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Brozek W, Clemens P, Ulmer H, Häring N, Concin H, Zitt E, Nagel G. Evaluation of a Population-Based Targeted Screening Approach for Skin Cancer with Long-Time Follow-Up in Austria including Potential Effects on Melanoma Mortality. Cancers (Basel) 2024; 16:1283. [PMID: 38610961 PMCID: PMC11011036 DOI: 10.3390/cancers16071283] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/26/2024] [Revised: 03/19/2024] [Accepted: 03/22/2024] [Indexed: 04/14/2024] Open
Abstract
BACKGROUND whether screening for skin cancer affects melanoma-specific mortality in a population-based setting remains unclear. METHODS in this population-based cohort study, we characterized and evaluated a skin cancer prevention program following a targeted screening approach conducted in 1989-1994 in the Austrian province Vorarlberg, with follow-up until 2019. The general population and attendees of a health examination program served for comparison. RESULTS in the screening program including full follow-up until 2019, 207 invasive and 187 in situ melanomas were identified in 8997 individuals. Incidences of invasive and in situ melanomas were elevated compared to the general population (IRR 2.92, 95%-CI 2.49-3.41, and IRR 4.13, 95%-CI 3.53-4.83, respectively) and the health examination program (HR 3.02, 95%-CI 2.59-3.52, and HR 3.90, 95%-CI 3.30-4.61, respectively). Breslow thickness and Clark's level at time of invasive diagnosis were significantly lower in 1989-2019, but the tumor characteristics of the melanomas diagnosed during 1989-1994 did not differ from the comparison groups. Moreover, melanoma mortality was significantly elevated in the screening program (IRR 1.66, 95%-CI 1.00-2.75 vs. the general population, HR 2.12, 95%-CI 1.25-3.61 vs. the health examination cohort). Melanoma mortality in Vorarlberg declined until 2004, though statistically non-significantly. CONCLUSIONS given the uncertain effectiveness and high public expenditures of population-wide mass screening programs, primary prevention and targeted risk-based skin cancer screening might be promising alternatives.
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Affiliation(s)
- Wolfgang Brozek
- Agency for Preventive and Social Medicine, 6900 Bregenz, Austria; (P.C.); (H.U.); (H.C.); (E.Z.); (G.N.)
| | - Patrick Clemens
- Agency for Preventive and Social Medicine, 6900 Bregenz, Austria; (P.C.); (H.U.); (H.C.); (E.Z.); (G.N.)
- Department of Radio-Oncology, Feldkirch Academic Teaching Hospital, 6800 Feldkirch, Austria
| | - Hanno Ulmer
- Agency for Preventive and Social Medicine, 6900 Bregenz, Austria; (P.C.); (H.U.); (H.C.); (E.Z.); (G.N.)
- Department of Medical Statistics, Informatics and Health Economics, Innsbruck Medical University, 6020 Innsbruck, Austria
| | - Nina Häring
- Department of Dermatology and Venerology, Feldkirch Academic Teaching Hospital, 6800 Feldkirch, Austria;
| | - Hans Concin
- Agency for Preventive and Social Medicine, 6900 Bregenz, Austria; (P.C.); (H.U.); (H.C.); (E.Z.); (G.N.)
| | - Emanuel Zitt
- Agency for Preventive and Social Medicine, 6900 Bregenz, Austria; (P.C.); (H.U.); (H.C.); (E.Z.); (G.N.)
- Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), 6800 Feldkirch, Austria
- Department of Internal Medicine 3 (Nephrology, Dialysis and Hypertension), Feldkirch Academic Teaching Hospital, 6800 Feldkirch, Austria
| | - Gabriele Nagel
- Agency for Preventive and Social Medicine, 6900 Bregenz, Austria; (P.C.); (H.U.); (H.C.); (E.Z.); (G.N.)
- Institute of Epidemiology and Medical Biometry, Ulm University, 89081 Ulm, Germany
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Saha A, Kolonin MG, DiGiovanni J. Obesity and prostate cancer - microenvironmental roles of adipose tissue. Nat Rev Urol 2023; 20:579-596. [PMID: 37198266 DOI: 10.1038/s41585-023-00764-9] [Citation(s) in RCA: 30] [Impact Index Per Article: 15.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 03/24/2023] [Indexed: 05/19/2023]
Abstract
Obesity is known to have important roles in driving prostate cancer aggressiveness and increased mortality. Multiple mechanisms have been postulated for these clinical observations, including effects of diet and lifestyle, systemic changes in energy balance and hormonal regulation and activation of signalling by growth factors and cytokines and other components of the immune system. Over the past decade, research on obesity has shifted towards investigating the role of peri-prostatic white adipose tissue as an important source of locally produced factors that stimulate prostate cancer progression. Cells that comprise white adipose tissue, the adipocytes and their progenitor adipose stromal cells (ASCs), which proliferate to accommodate white adipose tissue expansion in obesity, have been identified as important drivers of obesity-associated cancer progression. Accumulating evidence suggests that adipocytes are a source of lipids that are used by adjacent prostate cancer cells. However, results of preclinical studies indicate that ASCs promote tumour growth by remodelling extracellular matrix and supporting neovascularization, contributing to the recruitment of immunosuppressive cells, and inducing epithelial-mesenchymal transition through paracrine signalling. Because epithelial-mesenchymal transition is associated with cancer chemotherapy resistance and metastasis, ASCs are considered to be potential targets of therapies that could be developed to suppress cancer aggressiveness in patients with obesity.
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Affiliation(s)
- Achinto Saha
- Division of Pharmacology and Toxicology and Dell Paediatric Research Institute, The University of Texas at Austin, Austin, TX, USA
- Center for Molecular Carcinogenesis and Toxicology, The University of Texas at Austin, Austin, TX, USA
- Livestrong Cancer Institutes, Dell Medical School, The University of Texas at Austin, Austin, TX, USA
| | - Mikhail G Kolonin
- The Brown Foundation Institute of Molecular Medicine for the Prevention of Disease, The University of Texas Health Sciences Center at Houston, Houston, Texas, USA.
| | - John DiGiovanni
- Division of Pharmacology and Toxicology and Dell Paediatric Research Institute, The University of Texas at Austin, Austin, TX, USA.
- Center for Molecular Carcinogenesis and Toxicology, The University of Texas at Austin, Austin, TX, USA.
- Livestrong Cancer Institutes, Dell Medical School, The University of Texas at Austin, Austin, TX, USA.
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Arteaga DP, DeKraker C, Ennis M, Dewey N, Goebel EA, Welch S, Pimentel I, Ippolito JE, Lohmann AE. Body composition and endometrial cancer outcomes. J Natl Cancer Inst Monogr 2023; 2023:49-55. [PMID: 37139979 DOI: 10.1093/jncimonographs/lgad012] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/05/2022] [Revised: 02/24/2023] [Accepted: 03/06/2023] [Indexed: 05/05/2023] Open
Abstract
BACKGROUND Obesity is a known risk factor for developing endometrial cancer. However, the association of obesity with endometrial cancer (EC) outcomes has not been clearly established. This study examined how outcomes in women with early stage EC vary with body composition measured via computed tomography (CT). METHODS In this retrospective study, patients diagnosed with EC international Federation of Gynecology and Obstetrics stages I-III and available CT scans were included. Automatica software was used to assess the areas of visceral adipose tissue, subcutaneous adipose tissue (SAT), and intermuscular adipose tissue (IMAT) and skeletal muscle area. RESULTS Of 293 patient charts assessed, 199 met eligibility criteria. Median body mass index (BMI) was 32.8 kg/m2 (interquartile range [IQ] = 26.8-38.9); 61.8% had histologic subtype endometrioid carcinoma. Adjusted for age, international Federation of Gynecology and Obstetrics stage, and histologic subtype, a BMI of at least 30 vs less than 30 kg/m2 was associated with lower endometrial cancer-specific survival (ECSS) (hazard ratio [HR] = 2.32, 95% confidence interval [CI] = 1.27 to 4.25) and overall survival (OS) (HR = 2.7, 95% CI = 1.35 to 5.39). Higher IMAT 75th vs 25th percentile and SAT of at least 225.6 vs less than 225.6 cm2 were associated with lower ECSS (HR = 1.53, 95% CI = 1.1 to 2.13, and HR = 2.57, 95% CI = 1.13 to 5.88) and OS (HR = 1.50, 95% CI = 1.11 to 2.02, and HR = 2.46, 95% CI = 1.2 to 5.01), respectively. The association of visceral adipose tissue (75th vs 25th percentile) with ECSS and OS was not statistically significant (HR = 1.42, 95% CI = 0.91 to 2.22, and HR = 1.24, 95% CI = 0.81 to 1.89). CONCLUSION Higher BMI, IMAT, and SAT were associated with higher mortality from EC and lower OS. A better understanding of the mechanisms underlying these relationships could inform strategies to improve patient outcomes.
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Affiliation(s)
- Diana P Arteaga
- Department of Medicine, Schulich School of Medicine & Dentistry, Western University, London, ON, Canada
- Department of Oncology, Schulich School of Medicine & Dentistry, Western University, London, ON, Canada
| | - Corina DeKraker
- Department of Medicine, Schulich School of Medicine & Dentistry, Western University, London, ON, Canada
| | | | - Nicole Dewey
- Michener Institute of Education, University of Toronto, Toronto, ON, Canada
| | - Emily A Goebel
- Department of Medicine, Schulich School of Medicine & Dentistry, Western University, London, ON, Canada
- Department of Pathology and Laboratory Medicine, Schulich School of Medicine & Dentistry, Western University and London Health Science Centre, London, ON, Canada
| | - Stephen Welch
- Department of Medicine, Schulich School of Medicine & Dentistry, Western University, London, ON, Canada
- Department of Oncology, Schulich School of Medicine & Dentistry, Western University, London, ON, Canada
| | - Isabel Pimentel
- Department of Oncology, Vall d'Hebron Institute of Oncology (VHIO), Vall d'Hebron University Hospital, Barcelona, Catalonia, Spain
| | - Joseph E Ippolito
- Department of Radiology, Washington University School of Medicine, St Louis, MO, USA
| | - Ana Elisa Lohmann
- Department of Oncology, Schulich School of Medicine & Dentistry, Western University, London, ON, Canada
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4
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Sulu C, Bektas AB, Guzel SS, Tay K, Sahin S, Durcan E, Ozkaya HM, Kadioglu P. Effect of metformin on thyroid cancer risk in patients with acromegaly: A preliminary observational study. Growth Horm IGF Res 2022; 66:101484. [PMID: 35870256 DOI: 10.1016/j.ghir.2022.101484] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/19/2022] [Revised: 05/01/2022] [Accepted: 06/26/2022] [Indexed: 11/04/2022]
Abstract
PURPOSE To evaluate the role of metformin on thyroid cancer risk in patients with acromegaly. METHODS Medical charts of 534 patients with acromegaly that were followed-up between 1983 and 2019 were reviewed. Patients with follow-up duration at least 6 months were included. Cohort entry was defined as first visit date. The date of each case's thyroid cancer diagnosis was defined as index date. Patients were followed until the index date, death, or last visit date, whichever came first. Nested case-control study design was selected to evaluate the association between metformin and the thyroid cancer risk in patients with acromegaly. RESULTS 291 patients with acromegaly were included into final analysis. The mean age at acromegaly diagnosis was 42.3 ± 1.3 years. The median follow-up duration was 76 [34-132] months. Among 291 patients, 13 patients (4.5%) had thyroid cancer. Thirty-one percent (n = 92) of the patients used metformin for 6 months or longer. One standard deviation (SD) increase in average growth hormone increased the odds of having thyroid cancer by 1.164 folds (p = 0.017). One SD increase of the average insulin-like growth factor 1 to upper limit of normal ratio increased the odds of having thyroid cancer by 1.201 folds (p = 0.004). If a patient used metformin for at least 6 months, the odds to have thyroid cancer was decreased, multiplied by 0.62 with a 95% confidence interval of [0.47, 0.83] (p = 0.0013). The risk of thyroid cancer decreased with increasing duration of metformin use. CONCLUSION Metformin may decrease the thyroid cancer risk in patients with acromegaly.
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Affiliation(s)
- Cem Sulu
- Division of Endocrinology, Metabolism, and Diabetes-Department of Internal Medicine, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul 34098, Turkey
| | - Ayyuce Begum Bektas
- Graduate School of Sciences and Engineering, Koç University, Istanbul 34450, Turkey
| | - Suleyman Sami Guzel
- Department of Internal Medicine, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul 34098, Turkey
| | - Kubilay Tay
- Department of Internal Medicine, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul 34098, Turkey
| | - Serdar Sahin
- Division of Endocrinology, Metabolism, and Diabetes-Department of Internal Medicine, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul 34098, Turkey
| | - Emre Durcan
- Division of Endocrinology, Metabolism, and Diabetes-Department of Internal Medicine, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul 34098, Turkey
| | - Hande Mefkure Ozkaya
- Division of Endocrinology, Metabolism, and Diabetes-Department of Internal Medicine, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul 34098, Turkey
| | - Pinar Kadioglu
- Division of Endocrinology, Metabolism, and Diabetes-Department of Internal Medicine, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul 34098, Turkey.
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Alcala K, Mariosa D, Smith-Byrne K, Nasrollahzadeh Nesheli D, Carreras-Torres R, Ardanaz Aicua E, Bondonno NP, Bonet C, Brunström M, Bueno-de-Mesquita B, Chirlaque MD, Christakoudi S, Heath AK, Kaaks R, Katzke V, Krogh V, Ljungberg B, Martin RM, May A, Melander O, Palli D, Rodriguez-Barranco M, Sacerdote C, Stocks T, Tjønneland A, Travis RC, Vermeulen R, Chanock S, Purdue M, Weiderpass E, Muller D, Brennan P, Johansson M. The relationship between blood pressure and risk of renal cell carcinoma. Int J Epidemiol 2022; 51:1317-1327. [PMID: 35312764 PMCID: PMC9365619 DOI: 10.1093/ije/dyac042] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/12/2021] [Accepted: 03/07/2022] [Indexed: 11/23/2022] Open
Abstract
BACKGROUND The relation between blood pressure and kidney cancer risk is well established but complex and different study designs have reported discrepant findings on the relative importance of diastolic blood pressure (DBP) and systolic blood pressure (SBP). In this study, we sought to describe the temporal relation between diastolic and SBP with renal cell carcinoma (RCC) risk in detail. METHODS Our study involved two prospective cohorts: the European Prospective Investigation into Cancer and Nutrition study and UK Biobank, including >700 000 participants and 1692 incident RCC cases. Risk analyses were conducted using flexible parametric survival models for DBP and SBP both separately as well as with mutuality adjustment and then adjustment for extended risk factors. We also carried out univariable and multivariable Mendelian randomization (MR) analyses (DBP: ninstruments = 251, SBP: ninstruments = 213) to complement the analyses of measured DBP and SBP. RESULTS In the univariable analysis, we observed clear positive associations with RCC risk for both diastolic and SBP when measured ≥5 years before diagnosis and suggestive evidence for a stronger risk association in the year leading up to diagnosis. In mutually adjusted analysis, the long-term risk association of DBP remained, with a hazard ratio (HR) per standard deviation increment 10 years before diagnosis (HR10y) of 1.20 (95% CI: 1.10-1.30), whereas the association of SBP was attenuated (HR10y: 1.00, 95% CI: 0.91-1.10). In the complementary multivariable MR analysis, we observed an odds ratio for a 1-SD increment (ORsd) of 1.34 (95% CI: 1.08-1.67) for genetically predicted DBP and 0.70 (95% CI: 0.56-0.88) for genetically predicted SBP. CONCLUSION The results of this observational and MR study are consistent with an important role of DBP in RCC aetiology. The relation between SBP and RCC risk was less clear but does not appear to be independent of DBP.
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Affiliation(s)
- Karine Alcala
- International Agency for Research on Cancer (IARC/WHO), Genomic Epidemiology Branch, Lyon, France
| | - Daniela Mariosa
- International Agency for Research on Cancer (IARC/WHO), Genomic Epidemiology Branch, Lyon, France
| | - Karl Smith-Byrne
- Cancer Epidemiology Unit, Oxford Population Health, University of Oxford, Oxford, UK
| | | | - Robert Carreras-Torres
- Group of Digestive Diseases and Microbiota, Institut d'Investigació Biomèdica de Girona-IDIBGI, Salt, Spain
| | - Eva Ardanaz Aicua
- Navarra Public Health Institute, Pamplona, Spain
- idiSNA, Navarra Institute for Health Research, Pamplona, Spain
- CIBER in Epidemiology and Public Health (CIBERESP), Madrid, Spain
| | - Nicola P Bondonno
- Danish Cancer Society Research Center, Copenhagen, Denmark
- School of Biomedical Sciences, University of Western Australia, Royal Perth Hospital, Perth, Australia
- Institute for Nutrition Research, School of Medical and Health Sciences, Edith Cowan University, Perth, Australia
| | - Catalina Bonet
- Unit of Nutrition and Cancer, Catalan Institute of Oncology, ICO, Nutrition and Cancer Group, Bellvitge Biomedical Research Institute -(IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain
| | - Mattias Brunström
- Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden
| | - Bas Bueno-de-Mesquita
- Centre for Nutrition, Prevention and Health Services, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands
| | - María-Dolores Chirlaque
- CIBER in Epidemiology and Public Health (CIBERESP), Madrid, Spain
- Department of Epidemiology, Regional Health Council, IMIB-Arrixaca, Murcia University, Murcia, Spain
| | - Sofia Christakoudi
- Department of Epidemiology and Biostatistics, Imperial College London, Norfolk Place, St Mary’s Campus, London, UK
- MRC Centre for Transplantation, King's College London, London, UK
| | - Alicia K Heath
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK
| | - Rudolf Kaaks
- Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany
| | - Verena Katzke
- Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany
| | - Vittorio Krogh
- Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori di Milano, Milan, Italy
| | - Börje Ljungberg
- Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden
| | - Richard M Martin
- Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
| | - Anne May
- Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
| | - Olle Melander
- Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden
- Department of Emergency and Internal Medicine, Skåne University Hospital, Malmö, Sweden
| | - Domenico Palli
- Cancer Risk Factors and Life-Style Epidemiology Unit, Institute for Cancer Research, Prevention and Clinical Network (ISPRO), Florence, Italy
| | - Miguel Rodriguez-Barranco
- Escuela Andaluza de Salud Pública (EASP), Granada, Spain
- Instituto de Investigación Biosanitaria ibs. GRANADA, Granada, Spain
- Centro de Investigación Biomédica en Red de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain
| | - Carlotta Sacerdote
- Unit of Cancer Epidemiology, Città della Salute e della Scienza University-Hospital, Turin, Italy
| | - Tanja Stocks
- Department of Clinical Sciences Lund, Lund University, Lund, Sweden
| | - Anne Tjønneland
- Danish Cancer Society Research Center, Copenhagen, Denmark
- Department of Public Health, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - Ruth C Travis
- Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK
| | - Roel Vermeulen
- Institute for Risk Assessment Sciences (IRAS), Utrecht University, Utrecht, The Netherlands
| | - Stephen Chanock
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
| | - Mark Purdue
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
| | | | | | - Paul Brennan
- International Agency for Research on Cancer (IARC/WHO), Genomic Epidemiology Branch, Lyon, France
| | - Mattias Johansson
- International Agency for Research on Cancer (IARC/WHO), Genomic Epidemiology Branch, Lyon, France
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Bergantin LB. The Interactions among Hypertension, Cancer, and COVID-19: Perspectives from Ca2+/cAMP Signalling. Curr Cancer Drug Targets 2022; 22:351-360. [PMID: 35168520 DOI: 10.2174/1568009622666220215143805] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/09/2021] [Revised: 12/02/2021] [Accepted: 12/16/2021] [Indexed: 11/22/2022]
Abstract
BACKGROUND The hypothesis that hypertension is clinically associated with an enhanced risk for developing cancer has been highlighted. However, the working principles involved in this link are still under intensive discussion. A correlation among inflammation, hypertension, and cancer could accurately describe the clinical link between these diseases. In addition, a dyshomeostasis of Ca2+ has been considered as a topic involved in both cancer and hypertension and inflammation. There is a strong link between Ca2+ signalling, e.g. enhanced Ca2+ signals, and inflammatory outcomes. cAMP also modulates pro- and anti-inflammatory outcomes: pharmaceuticals, which increase intracellular cAMP levels, can decrease the production of proinflammatory mediators and enhance the production of anti-inflammatory outcomes. OBJECTIVE This article has discussed the participation of Ca2+/cAMP signalling in the clinical association among inflammation, hypertension, and an enhanced risk for the development of cancer. In addition, considering coronavirus disease 2019 (COVID-19) is a rapidly evolving field, this article also reviews recent reports about the role of Ca2+ channel blockers for restoring Ca2+ signalling disruption due to COVID-19, including the relationship among COVID-19, cancer, and hypertension. CONCLUSION Understanding the association among these diseases could expand current pharmacotherapy, including that involving Ca2+ channel blockers and pharmaceuticals which rise cAMP levels.
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Affiliation(s)
- Leandro Bueno Bergantin
- Department of Pharmacology - Universidade Federal de São Paulo - Escola Paulista de Medicina, Laboratory of Autonomic and Cardiovascular Pharmacology - 55 11 5576-4973, Rua Pedro de Toledo, 669 - Vila Clementino, São Paulo - SP, Brazil
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Abstract
Low birthweight has been related to an increased risk of adult cardiovascular disease (CVD). Transgenerational studies have been used to investigate likely mechanisms underlying this inverse association. However, previous studies mostly examined the association of offspring birthweight with CVD risk factors among parents. In this study, we investigated the association between offspring birthweight and individual CVD risk factors, an index of CVD risk factors, and education in their parents, aunts/uncles, and aunts'/uncles' partners. Birth data (Medical Birth Registry, Norway (MBRN) (1967-2012)) was linked to CVD risk factor data (the County Study, Age 40 Program, and Cohort Norway (CONOR)) for the parents, aunts/uncles, and their partners. For body mass index (BMI), resting heart rate (RHR), systolic blood pressure (SBP), total cholesterol (TC), triglycerides (TG), and a risk factor index, the associations were examined by linear regression. For smoking and education, they were examined by logistic regression. Low birthweight was associated with an unfavorable risk factor profile in all familial relationships. For each kg increase in birthweight, the mean risk factor index decreased by -0.14 units (-0.15, -0.13) in mothers, -0.11 (-0.12, -0.10) in fathers, and -0.02 (-0.05, -0.00) to -0.07 (-0.09, -0.06) in aunts/uncles and their partners. The association in mothers was stronger than fathers, but it was also stronger in aunts/uncles than their partners. Profound associations between birthweight and CVD risk factors in extended family members were observed that go beyond the expected genetic similarities in pedigrees, suggesting that mechanisms like environmental factors, assortative mating, and genetic nurturing may explain these associations.
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8
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Gudsoorkar P, Ruf R, Adnani H, Safdar K, Sparks MA. Onco-hypertension: An Emerging Specialty. Adv Chronic Kidney Dis 2021; 28:477-489.e1. [PMID: 35190114 DOI: 10.1053/j.ackd.2021.09.011] [Citation(s) in RCA: 9] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/17/2021] [Revised: 09/20/2021] [Accepted: 09/20/2021] [Indexed: 12/19/2022]
Abstract
Cancer is one of the leading causes of death worldwide. With the introduction of newer chemotherapeutic agents, targeted therapies, and immunotherapy, the prognosis and survival of patients with cancer has remarkably improved. As a result, patients are living longer and experiencing long-term cardiovascular complications. Hypertension is an important risk factor for cardiovascular diseases. Patients with malignancy have multiple etiologies of hypertension development, worsening, or association. This is because of the complex interplay between cancer type, chemotherapeutic agent, patient age, antihypertensive agent, and preexisting comorbidities in the etiology and pathogenesis of hypertension. Management of hypertension in patients with cancer requires accurate blood pressure measurement and considering factors such as adjuvant therapy and cancer-related pain. There are no set guidelines for management of hypertension in this unique cohort, and the therapy should be individualized based on the treatment guidelines for the general population. Onco-hypertension is an emerging subspeciality and entails a multidisciplinary approach between oncology, primary care physicians, nephrology, and cardiology.
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Wood AM, Jonsson H, Nagel G, Häggström C, Manjer J, Ulmer H, Engeland A, Zitt E, Jochems SHJ, Ghaderi S, Stattin P, Bjørge T, Stocks T. The Inverse Association of Body Mass Index with Lung Cancer: Exploring Residual Confounding, Metabolic Aberrations and Within-Person Variability in Smoking. Cancer Epidemiol Biomarkers Prev 2021; 30:1489-1497. [PMID: 34162656 DOI: 10.1158/1055-9965.epi-21-0058] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/14/2021] [Revised: 03/25/2021] [Accepted: 05/12/2021] [Indexed: 11/16/2022] Open
Abstract
BACKGROUND The inverse observational association between body mass index (BMI) and lung cancer risk remains unclear. We assessed whether the association is explained by metabolic aberrations, residual confounding, and within-person variability in smoking, and compared against other smoking-related cancers. METHODS We investigated the association between BMI, and its combination with a metabolic score (MS) of mid-blood pressure, glucose, and triglycerides, with lung cancer and other smoking-related cancers in 778,828 individuals. We used Cox regression, adjusted and corrected for within-person variability in smoking (status/pack-years), calculated from 600,201 measurements in 221,958 participants. RESULTS Over a median follow-up of 20 years, 20,242 smoking-related cancers (6,735 lung cancers) were recorded. Despite adjustment and correction for substantial within-person variability in smoking, BMI remained inversely associated with lung cancer [HR per standard deviation increase, 0.87 (95% confidence interval 0.85-0.89)]. Individuals with BMI less than 25 kg/m2 and high MS had the highest risk [HR 1.52 (1.44-1.60) vs. BMI ≥25 with low MS]. These associations were weaker and nonsignificant among nonsmokers. Similar associations were observed for head and neck cancers and esophageal squamous cell carcinoma, whereas for other smoking-related cancers, we generally observed positive associations with BMI. CONCLUSIONS The increased lung cancer risk with low BMI and high MS is unlikely due to residual confounding and within-person variability in smoking. However, similar results for other cancers strongly related to smoking suggest a remaining, unknown, effect of smoking. IMPACT Extensive smoking-adjustments may not capture all the effects of smoking on the relationship between obesity-related factors and risk of smoking-related cancers.
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Affiliation(s)
- Angela M Wood
- Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom.
| | - Håkan Jonsson
- Department of Radiation Sciences, Umeå University, Umeå, Sweden
| | - Gabriele Nagel
- Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany.,Agency for Preventive and Social Medicine, Bregenz, Austria
| | - Christel Häggström
- Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.,Department of Surgical Sciences, Uppsala University, Uppsala, Sweden
| | - Jonas Manjer
- Department of Surgery, Skåne University Hospital, Lund University, Malmö, Sweden
| | - Hanno Ulmer
- Department of Medical Statistics, Informatics and Health Economics, Innsbruck Medical University, Innsbruck, Austria
| | - Anders Engeland
- Department of Chronic Diseases and Ageing, Norwegian Institute of Public Health, Bergen, Norway.,Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway
| | - Emanuel Zitt
- Agency for Preventive and Social Medicine, Bregenz, Austria.,Department of Internal Medicine, Academic Teaching Hospital Feldkirch, Feldkirch, Austria
| | | | - Sara Ghaderi
- Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway
| | - Pär Stattin
- Department of Surgical Sciences, Uppsala University, Uppsala, Sweden
| | - Tone Bjørge
- Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway.,Cancer Registry of Norway, Oslo, Norway
| | - Tanja Stocks
- Department of Clinical Sciences Lund, Lund University, Lund, Sweden.
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10
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Bergantin LB. Diabetes and inflammatory diseases: An overview from the perspective of Ca 2+/3'-5'-cyclic adenosine monophosphate signaling. World J Diabetes 2021; 12:767-779. [PMID: 34168726 PMCID: PMC8192245 DOI: 10.4239/wjd.v12.i6.767] [Citation(s) in RCA: 13] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/02/2020] [Revised: 12/29/2020] [Accepted: 03/08/2021] [Indexed: 02/06/2023] Open
Abstract
A large amount of evidence has supported a clinical link between diabetes and inflammatory diseases, e.g., cancer, dementia, and hypertension. In addition, it is also suggested that dysregulations related to Ca2+ signaling could link these diseases, in addition to 3'-5'-cyclic adenosine monophosphate (cAMP) signaling pathways. Thus, revealing this interplay between diabetes and inflammatory diseases may provide novel insights into the pathogenesis of these diseases. Publications involving signaling pathways related to Ca2+ and cAMP, inflammation, diabetes, dementia, cancer, and hypertension (alone or combined) were collected by searching PubMed and EMBASE. Both signaling pathways, Ca2+ and cAMP signaling, control the release of neurotransmitters and hormones, in addition to neurodegeneration, and tumor growth. Furthermore, there is a clear relationship between Ca2+ signaling, e.g., increased Ca2+ signals, and inflammatory responses. cAMP also regulates pro- and anti-inflammatory responses. Due to the experience of our group in this field, this article discusses the role of Ca2+ and cAMP signaling in the correlation between diabetes and inflammatory diseases, including its pharmacological implications. As a novelty, this article also includes: (1) A timeline of the major events in Ca2+/cAMP signaling; and (2) As coronavirus disease 2019 (COVID-19) is an emerging and rapidly evolving situation, this article also discusses recent reports on the role of Ca2+ channel blockers for preventing Ca2+ signaling disruption due to COVID-19, including the correlation between COVID-19 and diabetes.
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11
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The Role of Visceral Obesity, Sarcopenia and Sarcopenic Obesity on Surgical Outcomes After Liver Resections for Colorectal Metastases. World J Surg 2021; 45:2218-2226. [PMID: 33842995 PMCID: PMC8154807 DOI: 10.1007/s00268-021-06073-9] [Citation(s) in RCA: 24] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 03/06/2021] [Indexed: 12/18/2022]
Abstract
Background The impact of body compositions on surgical results is controversially discussed. This study examined whether visceral obesity, sarcopenia or sarcopenic obesity influence the outcome after hepatic resections of synchronous colorectal liver metastases. Methods Ninety-four consecutive patients with primary hepatic resections of synchronous colorectal metastases were identified from a single center database between January 2013 and August 2018. Patient characteristics and 30-day morbidity were retrospectively analyzed. Body fat and skeletal muscle were calculated by planimetry from single-slice CT images at the level of L3. Results Fifty-nine patients (62.8%) underwent minor hepatectomies, and 35 patients underwent major resections (37.2%). Postoperative complications occurred in 60 patients (62.8%) including 35 patients with major complications (Clavien–Dindo grade III–V). The mortality was nil at 30 days and 2.1% at 90 days. The body mass index showed no influence on postoperative outcomes (p = 1.0). Visceral obesity was found in 66 patients (70.2%) and was significantly associated with overall and major complication rates (p = .002, p = .012, respectively). Sarcopenia was observed in 34 patients (36.2%) without a significant impact on morbidity (p = .461), however, with longer hospital stay. Sarcopenic obesity was found in 18 patients (19.1%) and was significantly associated with postoperative complications (p = .014). Visceral obesity, sarcopenia and sarcopenic obesity were all identified as significant risk factors for overall postoperative complications. Conclusion Visceral obesity, sarcopenic obesity and sarcopenia are independent risk factors for overall complications after resections of CRLM. Early recognition of extremes in body compositions could prompt to perioperative interventions and thus improve postoperative outcomes.
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12
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Nagel G, Bjørge T, Jaensch A, Peter RS, Häggström C, Lang A, Engeland A, Teleka S, Jirström K, Lindquist D, Stattin P, Ulmer H, Concin H, Stocks T. Metabolic factors and the risk of small intestine cancers: Pooled study of 800 000 individuals in the metabolic syndrome and cancer project. Int J Cancer 2021; 149:66-74. [PMID: 33634882 DOI: 10.1002/ijc.33530] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/16/2020] [Revised: 01/25/2021] [Accepted: 02/08/2021] [Indexed: 01/06/2023]
Abstract
To explore the largely unknown etiology of small intestine cancer, we examined metabolic factors and risk of small intestine cancer overall and by subtypes. Among 404 220 women and 403 265 men in six European cohorts, we applied Cox regression with adjustment for smoking and body mass index (BMI), to calculate sex-specific hazard ratios (HRs) of small intestine cancer by levels of BMI, mean arterial pressure (MAP) and plasma total cholesterol, triglycerides and glucose. We also calculated HRs for these factors combined (metabolic score; MetS) and used Wald test statistics to investigate pairwise interactions between metabolic factors on risk. We also performed analyses separately per subtype (neuroendocrine tumors [NETs] and adenocarcinomas). During a median follow-up of 16.9 years, 144 women and 195 men were diagnosed with small intestine cancer, including 184 NETs and 99 adenocarcinomas. Among men, no main associations or interactions between metabolic factors were observed in relation to the risk of small intestine cancer. Among women, triglycerides were positively and linearly associated with risk (HR per standard deviation [SD]: 1.23, 95% confidence interval [CI]: 1.04-1.46), and a positive association was also observed for the MetS (HR per SD: 1.25, 95% CI: 1.02-1.52). Positive interactions were observed among women between triglycerides and cholesterol (P = .0005), and between MAP and glucose (P = .009), on risk. Glucose was positively associated with adenocarcinomas among women. This large, prospective study suggests that elevated triglycerides, and metabolic factors in interaction, confer an increased risk of small intestine cancer among women, but not among men.
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Affiliation(s)
- Gabriele Nagel
- Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany.,Agency for Preventive and Social Medicine (aks), Bregenz, Austria
| | - Tone Bjørge
- Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway.,Cancer Registry of Norway, Oslo, Norway
| | - Andrea Jaensch
- Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany
| | - Raphael S Peter
- Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany
| | - Christel Häggström
- Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.,Department of Surgical Sciences, Uppsala University, Uppsala, Sweden
| | - Alois Lang
- Agency for Preventive and Social Medicine (aks), Bregenz, Austria
| | - Anders Engeland
- Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway.,Division of Mental and Physical Health, Norwegian Institute of Public Health, Bergen, Norway
| | - Stanley Teleka
- Department of Clinical Sciences Lund, Lund University, Lund, Sweden
| | - Karin Jirström
- Department of Clinical Sciences Lund, Lund University, Lund, Sweden
| | - David Lindquist
- Department of Clinical Sciences, Umeå University, Umeå, Sweden
| | - Pär Stattin
- Department of Surgical Sciences, Uppsala University, Uppsala, Sweden
| | - Hanno Ulmer
- Department of Medical Statistics, Informatics and Health Economics, Medical University of Innsbruck, Innsbruck, Austria
| | - Hans Concin
- Agency for Preventive and Social Medicine (aks), Bregenz, Austria
| | - Tanja Stocks
- Department of Clinical Sciences Lund, Lund University, Lund, Sweden
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13
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Teleka S, Jochems SHJ, Häggström C, Wood AM, Järvholm B, Orho‐Melander M, Liedberg F, Stocks T. Association between blood pressure and BMI with bladder cancer risk and mortality in 340,000 men in three Swedish cohorts. Cancer Med 2021; 10:1431-1438. [PMID: 33455057 PMCID: PMC7926028 DOI: 10.1002/cam4.3721] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/08/2020] [Revised: 12/22/2020] [Accepted: 12/24/2020] [Indexed: 12/13/2022] Open
Abstract
BACKGROUND The relation between obesity, blood pressure (BP) and bladder cancer (BC) risk and mortality remains unclear, partially due to potential confounding by smoking, the strongest risk factor for BC, and not accounting for tumor stage and grade in such studies. We investigated body mass index (BMI) and BP in relation to BC risk by stage and grade, and BC-specific mortality, including separately among never-smokers aimed at minimizing confounding by smoking. METHODS We analyzed 338,910 men from three Swedish cohorts, with 4895 incident BC's (940 among never-smokers) during follow-up. Cox regression was used to calculate hazard ratios (HR) and 95% confidence intervals adjusted for smoking status. HRs for BMI and BP were corrected for their regression dilution ratios, calculated from 280,456 individuals with 758,641 observations. RESULTS Body mass index was positively associated with non-muscle invasive BC (NMIBC, HR per 5 kg/m2 , 1.10 [1.02-1.19]) and NMIBC grade 3 (HR 1.17 [1.01-1.34]) in the full cohort, with similar effect sizes, albeit non-significant, among never-smokers. Systolic BP was positively associated with muscle-invasive BC (MIBC, HR per 10 mmHg, 1.25 [1.00-1.55]) and BC-specific mortality (HR 1.10 [1.01-1.20]) among never-smokers, with weaker and non-significant associations in the full cohort. CONCLUSIONS In an analyses of BMI, BP and BC risk by stage and grade among men, we found modest positive associations between BMI and NMIBC and NMIBC grade 3. SBP was positively associated with MIBC and BC-specific mortality in an analysis of never-smokers, which may reflect the association, un-confounded by smoking, also in a broader population.
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Affiliation(s)
- Stanley Teleka
- Department of Clinical Sciences in LundLund UniversityLundSweden
| | | | - Christel Häggström
- Department of Biobank ResearchUmeå UniversityUmeåSweden
- Department of Surgical SciencesUppsala UniversityUppsalaSweden
| | - Angela M. Wood
- MRC/BHF Cardiovascular Epidemiology UnitDepartment of Public Health and Primary CareUniversity of CambridgeCambridgeUK
| | - Bengt Järvholm
- Department of Public Health and Clinical MedicineUmeå UniversityUmeåSweden
| | | | - Fredrik Liedberg
- Division of Urological ResearchInstitution of Translational MedicineLund UniversityMalmöSweden
- Department of UrologySkåne University HospitalSkåneSweden
| | - Tanja Stocks
- Department of Clinical Sciences in LundLund UniversityLundSweden
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14
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Fritz J, Bjørge T, Nagel G, Manjer J, Engeland A, Häggström C, Concin H, Teleka S, Tretli S, Gylling B, Lang A, Stattin P, Stocks T, Ulmer H. The triglyceride-glucose index as a measure of insulin resistance and risk of obesity-related cancers. Int J Epidemiol 2020; 49:193-204. [PMID: 30945727 DOI: 10.1093/ije/dyz053] [Citation(s) in RCA: 61] [Impact Index Per Article: 12.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 03/11/2019] [Indexed: 01/19/2023] Open
Abstract
BACKGROUND The role of insulin resistance as a mediator in the association of body mass index (BMI) with site-specific cancer risk has, to our knowledge, never been systematically quantified. METHODS Altogether 510 471 individuals from six European cohorts, with a mean age of 43.1 years, were included. We used the triglyceride glucose product (TyG index) as a surrogate measure for insulin resistance. We fitted Cox models, adjusted for relevant confounders, to investigate associations of TyG index with 10 common obesity-related cancers, and quantified the proportion of the effect of BMI mediated through TyG index on the log-transformed hazard ratio (HR) scale. RESULTS During a median follow-up of 17.2 years, 16 052 individuals developed obesity-related cancers. TyG index was associated with the risk of cancers of the kidney HR per one standard deviation increase 1.13, 95% confidence interval: 1.07 to 1.20], liver (1.13, 1.04 to 1.23), pancreas (1.12, 1.06 to 1.19), colon (1.07, 1.03 to 1.10) and rectum (1.09, 1.04 to 1.14). Substantial proportions of the effect of BMI were mediated by TyG index for cancers of the pancreas (42%), rectum (34%) and colon (20%); smaller proportions for kidney (15%) and liver (11%). Little or no mediation was observed for breast (postmenopausal), endometrial and ovarian cancer. Results were similar for males and females, except for pancreatic cancer where the proportions mediated were 20% and 91%, respectively. CONCLUSIONS The TyG index was associated with increased risk of cancers of the digestive system and substantially mediated the effect of BMI, suggesting that insulin resistance plays a promoting role in the pathogenesis of gastrointestinal cancers.
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Affiliation(s)
- Josef Fritz
- Department of Medical Statistics, Informatics and Health Economics, Medical University of Innsbruck, Innsbruck, Austria
| | - Tone Bjørge
- Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway.,Cancer Registry of Norway, Oslo, Norway
| | - Gabriele Nagel
- Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany.,Agency for Preventive and Social Medicine, Bregenz (aks), Austria
| | - Jonas Manjer
- Department of Surgery, Skåne University Hospital, Lund University, Malmö, Sweden
| | - Anders Engeland
- Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway.,Division of Mental and Physical Health, Norwegian Institute of Public Health, Bergen, Norway
| | - Christel Häggström
- Department of Biobank Research, Umeå University, Umeå, Sweden.,Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.,Department of Public Health and Clinical Medicine, Nutritional Research, Umeå University, Umeå, Sweden
| | - Hans Concin
- Agency for Preventive and Social Medicine, Bregenz (aks), Austria
| | - Stanley Teleka
- Department of Clinical Sciences Lund, Lund University, Lund, Sweden
| | | | - Björn Gylling
- Department of Medical Biosciences, Pathology, Umeå University, Umeå, Sweden
| | - Alois Lang
- Agency for Preventive and Social Medicine, Bregenz (aks), Austria
| | - Pär Stattin
- Department of Surgical Sciences, Uppsala University, Uppsala, Sweden
| | - Tanja Stocks
- Department of Clinical Sciences Lund, Lund University, Lund, Sweden
| | - Hanno Ulmer
- Department of Medical Statistics, Informatics and Health Economics, Medical University of Innsbruck, Innsbruck, Austria
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15
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Christakoudi S, Kakourou A, Markozannes G, Tzoulaki I, Weiderpass E, Brennan P, Gunter M, Dahm CC, Overvad K, Olsen A, Tjønneland A, Boutron-Ruault MC, Madika AL, Severi G, Katzke V, Kühn T, Bergmann MM, Boeing H, Karakatsani A, Martimianaki G, Thriskos P, Masala G, Sieri S, Panico S, Tumino R, Ricceri F, Agudo A, Redondo-Sánchez D, Colorado-Yohar SM, Mokoroa O, Melander O, Stocks T, Häggström C, Harlid S, Bueno-de-Mesquita B, van Gils CH, Vermeulen RC, Khaw KT, Wareham NJ, Tong TY, Freisling H, Johansson M, Lennon H, Aune D, Riboli E, Trichopoulos D, Trichopoulou A, Tsilidis KK. Blood pressure and risk of cancer in the European Prospective Investigation into Cancer and Nutrition. Int J Cancer 2020; 146:2680-2693. [PMID: 31319002 PMCID: PMC7115826 DOI: 10.1002/ijc.32576] [Citation(s) in RCA: 46] [Impact Index Per Article: 9.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/11/2019] [Revised: 05/23/2019] [Accepted: 06/14/2019] [Indexed: 12/19/2022]
Abstract
Several studies have reported associations of hypertension with cancer, but not all results were conclusive. We examined the association of systolic (SBP) and diastolic (DBP) blood pressure with the development of incident cancer at all anatomical sites in the European Prospective Investigation into Cancer and Nutrition (EPIC). Hazard ratios (HRs) (95% confidence intervals) were estimated using multivariable Cox proportional hazards models, stratified by EPIC-participating center and age at recruitment, and adjusted for sex, education, smoking, body mass index, physical activity, diabetes and dietary (in women also reproductive) factors. The study included 307,318 men and women, with an average follow-up of 13.7 (standard deviation 4.4) years and 39,298 incident cancers. We confirmed the expected positive association with renal cell carcinoma: HR = 1.12 (1.08-1.17) per 10 mm Hg higher SBP and HR = 1.23 (1.14-1.32) for DBP. We additionally found positive associations for esophageal squamous cell carcinoma (SCC): HR = 1.16 (1.07-1.26) (SBP), HR = 1.31 (1.13-1.51) (DBP), weaker for head and neck cancers: HR = 1.08 (1.04-1.12) (SBP), HR = 1.09 (1.01-1.17) (DBP) and, similarly, for skin SCC, colon cancer, postmenopausal breast cancer and uterine adenocarcinoma (AC), but not for esophageal AC, lung SCC, lung AC or uterine endometroid cancer. We observed weak inverse associations of SBP with cervical SCC: HR = 0.91 (0.82-1.00) and lymphomas: HR = 0.97 (0.93-1.00). There were no consistent associations with cancers in other locations. Our results are largely compatible with published studies and support weak associations of blood pressure with cancers in specific locations and morphologies.
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Affiliation(s)
- Sofia Christakoudi
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary’s Campus, Norfolk place, London W2 1PG, United Kingdom
- MRC Centre for Transplantation, King’s College London, Great Maze Pond, London SE1 9RT, United Kingdom
| | - Artemisia Kakourou
- Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Ioannina, Greece
| | - Georgios Markozannes
- Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Ioannina, Greece
| | - Ioanna Tzoulaki
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary’s Campus, Norfolk place, London W2 1PG, United Kingdom
- Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Ioannina, Greece
| | - Elisabete Weiderpass
- International Agency for Research on Cancer, World Health Organization, 69372 Lyon CEDEX 08, France
| | - Paul Brennan
- International Agency for Research on Cancer, World Health Organization, 69372 Lyon CEDEX 08, France
| | - Marc Gunter
- International Agency for Research on Cancer, World Health Organization, 69372 Lyon CEDEX 08, France
| | - Christina C. Dahm
- Department of Public Health, Aarhus University, DK-8000, Aarhus, Denmark
| | - Kim Overvad
- Department of Public Health, Aarhus University, DK-8000, Aarhus, Denmark
- Department of Cardiology, Aalborg University Hospital, Aalborg, Denmark
| | - Anja Olsen
- Diet, Genes and Environment, Danish Cancer Society Research Center, DK-2100, Copenhagen, Denmark
| | - Anne Tjønneland
- Diet, Genes and Environment, Danish Cancer Society Research Center, DK-2100, Copenhagen, Denmark
- Department of Public Health, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - Marie-Christine Boutron-Ruault
- Centre de recherche en Epidemiologie et Sante des Populations (CESP), Fac. de médecine - Univ. Paris-Sud, Fac. de médecine - UVSQ, INSERM, Université Paris-Saclay, 94805, Villejuif, France
- Gustave Roussy, F-94805, Villejuif, France
| | - Anne-Laure Madika
- Centre de recherche en Epidemiologie et Sante des Populations (CESP), Fac. de médecine - Univ. Paris-Sud, Fac. de médecine - UVSQ, INSERM, Université Paris-Saclay, 94805, Villejuif, France
- Gustave Roussy, F-94805, Villejuif, France
- Université Lille, CHU Lille, EA2694, Lille, France
| | - Gianluca Severi
- Centre de recherche en Epidemiologie et Sante des Populations (CESP), Fac. de médecine - Univ. Paris-Sud, Fac. de médecine - UVSQ, INSERM, Université Paris-Saclay, 94805, Villejuif, France
- Gustave Roussy, F-94805, Villejuif, France
| | - Verena Katzke
- Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany
| | - Tilman Kühn
- Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany
| | - Manuela M. Bergmann
- Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE), Arthur-Scheunert-Allee 114-116, Nuthetal, Germany
| | - Heiner Boeing
- Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE), Arthur-Scheunert-Allee 114-116, Nuthetal, Germany
| | - Anna Karakatsani
- Hellenic Health Foundation, Athens, Greece
- 2 Pulmonary Medicine Department, School of Medicine, National and Kapodistrian University of Athens, “ATTIKON” University Hospital, Haidari, Greece
| | | | | | - Giovanna Masala
- Cancer Risk Factors and Life-Style Epidemiology Unit, Institute for Cancer Research, Prevention and Clinical Network - ISPRO, Florence, Italy
| | - Sabina Sieri
- Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori di Milano, 20133, Milano, Italy
| | - Salvatore Panico
- Dipartimento di Medicina Clinica e Chirurgia, Federico II University, Naples, Italy
| | - Rosario Tumino
- Cancer Registry and Histopathology Department, "M.P.Arezzo" Hospital, ASP Ragusa, Italy
| | - Fulvio Ricceri
- Department of Clinical and Biological Sciences, University of Turin, Italy
- Unit of Epidemiology, Regional Health Service ASL TO3, Grugliasco (TO), Italy
| | - Antonio Agudo
- Unit of Nutrition and Cancer. Cancer Epidemiology Research Program. Catalan Institute of Oncology-IDIBELL. L’Hospitalet de Llobregat, Barcelona, Spain
| | - Daniel Redondo-Sánchez
- Escuela Andaluza de Salud Pública. Instituto de Investigación Biosanitaria ibs.GRANADA, Universidad de Granada. Granada, Spain
- CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain
| | - Sandra M. Colorado-Yohar
- CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain
- Department of Epidemiology, Murcia Regional Health Council, IMIB-Arrixaca, Murcia, Spain
- Research Group on Demography and Health, National Faculty of Public Health, University of Antioquia, Medellín, Colombia
| | - Olatz Mokoroa
- Public Health Division of Gipuzkoa, BioDonostia Research Institute, San Sebastian, Spain
| | - Olle Melander
- Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden
| | - Tanja Stocks
- Department of Clinical Sciences Lund, Lund University, Lund, Sweden
| | - Christel Häggström
- Department of Biobank Research, Umeå University, Umeå, Sweden
- Department of Surgical Sciences, Uppsala University, Uppsala, Sweden
| | - Sophia Harlid
- Department of Radiation Sciences, Umeå University, Umeå, Sweden
| | - Bas Bueno-de-Mesquita
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary’s Campus, Norfolk place, London W2 1PG, United Kingdom
- Dept. for Determinants of Chronic Diseases (DCD), National Institute for Public Health and the Environment (RIVM), PO Box 1, 3720 BA Bilthoven, The Netherlands
- Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, The Netherlands
- Dept. of Social & Preventive Medicine, Faculty of Medicine, University of Malaya, Pantai Valley, 50603, Kuala Lumpur, Malaysia
| | - Carla H. van Gils
- Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, The Netherlands
| | - Roel C.H. Vermeulen
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary’s Campus, Norfolk place, London W2 1PG, United Kingdom
- Environmental Epidemiology Group, Institute of Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands
- Public Health Department, University Medical Center, Utrecht, The Netherlands
| | - Kay-Tee Khaw
- University of Cambridge, School of Clinical Medicine, Addenbrooke’s Hospital, Cambridge CB2 2QQ, United Kingdom
| | - Nicholas J. Wareham
- MRC Epidemiology Unit, Institute of Metabolic Science, School of Clinical Medicine, University of Cambridge, Cambridge CB2 0QQ, United Kingdom
| | - Tammy Y.N. Tong
- Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford. United Kingdom
| | - Heinz Freisling
- International Agency for Research on Cancer, World Health Organization, 69372 Lyon CEDEX 08, France
| | - Mattias Johansson
- International Agency for Research on Cancer, World Health Organization, 69372 Lyon CEDEX 08, France
| | - Hannah Lennon
- International Agency for Research on Cancer, World Health Organization, 69372 Lyon CEDEX 08, France
| | - Dagfinn Aune
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary’s Campus, Norfolk place, London W2 1PG, United Kingdom
- Department of Nutrition, Bjørknes University College, Oslo, Norway
- Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Oslo, Norway
| | - Elio Riboli
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary’s Campus, Norfolk place, London W2 1PG, United Kingdom
| | - Dimitrios Trichopoulos
- Hellenic Health Foundation, Athens, Greece
- Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA
- Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece
| | | | - Konstantinos K. Tsilidis
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary’s Campus, Norfolk place, London W2 1PG, United Kingdom
- Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Ioannina, Greece
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16
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Hektoen HH, Robsahm TE, Andreassen BK, Stenehjem JS, Axcrona K, Mondul A, Gislefoss RE. Lifestyle associated factors and risk of urinary bladder cancer: A prospective cohort study from Norway. Cancer Med 2020; 9:4420-4432. [PMID: 32319230 PMCID: PMC7300409 DOI: 10.1002/cam4.3060] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/13/2020] [Revised: 03/27/2020] [Accepted: 03/27/2020] [Indexed: 12/24/2022] Open
Abstract
A number of lifestyle associated factors, such as high body mass index (BMI), low physical activity, and related metabolic disorders, are associated with increased risk of cancer at several sites. For urinary bladder cancer (BC), such studies show inconsistent results, which could result from inadequate adjustment for smoking and occupational exposure. In the population‐based Janus Cohort (n = 292 851), we investigated the independent and combined impact of BMI, physical activity, blood pressure, and blood lipids on the risk of BC, by thorough adjustment for smoking and potential occupational exposure. We used cox proportional hazard regression to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) for the associations between the lifestyle associated factors and BC risk. The associations observed were dependent on smoking status and gender. Among men, diastolic blood pressure (DBP) (HR 1.07, 95% CI 1.02‐1.12) and systolic blood pressure (SBP) (HR 1.04, 95% CI 1.01‐1.07) were positively associated with BC risk. Stratification by smoking status revealed a positive association between DBP and BC risk in never smokers (HR 1.14, 95% CI 1.00‐1.30), while no association was seen for current and former smokers. A risk score, integrating information across the lifestyle factors was positively associated with BC risk in men (ptrend = 0.043). In women, physical activity was associated with a decreased BC risk, but only among never smokers (HR 0.65, 95% CI 0.45‐0.94). In conclusion, relations between lifestyle associated factors and BC risk were most evident in never smokers, suggesting that smoking dominates the relation in current smokers.
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Affiliation(s)
- Helga H Hektoen
- Department of Research, Cancer Registry of Norway, Oslo, Norway
| | - Trude E Robsahm
- Department of Research, Cancer Registry of Norway, Oslo, Norway
| | | | - Jo S Stenehjem
- Department of Research, Cancer Registry of Norway, Oslo, Norway.,Department of Biostatistics, Oslo Centre for Biostatistics and Epidemiology, University of Oslo, Oslo, Norway
| | - Karol Axcrona
- Department of Urology, Akershus University Hospital, Lørenskog, Norway
| | - Alison Mondul
- School of Public Health, University of Michigan, Ann Arbor, MI, USA
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17
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Dominic E, Brozek W, Peter RS, Fromm E, Ulmer H, Rapp K, Concin H, Nagel G. Metabolic factors and hip fracture risk in a large Austrian cohort study. Bone Rep 2020; 12:100244. [PMID: 31970265 PMCID: PMC6965713 DOI: 10.1016/j.bonr.2020.100244] [Citation(s) in RCA: 20] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/12/2019] [Revised: 01/07/2020] [Accepted: 01/10/2020] [Indexed: 12/11/2022] Open
Abstract
To explore the association of incident hip fractures with metabolic syndrome (MetS) and its single components, we designed a prospective cohort study of hip fracture incidence among 117,053 participants of a population-based health surveillance program in Vorarlberg, the westernmost Austrian province. Incident hip fractures were recorded between 5 and 10 years after inclusion at baseline from 2003 to 2009. Applying Cox proportional hazard models for each MetS component and for a composite z-score for MetS, hazards for fracture were estimated in quintiles, as continuous z-score variables, and as pathological cut off values. Mean age was 50.1 ± 15.6 years at baseline, 5-10 years after which 947 incident hip fractures occurred. An association of a higher composite MetS score with decreased hip fracture risk was observed in women (HR 0.80, 95%-CI 0.88-0.96, p < 0.01) which disappeared upon adjustment for BMI. BMI was inversely associated with hip fracture risk in women and men (HR for the highest compared with the lowest quintile: 0.83 (95%-CI: 0.63-1.10, p trend < 0.05) and 0.55 (95%-CI: 0.38-0.79, p trend < 0.001), respectively). Only in women, hip fracture risk was reduced at high cholesterol levels (HR for the highest relative to the lowest quintile: 0.64, 95%-CI: 0.48-0.84, p trend < 0.05) and in hypercholesterolemic patients (HR 0.82, 95%-CI: 0.67-0.99, p < 0.05), but elevated in hyperglycemic patients (HR 1.33, 95%-CI: 1.05-1.70, p < 0.05). Hypertriglyceridemia was associated with increased male hip fracture risk (HR 1.33, 95%-CI: 1.03-1.72, p < 0.05). The inverse association between the MetS and hip fracture risk is mainly driven by one single component, namely BMI.
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Affiliation(s)
- Erlangga Dominic
- Agency for Preventive and Social Medicine, Rheinstr. 61, 6900 Bregenz, Austria
| | - Wolfgang Brozek
- Agency for Preventive and Social Medicine, Rheinstr. 61, 6900 Bregenz, Austria
| | - Raphael Simon Peter
- Institute of Epidemiology and Medical Biometry, Ulm University, Helmholtzstr. 22, 89081 Ulm, Germany
| | - Ella Fromm
- Institute of Epidemiology and Medical Biometry, Ulm University, Helmholtzstr. 22, 89081 Ulm, Germany
| | - Hanno Ulmer
- Agency for Preventive and Social Medicine, Rheinstr. 61, 6900 Bregenz, Austria.,Department of Medical Statistics, Informatics and Health Economics, Innsbruck Medical University, Schöpfstr. 41/1, 6020 Innsbruck, Austria
| | - Kilian Rapp
- Clinic for Geriatric Rehabilitation, Robert-Bosch Hospital, Auerbachstr. 110, 70376 Stuttgart, Germany
| | - Hans Concin
- Agency for Preventive and Social Medicine, Rheinstr. 61, 6900 Bregenz, Austria
| | - Gabriele Nagel
- Agency for Preventive and Social Medicine, Rheinstr. 61, 6900 Bregenz, Austria.,Institute of Epidemiology and Medical Biometry, Ulm University, Helmholtzstr. 22, 89081 Ulm, Germany
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18
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Hansen MS, Licaj I, Braaten T, Langhammer A, Le Marchand L, Gram IT. Smoking related lung cancer mortality by education and sex in Norway. BMC Cancer 2019; 19:1132. [PMID: 31752755 PMCID: PMC6873553 DOI: 10.1186/s12885-019-6330-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/11/2019] [Accepted: 11/04/2019] [Indexed: 12/03/2022] Open
Affiliation(s)
- Merethe S Hansen
- Department of Community Medicine, Faculty of Health Sciences, The UiT Arctic University of Norway, Tromsø, Norway.
| | - Idlir Licaj
- Department of Community Medicine, Faculty of Health Sciences, The UiT Arctic University of Norway, Tromsø, Norway.,Clinical Research Department, Centre François Baclesse, Caen, France
| | - Tonje Braaten
- Department of Community Medicine, Faculty of Health Sciences, The UiT Arctic University of Norway, Tromsø, Norway
| | - Arnulf Langhammer
- Department of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, Trondheim, Norway
| | - Loic Le Marchand
- Cancer Epidemiology Program, University of Hawai`i Cancer Center-University of Hawai`i at Manoa, Honolulu, HI, USA
| | - Inger Torhild Gram
- Department of Community Medicine, Faculty of Health Sciences, The UiT Arctic University of Norway, Tromsø, Norway
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19
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Bjørge T, Häggström C, Ghaderi S, Nagel G, Manjer J, Tretli S, Ulmer H, Harlid S, Rosendahl AH, Lang A, Stattin P, Stocks T, Engeland A. BMI and weight changes and risk of obesity-related cancers: a pooled European cohort study. Int J Epidemiol 2019; 48:1872-1885. [DOI: 10.1093/ije/dyz188] [Citation(s) in RCA: 33] [Impact Index Per Article: 5.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 08/28/2019] [Indexed: 01/21/2023] Open
Abstract
Abstract
Background
Obesity is an established risk factor for several cancers. Adult weight gain has been associated with increased cancer risk, but studies on timing and duration of adult weight gain are relatively scarce. We examined the impact of BMI (body mass index) and weight changes over time, as well as the timing and duration of excess weight, on obesity- and non-obesity-related cancers.
Methods
We pooled health data from six European cohorts and included 221 274 individuals with two or more height and weight measurements during 1972–2014. Several BMI and weight measures were constructed. Cancer cases were identified through linkage with national cancer registries. Hazard ratios (HRs) of cancer with 95% confidence intervals (CIs) were derived from time-dependent Cox-regression models.
Results
During follow-up, 27 881 cancer cases were diagnosed; 9761 were obesity-related. The HR of all obesity-related cancers increased with increasing BMI at first and last measurement, maximum BMI and longer duration of overweight (men only) and obesity. Participants who were overweight before age 40 years had an HR of obesity-related cancers of 1.16 (95% CI 1.02, 1.32) and 1.15 (95% CI 1.04, 1.27) in men and women, respectively, compared with those who were not overweight. The risk increase was particularly high for endometrial (70%), male renal-cell (58%) and male colon cancer (29%). No positive associations were seen for cancers not regarded as obesity-related.
Conclusions
Adult weight gain was associated with increased risk of several major cancers. The degree, timing and duration of overweight and obesity also seemed to be important. Preventing weight gain may reduce the cancer risk.
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Affiliation(s)
- Tone Bjørge
- Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway
- Cancer Registry of Norway, Oslo, Norway
| | - Christel Häggström
- Department of Biobank Research, Umeå University, Umeå, Sweden
- Department of Surgical Sciences, Uppsala University, Uppsala, Sweden
- Department of Public Health and Clinical Medicine, Nutritional Research, Umeå University, Umeå, Sweden
| | - Sara Ghaderi
- Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway
| | - Gabriele Nagel
- Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany
- Agency for Preventive and Social Medicine, Bregenz (aks), Austria
| | - Jonas Manjer
- Department of Surgery, Skåne University Hospital, Lund University, Malmö, Sweden
| | | | - Hanno Ulmer
- Department of Medical Statistics, Informatics and Health Economics, Innsbruck Medical University, Innsbruck, Austria
| | - Sophia Harlid
- Department of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden
| | - Ann H Rosendahl
- Department of Clinical Sciences Lund, Lund University, Lund, Sweden
| | - Alois Lang
- Agency for Preventive and Social Medicine, Bregenz (aks), Austria
| | - Pär Stattin
- Department of Surgical Sciences, Uppsala University, Uppsala, Sweden
| | - Tanja Stocks
- Department of Clinical Sciences Lund, Lund University, Lund, Sweden
| | - Anders Engeland
- Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway
- Division of Mental and Physical Health, Norwegian Institute of Public Health, Bergen, Norway
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20
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Häggström C, Jonsson H, Bjørge T, Nagel G, Manjer J, Ulmer H, Drake I, Ghaderi S, Lang A, Engeland A, Stattin P, Stocks T. Linear age‐course effects on the associations between body mass index, triglycerides, and female breast and male liver cancer risk: An internal replication study of 800,000 individuals. Int J Cancer 2019; 146:58-67. [DOI: 10.1002/ijc.32240] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/02/2018] [Revised: 01/28/2019] [Accepted: 02/14/2019] [Indexed: 12/17/2022]
Affiliation(s)
- Christel Häggström
- Department of Biobank ResearchUmeå University Umeå Sweden
- Department of Surgical SciencesUppsala University Uppsala Sweden
- Department of Public Health and Clinical Medicine, Nutritional ResearchUmeå University Umeå Sweden
| | - Håkan Jonsson
- Department of Radiation SciencesUmeå University Umeå Sweden
| | - Tone Bjørge
- Department of Global Public Health and Primary CareUniversity of Bergen Bergen Norway
- Cancer Registry of Norway Oslo Norway
| | - Gabriele Nagel
- Institute of Epidemiology and Medical BiometryUlm University Ulm Germany
- Vorarlberg Cancer RegistryAgency for Preventive and Social Medicine Bregenz (aks) Austria
| | - Jonas Manjer
- Department of SurgerySkåne University Hospital, Lund University Malmö Sweden
| | - Hanno Ulmer
- Department of Medical Statistics, Informatics and Health EconomicsInnsbruck Medical University Innsbruck Austria
| | - Isabel Drake
- Department of Clinical Sciences in MalmöLund University Lund Sweden
| | - Sara Ghaderi
- Department of Global Public Health and Primary CareUniversity of Bergen Bergen Norway
| | - Alois Lang
- Vorarlberg Cancer RegistryAgency for Preventive and Social Medicine Bregenz (aks) Austria
| | - Anders Engeland
- Department of Global Public Health and Primary CareUniversity of Bergen Bergen Norway
- Norwegian Institute of Public Health Bergen/Oslo Norway
| | - Pär Stattin
- Department of Surgical SciencesUppsala University Uppsala Sweden
| | - Tanja Stocks
- Department of Clinical Sciences in LundLund University Lund Sweden
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21
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Teleka S, Häggström C, Nagel G, Bjørge T, Manjer J, Ulmer H, Liedberg F, Ghaderi S, Lang A, Jonsson H, Jahnson S, Orho-Melander M, Tretli S, Stattin P, Stocks T. Risk of bladder cancer by disease severity in relation to metabolic factors and smoking: A prospective pooled cohort study of 800,000 men and women. Int J Cancer 2018; 143:3071-3082. [DOI: 10.1002/ijc.31597] [Citation(s) in RCA: 24] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/15/2017] [Revised: 04/09/2018] [Accepted: 04/16/2018] [Indexed: 12/21/2022]
Affiliation(s)
- Stanley Teleka
- Department of Clinical Sciences in Malmö; Lund University; Lund Sweden
| | - Christel Häggström
- Department of Biobank Research; Umeå University; Umeå Sweden
- Department of Surgical Sciences; Uppsala University; Uppsala Sweden
- Department of Public Health and Clinical Medicine, Nutritional Research; Umeå University; Umeå Sweden
| | - Gabriele Nagel
- Institute of Epidemiology and Medical Biometry; Ulm University; Ulm Germany
- Vorarlberg Cancer Registry; Agency for Preventive and Social Medicine; Bregenz (aks) Austria
| | - Tone Bjørge
- Department of Global Public Health and Primary Care; University of Bergen; Bergen Norway
- Cancer Registry of Norway; Oslo Norway
| | - Jonas Manjer
- Department of Surgery; Skåne University Hospital; Lund University Malmö Sweden
| | - Hanno Ulmer
- Department of Medical Statistics, Informatics and Health Economics; Innsbruck Medical University; Innsbruck Austria
| | - Fredrik Liedberg
- Division of Urological Research, Institution of Translational Medicine; Lund University; Malmö Sweden
| | - Sara Ghaderi
- Department of Global Public Health and Primary Care; University of Bergen; Bergen Norway
| | - Alois Lang
- Vorarlberg Cancer Registry; Agency for Preventive and Social Medicine; Bregenz (aks) Austria
| | - Håkan Jonsson
- Department of Radiation Sciences; Umeå University; Umeå Sweden
| | - Staffan Jahnson
- Department of Urology and IKE; Linköping University; Linköping Sweden
| | | | | | - Pär Stattin
- Department of Surgical Sciences; Uppsala University; Uppsala Sweden
| | - Tanja Stocks
- Department of Clinical Sciences in Malmö; Lund University; Lund Sweden
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22
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Hjerkind KV, Gislefoss RE, Tretli S, Nystad W, Bjørge T, Engeland A, Meyer HE, Holvik K, Ursin G, Langseth H. Cohort Profile Update: The Janus Serum Bank Cohort in Norway. Int J Epidemiol 2018; 46:1101-1102f. [PMID: 28087783 DOI: 10.1093/ije/dyw302] [Citation(s) in RCA: 22] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 09/21/2016] [Indexed: 11/14/2022] Open
Affiliation(s)
- Kirsti Vik Hjerkind
- Cancer Registry of Norway, Institute of Population-based Cancer Research, Oslo, Norway
| | - Randi E Gislefoss
- Cancer Registry of Norway, Institute of Population-based Cancer Research, Oslo, Norway
| | - Steinar Tretli
- Cancer Registry of Norway, Institute of Population-based Cancer Research, Oslo, Norway
| | - Wenche Nystad
- Division of Mental and Physical Health, Norwegian Institute for Public Health, Oslo, Norway
| | - Tone Bjørge
- Cancer Registry of Norway, Institute of Population-based Cancer Research, Oslo, Norway.,Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway
| | - Anders Engeland
- Division of Mental and Physical Health, Norwegian Institute for Public Health, Oslo, Norway.,Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway
| | - Haakon E Meyer
- Division of Mental and Physical Health, Norwegian Institute for Public Health, Oslo, Norway
| | - Kristin Holvik
- Division of Mental and Physical Health, Norwegian Institute for Public Health, Oslo, Norway
| | - Giske Ursin
- Cancer Registry of Norway, Institute of Population-based Cancer Research, Oslo, Norway.,Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.,Department of Preventive Medicine, University of Southern California, Los Angeles, CA, USA
| | - Hilde Langseth
- Cancer Registry of Norway, Institute of Population-based Cancer Research, Oslo, Norway
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23
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Yin DT, He H, Yu K, Xie J, Lei M, Ma R, Li H, Wang Y, Liu Z. The association between thyroid cancer and insulin resistance, metabolic syndrome and its components: A systematic review and meta-analysis. Int J Surg 2018; 57:66-75. [PMID: 30081182 DOI: 10.1016/j.ijsu.2018.07.013] [Citation(s) in RCA: 58] [Impact Index Per Article: 8.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/25/2018] [Revised: 06/15/2018] [Accepted: 07/28/2018] [Indexed: 12/18/2022]
Abstract
BACKGROUND Thyroid cancer is rapidly increasing in incidence worldwide in the past several decades, same as the incidence of metabolic syndrome. We performed a system review and meta-analysis of the association between metabolic syndrome, its components and insulin resistance and thyroid cancer incidence. METHODS We searched several computer-assisted databases PUBMED, EMBASE and ISI Web of Science to identify studies published before 31st January 2018. Every study must report either risk estimates of thyroid cancer incidence with 95% confidence interval (CI) or related data can speculate. Two investigators independently identified eligible studies and extracted data. Evaluating the summaries of relative risk estimates use both fixed and random effects methods. RESULTS We found 42 articles met the inclusion criteria of this review. There is an increased risk for thyroid cancer for patients with insulin resistance (relative risk [RR] = 1.59, 95%confidence interval [CI] = 1.12-2.27, P = 0.01), dysglycemia (RR = 1.40, 95%CI = 1.15-1.70,P < 0.001), high BMI (RR = 1.35,95%CI = 1.23-1.48,P < 0.001) and hypertension(RR = 1.34,95%CI = 1.22-1.47, p < 0.001). However, patients with dyslipidemia, both total cholesterol (RR = 1.09, 95%CI = 0.98-1.21, P = 0.13) and triglyceride (RR = 1.01, 95%CI = 0.91-1.12, P = 0.82) was not associated with thyroid cancer. CONCLUSIONS Our meta-analysis showed Insulin Resistance, dysglycemia, high BMI and hypertension significantly increased the thyroid cancer risk. These results may help identify people with high risk of thyroid cancer and change to healthy life style.
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Affiliation(s)
- De-Tao Yin
- Department of Thyroid Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, PR China; Key Discipline Laboratory of Clinical Medicine Henan, Zhengzhou, 450052, PR China.
| | - Huanan He
- Department of Thyroid Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, PR China; Key Discipline Laboratory of Clinical Medicine Henan, Zhengzhou, 450052, PR China; Department of General Surgery, the First People's Hospital of Pingdingshan, Pingdingshan, 467000, PR China
| | - Kun Yu
- Department of Thyroid Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, PR China; Key Discipline Laboratory of Clinical Medicine Henan, Zhengzhou, 450052, PR China
| | - Jing Xie
- Center for Eye Research Australia, Royal Victorian Eye and Ear Hospital, University of Melbourne, Melbourne, Australia
| | - Mengyuan Lei
- Department of Thyroid Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, PR China; Key Discipline Laboratory of Clinical Medicine Henan, Zhengzhou, 450052, PR China
| | - Runsheng Ma
- Department of Thyroid Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, PR China; Key Discipline Laboratory of Clinical Medicine Henan, Zhengzhou, 450052, PR China
| | - Hongqiang Li
- Department of Thyroid Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, PR China; Key Discipline Laboratory of Clinical Medicine Henan, Zhengzhou, 450052, PR China
| | - Yongfei Wang
- Department of Thyroid Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, PR China; Key Discipline Laboratory of Clinical Medicine Henan, Zhengzhou, 450052, PR China
| | - Zhen Liu
- Department of Thyroid Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, PR China; Key Discipline Laboratory of Clinical Medicine Henan, Zhengzhou, 450052, PR China
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24
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Hansen MS, Licaj I, Braaten T, Langhammer A, Le Marchand L, Gram IT. Sex Differences in Risk of Smoking-Associated Lung Cancer: Results From a Cohort of 600,000 Norwegians. Am J Epidemiol 2018; 187:971-981. [PMID: 29087432 DOI: 10.1093/aje/kwx339] [Citation(s) in RCA: 23] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/10/2017] [Accepted: 10/10/2017] [Indexed: 11/14/2022] Open
Abstract
Whether women are more susceptible than men to smoking-related lung cancer has been a topic of controversy. To address this question, we compared risks of lung cancer associated with smoking by sex. Altogether, 585,583 participants from 3 Norwegian cohorts (Norwegian Counties Study, 40 Years Study, and Cohort of Norway (CONOR) Study) were followed until December 31, 2013, through linkage of data to national registries. We used Cox proportional hazards models and 95% confidence intervals to estimate risks. During nearly 12 million person-years of follow-up, 6,534 participants (43% women) were diagnosed with lung cancer. More men than women were heavier smokers. Compared with never smokers, male and female current smokers with ≥16 pack-years of smoking had hazard ratios for lung cancer of 27.24 (95% confidence interval (CI): 22.42, 33.09) and 23.90 (95% CI: 20.57, 27.76), respectively (P for heterogeneity = 0.30). In contrast, for current smokers, in a model with pack-years measured continuously, men had a hazard ratio of 1.43 (95% CI: 1.39, 1.48) and women a hazard ratio of 1.64 (95% CI: 1.57, 1.71) for each 10-pack-year increment of smoking (P for heterogeneity < 0.01). Our results suggest that women have an increased susceptibility to lung cancer compared with men, given the same lifetime smoking exposure.
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Affiliation(s)
- Merethe S Hansen
- Department of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway
| | - Idlir Licaj
- Department of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway
- Clinical Research Department, Centre François Baclesse, Caen, France
| | - Tonje Braaten
- Department of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway
| | - Arnulf Langhammer
- General Practice Research Unit, Department of Public Health and Nursing, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway
| | - Loic Le Marchand
- Epidemiology Program, University of Hawaii Cancer Center, Honolulu, Hawaii
| | - Inger T Gram
- Department of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway
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25
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Offspring birth weight and cardiovascular mortality among parents: the role of cardiovascular risk factors. J Dev Orig Health Dis 2018; 9:351-357. [DOI: 10.1017/s2040174418000065] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/07/2022]
Abstract
AbstractAn inverse association between offspring birth weight (BW) and higher risk of parental cardiovascular disease (CVD) mortality and morbidity has been reported. Shared environmental, genetic and intrauterine factors may be responsible for explaining these associations. We studied the role of parental CVD risk factors in the association between offspring BW and CVD mortality among mothers and fathers. All births registered in Medical Birth Registry Norway (1967–2012) were linked to three health surveys, National Educational Registry and Cause of Death Registry. Number of births with information of parental CVD risk factors available for the analyses was 1,006,557 (520,670 for mothers and 485,887 for fathers). Cox proportional hazards regression models were used, following CVD deaths in parents from 1974 to 2012. An inverse association between offspring BW and CVD mortality was observed among both parents: hazard ratio 1.60 (1.44–1.75) for mothers and 1.16 (1.10–1.23) for fathers. Among mothers, adjustment for smoking, triglycerides and diabetes reduced the risk to 1.36 (1.25–1.52), 1.57 (1.43–1.73) and 1.58 (1.43–1.79), respectively. Adjustment for diastolic blood pressure (DBP) and systolic blood pressure (SBP) both reduced the risk to 1.53 (1.37–1.66). Among fathers, adjustments for smoking, DBP, SBP reduced the risk to 1.08 (1.02–1.15), 1.13 (1.06–1.19) and 1.14 (1.08–1.22), respectively. Triglycerides and diabetes both reduced the risk to 1.15 (1.09–1.12). Our results indicate that shared environmental factors might be important in the association. A stronger association in mothers suggest that intrauterine factors also are at play.
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26
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Flegal KM, Ioannidis JPA. A meta-analysis but not a systematic review: an evaluation of the Global BMI Mortality Collaboration. J Clin Epidemiol 2017; 88:21-29. [PMID: 28435099 DOI: 10.1016/j.jclinepi.2017.04.007] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/12/2016] [Accepted: 04/04/2017] [Indexed: 01/25/2023]
Abstract
Meta-analyses of individual participant data (MIPDs) offer many advantages and are considered the highest level of evidence. However, MIPDs can be seriously compromised when they are not solidly founded upon a systematic review. These data-intensive collaborative projects may be led by experts who already have deep knowledge of the literature in the field and of the results of published studies and how these results vary based on different analytical approaches. If investigators tailor the searches, eligibility criteria, and analysis plan of the MIPD, they run the risk of reaching foregone conclusions. We exemplify this potential bias in a MIPD on the association of body mass index with mortality conducted by a collaboration of outstanding and extremely knowledgeable investigators. Contrary to a previous meta-analysis of group data that used a systematic review approach, the MIPD did not seem to use a formal search: it considered 239 studies, of which the senior author was previously aware of at least 238, and it violated its own listed eligibility criteria to include those studies and exclude other studies. It also preferred an analysis plan that was also known to give a specific direction of effects in already published results of most of the included evidence. MIPDs where results of constituent studies are already largely known need safeguards to their validity. These may include careful systematic searches, adherence to the Preferred Reporting Items for Systematic Review and Meta-Analyses of individual participant data guidelines, and exploration of the robustness of results with different analyses. They should also avoid selective emphasis on foregone conclusions based on previously known results with specific analytical choices.
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Affiliation(s)
- Katherine M Flegal
- Stanford Prevention Research Center, Department of Medicine, Stanford University School of Medicine, Medical School Office Building, 1265 Welch Road, Mail Code 5411, Stanford, CA 94305-5411, USA.
| | - John P A Ioannidis
- Stanford Prevention Research Center, Department of Medicine, Stanford University School of Medicine, Medical School Office Building, 1265 Welch Road, Mail Code 5411, Stanford, CA 94305-5411, USA; Department of Health Research and Policy, 150 Governor's Lane, HRP Redwood Building, Stanford University School of Medicine, Stanford, CA 94305-5405 USA; Department of Statistics, Stanford University School of Humanities and Sciences, Sequoia Hall, Mail Code 4065, 390 Serra Mall, Stanford University, Stanford, CA 94305-4020, USA; Meta-Research Innovation Center at Stanford (METRICS), Stanford University, 1070 Arastradero Road, Palo Alto, CA 94304, USA
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27
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Schwartzbaum J, Edlinger M, Zigmont V, Stattin P, Rempala GA, Nagel G, Hammar N, Ulmer H, Föger B, Walldius G, Manjer J, Malmström H, Feychting M. Associations between prediagnostic blood glucose levels, diabetes, and glioma. Sci Rep 2017; 7:1436. [PMID: 28469238 PMCID: PMC5431098 DOI: 10.1038/s41598-017-01553-2] [Citation(s) in RCA: 17] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/13/2016] [Accepted: 03/31/2017] [Indexed: 12/11/2022] Open
Abstract
Previous literature indicates that pre-diagnostic diabetes and blood glucose levels are inversely related to glioma risk. To replicate these findings and determine whether they could be attributed to excess glucose consumption by the preclinical tumour, we used data from the Apolipoprotein MOrtality RISk (AMORIS) (n = 528,580) and the Metabolic syndrome and Cancer project (Me-Can) cohorts (n = 269,365). We identified individuals who were followed for a maximum of 15 years after their first blood glucose test until glioma diagnosis, death, emigration or the end of follow-up. Hazard ratios (HRs), 95% confidence intervals (CIs) and their interactions with time were estimated using Cox time-dependent regression. As expected, pre-diagnostic blood glucose levels were inversely related to glioma risk (AMORIS, Ptrend = 0.002; Me-Can, Ptrend = 0.04) and pre-diagnostic diabetes (AMORIS, HR = 0.30, 95% CI 0.17 to 0.53). During the year before diagnosis, blood glucose was inversely associated with glioma in the AMORIS (HR = 0.78, 95% CI 0.66 to 0.93) but not the Me-Can cohort (HR = 0.99, 95% CI 0.63 to 1.56). This AMORIS result is consistent with our hypothesis that excess glucose consumption by the preclinical tumour accounts for the inverse association between blood glucose and glioma. We discuss additional hypothetical mechanisms that may explain our paradoxical findings.
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Affiliation(s)
- Judith Schwartzbaum
- Division of Epidemiology, College of Public Health, Ohio State University, Columbus, Ohio, 43210, United States of America. .,Comprehensive Cancer Center, Ohio State University, Columbus, Ohio, 43210, United States of America.
| | - Michael Edlinger
- Department of Medical Statistics, Informatics, and Health Economics, Medical University, Innsbruck, Austria.
| | - Victoria Zigmont
- Division of Epidemiology, College of Public Health, Ohio State University, Columbus, Ohio, 43210, United States of America.,Department of Public Health, Southern Connecticut State University, New Haven, CT, 06515, United States of America
| | - Pär Stattin
- Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden
| | - Grzegorz A Rempala
- Division of Epidemiology, College of Public Health, Ohio State University, Columbus, Ohio, 43210, United States of America.,Division of Biostatistics, College of Public Health, Ohio State University, Columbus, Ohio, 43210, United States of America.,Mathematical Biosciences Institute, Columbus, Ohio, 43210, United States of America
| | - Gabriele Nagel
- Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany.,Agency for Preventive and Social Medicine, Bregenz, Austria
| | - Niklas Hammar
- Medical Evidence & Observational Research, Global Medical Affairs, Astra Zeneca R&D, Mölndal, 43150, Sweden.,Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, SE-17177, Stockholm, Sweden
| | - Hanno Ulmer
- Department of Medical Statistics, Informatics, and Health Economics, Medical University, Innsbruck, Austria
| | - Bernhard Föger
- Agency for Preventive and Social Medicine, Bregenz, Austria
| | - Göran Walldius
- Unit of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, SE-17177, Stockholm, Sweden
| | - Jonas Manjer
- Department of Surgery, Skåne University Hospital, Malmö, Sweden
| | - Håkan Malmström
- Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, SE-17177, Stockholm, Sweden
| | - Maria Feychting
- Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, SE-17177, Stockholm, Sweden
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Licaj I, Jacobsen BK, Selmer RM, Maskarinec G, Weiderpass E, Gram IT. Smoking and risk of ovarian cancer by histological subtypes: an analysis among 300 000 Norwegian women. Br J Cancer 2017; 116:270-276. [PMID: 27959888 PMCID: PMC5243998 DOI: 10.1038/bjc.2016.418] [Citation(s) in RCA: 21] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Revised: 10/19/2016] [Accepted: 11/18/2016] [Indexed: 12/18/2022] Open
Abstract
BACKGROUND We prospectively investigated the association between different measures of smoking exposure and the risk of serous, mucinous, and endometrioid ovarian cancers (OC) in a cohort of more than 300 000 Norwegian women. METHODS We followed 300 398 women aged 19-67 years at enrolment until 31 December 2013 for OC incidence through linkage to national registries. We used Cox proportional hazards models with attained age as the underlying time scale to estimate multivariable-adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) adjusted for relevant confounders. RESULTS During more than 5.9 million person-years and a median follow-up time of 19 years, 2336 primary invasive (1647, 71%) and borderline (689, 29%) OC were identified (53% serous, 19% mucinous). Compared with never smokers, current smokers who had smoked for ⩾10 years had a higher risk of mucinous OC (HR10-19 years vs never=1.73, 95% CI 1.24-2.42; HR⩾20 vs never=2.26, 95% CI 1.77-2.89, Ptrend <0.001). When stratified by invasiveness, current smokers had a higher risk of invasive mucinous OC (HR=1.78, 95% CI 1.20-2.64) and borderline mucinous OC (HR=2.26 95% CI, 1.71-2.97) (Pheterogeneity=0.34) than never smokers. Smoking was not associated with serous or endometrioid OC. CONCLUSIONS Using a very large cohort of women, the current analysis provides an important replication for a similar risk of invasive and borderline mucinous OC related to smoking.
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Affiliation(s)
- Idlir Licaj
- Department of Community Medicine, Faculty of Health Sciences, The UiT Arctic University of Norway, Tromsø, Norway
| | - Bjarne Koster Jacobsen
- Department of Community Medicine, Faculty of Health Sciences, The UiT Arctic University of Norway, Tromsø, Norway
| | | | | | - Elisabete Weiderpass
- Department of Community Medicine, Faculty of Health Sciences, The UiT Arctic University of Norway, Tromsø, Norway
- Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
- Department of Research, Cancer Registry of Norway, Institute of Population-Based Cancer Research, Oslo, Norway
- Genetic Epidemiology Group, Folkhälsan Research Center, Helsinki, Finland
| | - Inger Torhild Gram
- Department of Community Medicine, Faculty of Health Sciences, The UiT Arctic University of Norway, Tromsø, Norway
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Malaguarnera R, Vella V, Nicolosi ML, Belfiore A. Insulin Resistance: Any Role in the Changing Epidemiology of Thyroid Cancer? Front Endocrinol (Lausanne) 2017; 8:314. [PMID: 29184536 PMCID: PMC5694441 DOI: 10.3389/fendo.2017.00314] [Citation(s) in RCA: 37] [Impact Index Per Article: 4.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/04/2017] [Accepted: 10/30/2017] [Indexed: 12/13/2022] Open
Abstract
In the past few decades, the incidence of thyroid cancer (TC), namely of its papillary hystotype (PTC), has shown a steady increase worldwide, which has been attributed at least in part to the increasing diagnosis of early stage tumors. However, some evidence suggests that environmental and lifestyle factors can also play a role. Among the potential risk factors involved in the changing epidemiology of TC, particular attention has been drawn to insulin-resistance and related metabolic disorders, such as obesity, type 2 diabetes, and metabolic syndrome, which have been also rapidly increasing worldwide due to widespread dietary and lifestyle changes. In accordance with this possibility, various epidemiological studies have indeed gathered substantial evidence that insulin resistance-related metabolic disorders might be associated with an increased TC risk either through hyperinsulinemia or by affecting other TC risk factors including iodine deficiency, elevated thyroid stimulating hormone, estrogen-dependent signaling, chronic autoimmune thyroiditis, and others. This review summarizes the current literature evaluating the relationship between metabolic disorders characterized by insulin resistance and the risk for TC as well as the possible underlying mechanisms. The potential implications of such association in TC prevention and therapy are discussed.
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Affiliation(s)
- Roberta Malaguarnera
- Endocrinology, Department of Health Sciences, University Magna Graecia of Catanzaro, Catanzaro, Italy
| | - Veronica Vella
- School of Human and Social Sciences, “Kore” University of Enna, Enna, Italy
- *Correspondence: Veronica Vella, ; Antonino Belfiore,
| | - Maria Luisa Nicolosi
- Endocrinology, Department of Health Sciences, University Magna Graecia of Catanzaro, Catanzaro, Italy
| | - Antonino Belfiore
- Endocrinology, Department of Health Sciences, University Magna Graecia of Catanzaro, Catanzaro, Italy
- *Correspondence: Veronica Vella, ; Antonino Belfiore,
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30
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Ko S, Yoon SJ, Kim D, Kim AR, Kim EJ, Seo HY. Metabolic Risk Profile and Cancer in Korean Men and Women. J Prev Med Public Health 2016; 49:143-52. [PMID: 27255073 PMCID: PMC4898898 DOI: 10.3961/jpmph.16.021] [Citation(s) in RCA: 40] [Impact Index Per Article: 4.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/22/2016] [Accepted: 04/05/2016] [Indexed: 01/10/2023] Open
Abstract
OBJECTIVES Metabolic syndrome is a cluster of risk factors for type 2 diabetes mellitus and cardiovascular disease. Associations between metabolic syndrome and several types of cancer have recently been documented. METHODS We analyzed the sample cohort data from the Korean National Health Insurance Service from 2002, with a follow-up period extending to 2013. The cohort data included 99 565 individuals who participated in the health examination program and whose data were therefore present in the cohort database. The metabolic risk profile of each participant was assessed based on obesity, high serum glucose and total cholesterol levels, and high blood pressure. The occurrence of cancer was identified using Korean National Health Insurance claims data. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models, adjusting for age group, smoking status, alcohol intake, and regular exercise. RESULTS A total of 5937 cases of cancer occurred during a mean follow-up period of 10.4 years. In men with a high-risk metabolic profile, the risk of colon cancer was elevated (HR, 1.40; 95% CI, 1.14 to 1.71). In women, a high-risk metabolic profile was associated with a significantly increased risk of gallbladder and biliary tract cancer (HR, 2.05; 95% CI, 1.24 to 3.42). Non-significantly increased risks were observed in men for pharynx, larynx, rectum, and kidney cancer, and in women for colon, liver, breast, and ovarian cancer. CONCLUSIONS The findings of this study support the previously suggested association between metabolic syndrome and the risk of several cancers. A high-risk metabolic profile may be an important risk factor for colon cancer in Korean men and gallbladder and biliary tract cancer in Korean women.
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Affiliation(s)
- Seulki Ko
- Department of Preventive Medicine, Korea University College of Medicine, Seoul, Korea
| | - Seok-Jun Yoon
- Department of Preventive Medicine, Korea University College of Medicine, Seoul, Korea
| | - Dongwoo Kim
- Department of Preventive Medicine, Korea University College of Medicine, Seoul, Korea
| | - A-Rim Kim
- Department of Public Health, Graduate School of Korea University, Seoul, Korea
| | - Eun-Jung Kim
- Department of Economics, Economic Research Institute, Korea University, Seoul, Korea
| | - Hye-Young Seo
- Department of Public Health, Graduate School of Korea University, Seoul, Korea
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Häggström C, Stattin P, Stocks T, Garmo H, Holmberg L, Van Hemelrijck M. Interpretation of conventional survival analysis and competing-risk analysis: an example of hypertension and prostate cancer. BJU Int 2016; 118:850-852. [PMID: 27037631 DOI: 10.1111/bju.13494] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/28/2022]
Affiliation(s)
- Christel Häggström
- Department of Surgical and Perioperative sciences, Urology and Andrology, Umeå University, Umeå, Sweden.,Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.,Department of Biobank Research, Umeå University, Umeå, Sweden
| | - Pär Stattin
- Department of Surgical and Perioperative sciences, Urology and Andrology, Umeå University, Umeå, Sweden.,Department of Surgical Sciences, Uppsala University, Uppsala, Sweden
| | - Tanja Stocks
- Department of Surgical and Perioperative sciences, Urology and Andrology, Umeå University, Umeå, Sweden.,Department of Clinical Sciences, Diabetes and Cardiovascular Diseases, Genetic Epidemiology, Lund University, Lund, Sweden
| | - Hans Garmo
- Regional Cancer Centre Uppsala/Örebro, Uppsala, Sweden.,King's College London, Faculty of Life Sciences and Medicine, Division of Cancer Studies, London, UK
| | - Lars Holmberg
- Regional Cancer Centre Uppsala/Örebro, Uppsala, Sweden.,King's College London, Faculty of Life Sciences and Medicine, Division of Cancer Studies, London, UK
| | - Mieke Van Hemelrijck
- King's College London, Faculty of Life Sciences and Medicine, Division of Cancer Studies, London, UK.,Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden
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Abstract
Supplemental Digital Content is available in the text. Background: Few previous studies of metabolic aberrations and prostate cancer risk have taken into account the fact that men with metabolic aberrations have an increased risk of death from causes other than prostate cancer. The aim of this study was to calculate, in a real-life scenario, the risk of prostate cancer diagnosis, prostate cancer death, and death from other causes. Methods: In the Metabolic Syndrome and Cancer Project, prospective data on body mass index, blood pressure, glucose, cholesterol, and triglycerides were collected from 285,040 men. Risks of prostate cancer diagnosis, prostate cancer death, and death from other causes were calculated by use of competing risk analysis for men with normal (bottom 84%) and high (top 16%) levels of each factor, and a composite score. Results: During a mean follow-up period of 12 years, 5,893 men were diagnosed with prostate cancer, 1,013 died of prostate cancer, and 26,328 died of other causes. After 1996, when prostate-specific antigen testing was introduced, men up to age 80 years with normal metabolic levels had 13% risk of prostate cancer, 2% risk of prostate cancer death, and 30% risk of death from other causes, whereas men with metabolic aberrations had corresponding risks of 11%, 2%, and 44%. Conclusions: In contrast to recent studies using conventional survival analysis, in a real-world scenario taking risk of competing events into account, men with metabolic aberrations had lower risk of prostate cancer diagnosis, similar risk of prostate cancer death, and substantially higher risk of death from other causes compared with men who had normal metabolic levels.
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Bjerkaas E, Parajuli R, Engeland A, Maskarinec G, Weiderpass E, Gram IT. Social inequalities and smoking-associated breast cancer - Results from a prospective cohort study. Prev Med 2015; 73:125-9. [PMID: 25620729 DOI: 10.1016/j.ypmed.2015.01.004] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/25/2014] [Revised: 12/15/2014] [Accepted: 01/05/2015] [Indexed: 10/24/2022]
Abstract
OBJECTIVE The association between smoking and breast cancer has been found in most recent, large cohort studies. We wanted to investigate how smoking-associated breast cancer varies by level of education, a well-established measure of socioeconomic status. METHODS We included 302,865 women with 7490 breast cancer cases. Participants were assigned to low, moderate or high level of education and analyzed by smoking status (ever/never), and stratified by birth cohorts (≤1950>). We used Cox proportional hazard to estimate hazard ratios (HRs) and confidence intervals (CIs), adjusting for age, number of children, age at first childbirth, BMI, age at enrollment and physical activity. RESULTS Women born ≤1950 with low and moderate levels of education had a 40% increase in smoking-associated breast cancer risk (HR=1.40, 95% CI 1.25-1.57 and HR=1.14, 95% CI 1.05-1.24, respectively). Women in the same age group with high level of education did not have an increase in risk. No increased breast cancer risk was found among women born after 1950 for any level of education, when analyzed by smoking status. Longer duration of smoking before first childbirth was consistently associated with increasing risk of breast cancer in all three categories of education (all p for trends<0.01). CONCLUSION Smoking for several years before first childbirth increases the risk of breast cancer, regardless of educational level.
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Affiliation(s)
- Eivind Bjerkaas
- Department of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of Norway, N-9037 Tromsø, Norway
| | - Ranjan Parajuli
- Department of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of Norway, N-9037 Tromsø, Norway
| | - Anders Engeland
- Division of Epidemiology, Department of Pharmacoepidemiology, Norwegian Institute of Public Health, Oslo, Norway; Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway
| | | | - Elisabete Weiderpass
- Department of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of Norway, N-9037 Tromsø, Norway; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Genetic Epidemiology, Folkhälsan Research Center, Samfundet Folkhälsan, Helsinki, Finland; Department of Research, Cancer Registry of Norway, Oslo, Norway
| | - Inger Torhild Gram
- Department of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of Norway, N-9037 Tromsø, Norway
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Visceral Fat Content Correlates with Retroperitoneal Soft Tissue Sarcoma (STS) Local Recurrence and Survival. World J Surg 2015; 39:1895-901. [DOI: 10.1007/s00268-015-3038-0] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/01/2023]
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35
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Stocks T, Bjørge T, Ulmer H, Manjer J, Häggström C, Nagel G, Engeland A, Johansen D, Hallmans G, Selmer R, Concin H, Tretli S, Jonsson H, Stattin P. Metabolic risk score and cancer risk: pooled analysis of seven cohorts. Int J Epidemiol 2015; 44:1353-63. [PMID: 25652574 PMCID: PMC4588859 DOI: 10.1093/ije/dyv001] [Citation(s) in RCA: 101] [Impact Index Per Article: 10.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 01/08/2015] [Indexed: 01/10/2023] Open
Abstract
Background: There are few data on the joint influence of metabolic factors on risk of separate cancers. Methods: We analysed data on body mass index, blood pressure and plasma levels of glucose, total cholesterol and triglycerides from seven European cohorts comprising 564 596 men and women with a mean age of 44 years. We weighted those factors equally into a standardized metabolic risk score [MRS, mean = 0, standard deviation (SD) = 1], with an individual’s level indicated as SDs from the sex- and cohort-specific means. Cancer hazard ratios were calculated by Cox regression with age as timescale and with relevant adjustments including smoking status. All statistical tests were two-sided. Results: During a mean follow-up of 12 years, 21 593 men and 14 348 women were diagnosed with cancer. MRS was linearly and positively associated with incident cancer in total and at sites (P < 0.05). In men, risk per SD MRS was increased by 43% (95% confidence interval: 27–61) for renal cell cancer, 43% (16–76) for liver cancer, 29% (20–38) for colon cancer, 27% (5–54) for oesophageal cancer, 20% (9–31) for rectal cancer, 19% (4–37) for leukaemias, 15% (1–30) for oral cancer and 10% (2–19) for bladder cancer. In women, risk increases per SD MRS were 56% (42–70) for endometrial cancer, 53% (29–81) for pancreatic cancer, 40% (16–67) for renal cell cancer, 27% (9–47) for cervical cancer and 17% (3–32) for rectal cancer. Conclusion: This largest study to date on the joint influence of metabolic factors on risk of separate cancers showed increased risks for several cancers, in particular renal cell and liver cancer in men and endometrial and pancreatic cancer in women.
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Affiliation(s)
- Tanja Stocks
- Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden, Department of Clinical Sciences in Malmö, Diabetes and Cardiovascular Diseases, Genetic Epidemiology, Lund University, Lund, Sweden,
| | - Tone Bjørge
- Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway, Institute of Population-based Cancer Research, Cancer Registry of Norway, Oslo, Norway
| | - Hanno Ulmer
- Department of Medical Statistics, Informatics and Health Economics, Innsbruck Medical University, Innsbruck, Austria
| | - Jonas Manjer
- Department of Surgery, Skåne University Hospital, Lund University, Malmö, Sweden
| | - Christel Häggström
- Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden
| | - Gabriele Nagel
- Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany, Agency for Preventive and Social Medicine, Bregenz, Austria
| | - Anders Engeland
- Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway, Department of Pharmacoepidemiology, Norwegian Institute of Public Health, Oslo, Norway
| | - Dorthe Johansen
- Department of Surgery, Skåne University Hospital, Lund University, Malmö, Sweden
| | - Göran Hallmans
- Department of Public Health and Clinical Medicine, Nutritional Research, and
| | - Randi Selmer
- Department of Pharmacoepidemiology, Norwegian Institute of Public Health, Oslo, Norway
| | - Hans Concin
- Agency for Preventive and Social Medicine, Bregenz, Austria
| | - Steinar Tretli
- Institute of Population-based Cancer Research, Cancer Registry of Norway, Oslo, Norway
| | - Håkan Jonsson
- Department of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden
| | - Pär Stattin
- Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden
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Bjerkaas E, Parajuli R, Engeland A, Maskarinec G, Weiderpass E, Gram IT. The association between lifetime smoking exposure and breast cancer mortality--results from a Norwegian cohort. Cancer Med 2014; 3:1448-57. [PMID: 25073713 PMCID: PMC4302695 DOI: 10.1002/cam4.304] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/07/2014] [Revised: 05/23/2014] [Accepted: 06/11/2014] [Indexed: 12/30/2022] Open
Abstract
Several recent cohort studies have found an association between smoking and breast cancer, but the association between lifetime smoking exposure and breast cancer mortality is less well described. We examined whether smoking before breast cancer diagnosis is a predictor of breast cancer mortality in a large cohort with more than 4.1 million years of follow-up, with a special focus on women who initiated smoking before first childbirth. Information on smoking status was collected before breast cancer diagnosis and used to estimate hazard ratios (HRs) and corresponding 95% confidence intervals (CIs) of breast cancer mortality in a cohort of 302,865 Norwegian women with 1106 breast cancer deaths. Women were enrolled between 1974 and 2003 and followed up through linkages to national registries until 31 December 2007. We found that breast cancer mortality was slightly but significantly increased for current (HR = 1.15, 95% CI 1.01-1.32) and ever (HR = 1.15, 95% CI 1.02-1.30) smokers as compared to never smokers. No statistically significantly increased mortality was found for women who initiated smoking before first childbirth, and no dose-response association was revealed for any of the different measures of smoking exposure. A large proportion of heavy smokers may have died from other causes than breast cancer during follow-up, possibly diluting our results. This study found that lifetime smoking exposure had a significantly increased risk of breast cancer mortality compared with never smokers.
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Affiliation(s)
- Eivind Bjerkaas
- Department of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of NorwayN-9037, Tromsø, Norway
| | - Ranjan Parajuli
- Department of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of NorwayN-9037, Tromsø, Norway
| | - Anders Engeland
- Division of Epidemiology, Department of Pharmacoepidemiology, Norwegian Institute of Public HealthOslo, Norway
- Department of Global Public Health and Primary Care, University of BergenBergen, Norway
| | | | - Elisabete Weiderpass
- Department of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of NorwayN-9037, Tromsø, Norway
- Department of Medical Epidemiology and Biostatistics, Karolinska InstitutetStockholm, Sweden
- Department of Genetic Epidemiology, Folkhälsan Research Center, Samfundet FolkhälsanHelsinki, Finland
- Department of Research, Cancer Registry of NorwayOslo, Norway
| | - Inger Torhild Gram
- Department of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of NorwayN-9037, Tromsø, Norway
- Norwegian Centre for Integrated Care and Telemedicine, University Hospital of North NorwayTromsø, Norway
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37
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Andreassen OA, Zuber V, Thompson WK, Schork AJ, Bettella F, Djurovic S, Desikan RS, Mills IG, Dale AM. Shared common variants in prostate cancer and blood lipids. Int J Epidemiol 2014; 43:1205-14. [PMID: 24786909 PMCID: PMC4121563 DOI: 10.1093/ije/dyu090] [Citation(s) in RCA: 39] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 03/20/2014] [Indexed: 02/07/2023] Open
Abstract
BACKGROUND Epidemiological and clinical studies suggest comorbidity between prostate cancer (PCA) and cardiovascular disease (CVD) risk factors. However, the relationship between these two phenotypes is still not well understood. Here we sought to identify shared genetic loci between PCA and CVD risk factors. METHODS We applied a genetic epidemiology method based on conjunction false discovery rate (FDR) that combines summary statistics from different genome-wide association studies (GWAS), and allows identification of genetic overlap between two phenotypes. We evaluated summary statistics from large, multi-centre GWA studies of PCA (n=50 000) and CVD risk factors (n=200 000) [triglycerides (TG), low-density lipoprotein (LDL) cholesterol and high-density lipoprotein (HDL) cholesterol, systolic blood pressure, body mass index, waist-hip ratio and type 2 diabetes (T2D)]. Enrichment of single nucleotide polymorphisms (SNPs) associated with PCA and CVD risk factors was assessed with conditional quantile-quantile plots and the Anderson-Darling test. Moreover, we pinpointed shared loci using conjunction FDR. RESULTS We found the strongest enrichment of P-values in PCA was conditional on LDL and conditional on TG. In contrast, we found only weak enrichment conditional on HDL or conditional on the other traits investigated. Conjunction FDR identified altogether 17 loci; 10 loci were associated with PCA and LDL, 3 loci were associated with PCA and TG and additionally 4 loci were associated with PCA, LDL and TG jointly (conjunction FDR <0.01). For T2D, we detected one locus adjacent to HNF1B. CONCLUSIONS We found polygenic overlap between PCA predisposition and blood lipids, in particular LDL and TG, and identified 17 pleiotropic gene loci between PCA and LDL, and PCA and TG, respectively. These findings provide novel pathobiological insights and may have implications for trials using targeting lipid-lowering agents in a prevention or cancer setting.
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Affiliation(s)
- Ole A Andreassen
- NORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway, Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway, Prostate Cancer Research Group, Centre for Molecular Medicine Norway, Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, Oslo, Norway, Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA, Multimodal Imaging Laboratory, University of California at San Diego, La Jolla, CA, USA, Cognitive Sciences Graduate Program, University of California, San Diego, La Jolla, CA, USA, Center for Human Development, University of California at San Diego, La Jolla, CA, USA, the participants acknowledged in Supplementary data, available at IJE online, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway, Department of Radiology, University of California, San Diego, La Jolla, CA, USA, Department of Cancer Prevention, Institute of Cancer Research and Department of Urology, Oslo University Hospital, Oslo, Norway and Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA
| | - Verena Zuber
- NORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway, Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway, Prostate Cancer Research Group, Centre for Molecular Medicine Norway, Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, Oslo, Norway, Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA, Multimodal Imaging Laboratory, University of California at San Diego, La Jolla, CA, USA, Cognitive Sciences Graduate Program, University of California, San Diego, La Jolla, CA, USA, Center for Human Development, University of California at San Diego, La Jolla, CA, USA, the participants acknowledged in Supplementary data, available at IJE online, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway, Department of Radiology, University of California, San Diego, La Jolla, CA, USA, Department of Cancer Prevention, Institute of Cancer Research and Department of Urology, Oslo University Hospital, Oslo, Norway and Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA
| | - Wesley K Thompson
- NORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway, Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway, Prostate Cancer Research Group, Centre for Molecular Medicine Norway, Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, Oslo, Norway, Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA, Multimodal Imaging Laboratory, University of California at San Diego, La Jolla, CA, USA, Cognitive Sciences Graduate Program, University of California, San Diego, La Jolla, CA, USA, Center for Human Development, University of California at San Diego, La Jolla, CA, USA, the participants acknowledged in Supplementary data, available at IJE online, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway, Department of Radiology, University of California, San Diego, La Jolla, CA, USA, Department of Cancer Prevention, Institute of Cancer Research and Department of Urology, Oslo University Hospital, Oslo, Norway and Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA
| | - Andrew J Schork
- NORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway, Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway, Prostate Cancer Research Group, Centre for Molecular Medicine Norway, Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, Oslo, Norway, Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA, Multimodal Imaging Laboratory, University of California at San Diego, La Jolla, CA, USA, Cognitive Sciences Graduate Program, University of California, San Diego, La Jolla, CA, USA, Center for Human Development, University of California at San Diego, La Jolla, CA, USA, the participants acknowledged in Supplementary data, available at IJE online, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway, Department of Radiology, University of California, San Diego, La Jolla, CA, USA, Department of Cancer Prevention, Institute of Cancer Research and Department of Urology, Oslo University Hospital, Oslo, Norway and Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA
| | - Francesco Bettella
- NORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway, Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway, Prostate Cancer Research Group, Centre for Molecular Medicine Norway, Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, Oslo, Norway, Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA, Multimodal Imaging Laboratory, University of California at San Diego, La Jolla, CA, USA, Cognitive Sciences Graduate Program, University of California, San Diego, La Jolla, CA, USA, Center for Human Development, University of California at San Diego, La Jolla, CA, USA, the participants acknowledged in Supplementary data, available at IJE online, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway, Department of Radiology, University of California, San Diego, La Jolla, CA, USA, Department of Cancer Prevention, Institute of Cancer Research and Department of Urology, Oslo University Hospital, Oslo, Norway and Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA
| | - the PRACTICAL Consortium
- NORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway, Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway, Prostate Cancer Research Group, Centre for Molecular Medicine Norway, Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, Oslo, Norway, Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA, Multimodal Imaging Laboratory, University of California at San Diego, La Jolla, CA, USA, Cognitive Sciences Graduate Program, University of California, San Diego, La Jolla, CA, USA, Center for Human Development, University of California at San Diego, La Jolla, CA, USA, the participants acknowledged in Supplementary data, available at IJE online, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway, Department of Radiology, University of California, San Diego, La Jolla, CA, USA, Department of Cancer Prevention, Institute of Cancer Research and Department of Urology, Oslo University Hospital, Oslo, Norway and Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA
| | - and the CRUK GWAS
- NORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway, Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway, Prostate Cancer Research Group, Centre for Molecular Medicine Norway, Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, Oslo, Norway, Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA, Multimodal Imaging Laboratory, University of California at San Diego, La Jolla, CA, USA, Cognitive Sciences Graduate Program, University of California, San Diego, La Jolla, CA, USA, Center for Human Development, University of California at San Diego, La Jolla, CA, USA, the participants acknowledged in Supplementary data, available at IJE online, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway, Department of Radiology, University of California, San Diego, La Jolla, CA, USA, Department of Cancer Prevention, Institute of Cancer Research and Department of Urology, Oslo University Hospital, Oslo, Norway and Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA
| | - Srdjan Djurovic
- NORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway, Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway, Prostate Cancer Research Group, Centre for Molecular Medicine Norway, Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, Oslo, Norway, Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA, Multimodal Imaging Laboratory, University of California at San Diego, La Jolla, CA, USA, Cognitive Sciences Graduate Program, University of California, San Diego, La Jolla, CA, USA, Center for Human Development, University of California at San Diego, La Jolla, CA, USA, the participants acknowledged in Supplementary data, available at IJE online, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway, Department of Radiology, University of California, San Diego, La Jolla, CA, USA, Department of Cancer Prevention, Institute of Cancer Research and Department of Urology, Oslo University Hospital, Oslo, Norway and Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA
| | - Rahul S Desikan
- NORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway, Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway, Prostate Cancer Research Group, Centre for Molecular Medicine Norway, Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, Oslo, Norway, Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA, Multimodal Imaging Laboratory, University of California at San Diego, La Jolla, CA, USA, Cognitive Sciences Graduate Program, University of California, San Diego, La Jolla, CA, USA, Center for Human Development, University of California at San Diego, La Jolla, CA, USA, the participants acknowledged in Supplementary data, available at IJE online, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway, Department of Radiology, University of California, San Diego, La Jolla, CA, USA, Department of Cancer Prevention, Institute of Cancer Research and Department of Urology, Oslo University Hospital, Oslo, Norway and Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA
| | - Ian G Mills
- NORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway, Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway, Prostate Cancer Research Group, Centre for Molecular Medicine Norway, Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, Oslo, Norway, Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA, Multimodal Imaging Laboratory, University of California at San Diego, La Jolla, CA, USA, Cognitive Sciences Graduate Program, University of California, San Diego, La Jolla, CA, USA, Center for Human Development, University of California at San Diego, La Jolla, CA, USA, the participants acknowledged in Supplementary data, available at IJE online, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway, Department of Radiology, University of California, San Diego, La Jolla, CA, USA, Department of Cancer Prevention, Institute of Cancer Research and Department of Urology, Oslo University Hospital, Oslo, Norway and Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA
| | - Anders M Dale
- NORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway, Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway, Prostate Cancer Research Group, Centre for Molecular Medicine Norway, Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, Oslo, Norway, Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA, Multimodal Imaging Laboratory, University of California at San Diego, La Jolla, CA, USA, Cognitive Sciences Graduate Program, University of California, San Diego, La Jolla, CA, USA, Center for Human Development, University of California at San Diego, La Jolla, CA, USA, the participants acknowledged in Supplementary data, available at IJE online, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway, Department of Radiology, University of California, San Diego, La Jolla, CA, USA, Department of Cancer Prevention, Institute of Cancer Research and Department of Urology, Oslo University Hospital, Oslo, Norway and Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA
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Parajuli R, Bjerkaas E, Tverdal A, Le Marchand L, Weiderpass E, Gram IT. Smoking increases rectal cancer risk to the same extent in women as in men: results from a Norwegian cohort study. BMC Cancer 2014; 14:321. [PMID: 24884601 PMCID: PMC4024272 DOI: 10.1186/1471-2407-14-321] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/08/2013] [Accepted: 05/01/2014] [Indexed: 11/10/2022] Open
Abstract
Background Smoking has recently been established as a risk factor for rectal cancer. We examined whether the smoking-related increase in rectal cancer differed by gender. Methods We followed 602,242 participants (49% men), aged 19 to 67 years at enrollment from four Norwegian health surveys carried out between 1972 and 2003, by linkage to Norwegian national registries through December 2007. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated by fitting Cox proportional hazard models and adjusting for relevant confounders. Heterogeneity by gender in the effect of smoking and risk of rectal cancer was tested with Wald χ2. Results During a mean follow-up of 14 years, 1,336 men and 840 women developed invasive rectal cancer. Ever smokers had a significantly increased risk of rectal cancer of more than 25% for both men (HR = 1.27, 95% CI = 1.11-1.45) and women (HR = 1.28, 95% CI = 1.11-1.48) compared with gender-specific never smokers. Men smoking ≥20 pack-years had a significantly increased risk of rectal cancer of 35% (HR = 1.35, 95% CI = 1.14-1.58), whereas for women, it was 47% (HR = 1.47, 95% CI = 1.13-1.91) compared with gender-specific never smokers. For both men and women, we observed significant dose–response associations between the risk of rectal cancer for four variables [Age at smoking initiation in years (both ptrend <0.05), number of cigarettes smoked per day (both ptrend <0.0001), smoking duration in years (ptrend <0.05, <0.0001) and number of pack-years smoked (both ptrend <0.0001)]. The test for heterogeneity by gender was not significant between smoking status and the risk of rectal cancer (Wald χ2, p -value; current smokers = 0.85; former smokers = 0.87; ever smokers = 1.00). Conclusions Smoking increases the risk of rectal cancer to the same extent in women as in men.
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Affiliation(s)
| | | | | | | | | | - Inger T Gram
- Department of Community Medicine, Faculty of Health Sciences, UiT, The Arctic University of Tromsø, Tromsø, Norway.
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Parajuli R, Bjerkaas E, Tverdal A, Le Marchand L, Weiderpass E, Gram IT. Cigarette smoking and colorectal cancer mortality among 602,242 Norwegian males and females. Clin Epidemiol 2014; 6:137-45. [PMID: 24741327 PMCID: PMC3984060 DOI: 10.2147/clep.s58722] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022] Open
Abstract
BACKGROUND Colorectal cancer (CRC) is one of the main cancer types, with high incidence and mortality in Norway. We examined the association between different measures of smoking exposure and CRC mortality overall and by subsite in a large Norwegian cohort. METHODS We followed 602,242 participants from four Norwegian health surveys, aged 19-67 years at enrollment between 1972 and 2003 by linkage to the national registries through December 2007. We used Cox proportional hazard models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) by smoking categories for different CRC endpoints. RESULTS During a mean follow-up of 14 years, 2,333 Norwegian males and females died of CRC (60% men). Male and female ever smokers had a 20% (HR 1.23, CI 1.08-1.40 and HR 1.22, 95% CI 1.06-1.40, respectively) increased risk of death from CRC compared with sex-specific never smokers. For proximal colon cancer mortality, female ever smokers had a 50% (HR 1.49, 95% CI 1.20-1.87) increased risk compared with female never smokers. The increased risk of rectal cancer mortality was about 40% higher for male ever smokers (HR 1.43, 95% CI 1.14-1.81) compared with male never smokers. A test for heterogeneity by sex showed an increased risk of rectal cancer mortality among men which was significant for former smokers (Wald χ(2) =0.02) and an increased risk of proximal colon cancer mortality among women which was significant for ever and former smokers (Wald χ(2) =0.02 and χ(2) =0.04, respectively). CONCLUSION Smoking is associated with increased CRC mortality in both sexes. The risk of rectal and proximal colon cancer mortality was most pronounced among male and female smokers respectively.
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Affiliation(s)
- Ranjan Parajuli
- Department of Community Medicine, Faculty of Health Sciences UiT, The Arctic University of Norway, Tromsø, Norway
| | - Eivind Bjerkaas
- Department of Community Medicine, Faculty of Health Sciences UiT, The Arctic University of Norway, Tromsø, Norway
| | - Aage Tverdal
- Division of Epidemiology, Department of Pharmacoepidemiology, Norwegian Institute of Public Health, Oslo, Norway
| | - Loïc Le Marchand
- Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI, USA
| | - Elisabete Weiderpass
- Department of Community Medicine, Faculty of Health Sciences UiT, The Arctic University of Norway, Tromsø, Norway ; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden ; Department of Genetic Epidemiology, Samfundet Folkhälsan, Helsinki, Finland ; Department of Research, Cancer Registry of Norway, Oslo, Norway
| | - Inger T Gram
- Department of Community Medicine, Faculty of Health Sciences UiT, The Arctic University of Norway, Tromsø, Norway ; Norwegian Centre for Integrated Care and Telemedicine, University Hospital of North Norway, Tromsø, Norway
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Abstract
Nearly 36 % of adults and 20 % of children in the USA are obese, defined as a body mass index (BMI) ≥30 kg/m(2). Obesity, which is accompanied by metabolic dysregulation often manifesting in the metabolic syndrome, is an established risk factor for many cancers. Within the growth-promoting, proinflammatory environment of the obese state, cross talk between macrophages, adipocytes, and epithelial cells occurs via obesity-associated hormones, cytokines, and other mediators that may enhance cancer risk and/or progression. This chapter synthesizes the evidence on key biological mechanisms underlying the obesity-cancer link, with particular emphasis on obesity-associated enhancements in growth factor signaling, inflammation, and vascular integrity processes, as well as obesity-dependent microenvironmental perturbations, including the epithelial-to-mesenchymal transition. These interrelated pathways represent possible mechanistic targets for disrupting the obesity-cancer link.
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Affiliation(s)
- Stephen D Hursting
- Department of Nutritional Sciences, Dell Pediatric Research Institute, University of Texas at Austin, 1400 Barbara Jordan Blvd, Austin, TX, 78723, United States,
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A prospective study on metabolic risk factors and gallbladder cancer in the metabolic syndrome and cancer (Me-Can) collaborative study. PLoS One 2014; 9:e89368. [PMID: 24586723 PMCID: PMC3931760 DOI: 10.1371/journal.pone.0089368] [Citation(s) in RCA: 34] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/22/2013] [Accepted: 01/19/2014] [Indexed: 01/18/2023] Open
Abstract
OBJECTIVE To investigate the association between metabolic risk factors (individually and in combination) and risk of gallbladder cancer (GBC). METHODS The metabolic syndrome and cancer project (Me-Can) includes cohorts from Norway, Austria, and Sweden with data on 578,700 men and women. We used Cox proportional hazard regression models to calculate relative risks of GBC by body mass index (BMI), blood pressure, and plasma levels of glucose, cholesterol, and triglycerides as continuous standardised variables and their standardised sum of metabolic syndrome (MetS) z-score. The risk estimates were corrected for random error in measurements. RESULTS During an average follow-up of 12.0 years (SD = 7.8), 184 primary gallbladder cancers were diagnosed. Relative risk of gallbladder cancer per unit increment of z-score adjusted for age, smoking status and BMI (except for BMI itself) and stratified by birth year, sex and sub-cohorts, was for BMI 1.31 (95% confidence interval 1.11, 1.57) and blood glucose 1.76 (1.10, 2.85). Further analysis showed that the effect of BMI on GBC risk is larger among women in the premenopausal age group (1.84 (1.23, 2.78)) compared to those in the postmenopausal age group (1.29 (0.93, 1.79)). For the other metabolic factors no significant association was found (mid blood pressure 0.96 (0.71, 1.31), cholesterol 0.84 (0.66, 1.06) and serum triglycerides 1.16 (0.82, 1.64)). The relative risk per one unit increment of the MetS z-score was 1.37 (1.07, 1.73). CONCLUSION This study showed that increasing BMI and impaired glucose metabolism pose a possible risk for gallbladder cancer. Beyond the individual factors, the results also showed that the metabolic syndrome as an entity presents a risk constellation for the occurrence of gallbladder cancer.
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Lindkvist B, Johansen D, Stocks T, Concin H, Bjørge T, Almquist M, Häggström C, Engeland A, Hallmans G, Nagel G, Jonsson H, Selmer R, Ulmer H, Tretli S, Stattin P, Manjer J. Metabolic risk factors for esophageal squamous cell carcinoma and adenocarcinoma: a prospective study of 580,000 subjects within the Me-Can project. BMC Cancer 2014; 14:103. [PMID: 24548688 PMCID: PMC3929907 DOI: 10.1186/1471-2407-14-103] [Citation(s) in RCA: 79] [Impact Index Per Article: 7.2] [Reference Citation Analysis] [Abstract] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/27/2013] [Accepted: 02/06/2014] [Indexed: 01/24/2023] Open
Abstract
Background Obesity is associated with an increased risk of esophageal adenocarcinoma (EAC) and a decreased risk of esophageal squamous cell carcinoma (ESCC). However, little is known about the risk of EAC and ESCC related to other metabolic risk factors. We aimed to examine the risk of EAC and ESCC in relation to metabolic risk factors, separately and combined in a prospective cohort study. Methods The Metabolic Syndrome and Cancer cohort includes prospective cohorts in Austria, Norway and Sweden, with blood pressure, lipids, glucose and BMI available from 578 700 individuals. Relative risk (RR) for EAC and ESCC was calculated using Cox’s proportional hazards analysis for metabolic risk factors categorized into quintiles and transformed into z-scores. The standardized sum of all z-scores was used as a composite score for the metabolic syndrome (MetS). Results In total, 324 histologically verified cases of esophageal cancer were identified (114 EAC, 184 ESCC and 26 with other histology). BMI was associated with an increased risk of EAC (RR 7.34 (95% confidence interval, 2.88-18.7) top versus bottom quintile) and negatively associated with the risk of ESCC (RR 0.38 (0.23-0.62)). The mean value of systolic and diastolic blood pressure (mid blood pressure) was associated with the risk of ESCC (RR 1.77 (1.37-2.29)). The composite MetS score was associated with the risk of EAC (RR 1.56 (1.19-2.05) per one unit increase of z-score) but not ESCC. Conclusions In accordance with previous studies, high BMI was associated with an increased risk of EAC and a decreased risk of ESCC. An association between high blood pressure and risk of ESCC was observed but alcohol consumption is a potential confounding factor that we were not able to adjust for in the analysis. The MetS was associated with EAC but not ESCC. However this association was largely driven by the strong association between BMI and EAC. We hypothesize that this association is more likely to be explained by factors directly related to obesity than the metabolic state of the MetS, considering that no other metabolic factor than BMI was associated with EAC.
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Affiliation(s)
- Björn Lindkvist
- Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
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Wirén S, Häggström C, Ulmer H, Manjer J, Bjørge T, Nagel G, Johansen D, Hallmans G, Engeland A, Concin H, Jonsson H, Selmer R, Tretli S, Stocks T, Stattin P. Pooled cohort study on height and risk of cancer and cancer death. Cancer Causes Control 2013; 25:151-9. [PMID: 24173535 PMCID: PMC3929024 DOI: 10.1007/s10552-013-0317-7] [Citation(s) in RCA: 70] [Impact Index Per Article: 5.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/28/2013] [Accepted: 10/21/2013] [Indexed: 10/26/2022]
Abstract
PURPOSE To assess the association between height and risk of cancer and cancer death. METHODS The metabolic syndrome and cancer project is a prospective pooled cohort study of 585,928 participants from seven cohorts in Austria, Norway, and Sweden. Hazard ratios (HRs) and 95 % confidence intervals (CIs) for cancer incidence and death were estimated in height categories and per 5-cm increment for each cancer site using Cox proportional hazards model. RESULTS During a mean follow-up of 12.7 years (SD = 7.2), 38,862 participants were diagnosed with cancer and 13,547 participants died of cancer. Increased height (per 5-cm increment) was associated with an increased overall cancer risk in women, HR 1.07 (95 % CI 1.06-1.09), and in men, HR 1.04 (95 % CI 1.03-1.06). The highest HR was seen for malignant melanoma in women, HR 1.17 (95 % CI 1.11-1.24), and in men HR 1.12 (95 % CI 1.08-1.19). Height was also associated with increased risk of cancer death in women, HR 1.03 (95 % CI 1.01-1.16), and in men, HR 1.03 (95 % CI 1.01-1.05). The highest HR was observed for breast cancer death in postmenopausal women (>60 years), HR 1.10 (95 % CI 1.00-1.21), and death from renal cell carcinoma in men, HR 1.18 (95 % CI 1.07-1.30). All these associations were independent of body mass index. CONCLUSION Height was associated with risk of cancer and cancer death indicating that factors related to height such as hormonal and genetic factors stimulate both cancer development and progression.
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Affiliation(s)
- Sara Wirén
- Department of Surgery and Perioperative Sciences, Urology and Andrology, Umeå University, 901 87, Umeå, Sweden,
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Gallagher EJ, LeRoith D. Epidemiology and molecular mechanisms tying obesity, diabetes, and the metabolic syndrome with cancer. Diabetes Care 2013; 36 Suppl 2:S233-9. [PMID: 23882051 PMCID: PMC3920794 DOI: 10.2337/dcs13-2001] [Citation(s) in RCA: 100] [Impact Index Per Article: 8.3] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]
Affiliation(s)
- Emily J Gallagher
- Division of Endocrinology, Diabetes and Bone Disease, Samuel Bronfman Department of Medicine, Mount Sinai School of Medicine, New York, New York, USA
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Smoking duration before first childbirth: an emerging risk factor for breast cancer? Results from 302,865 Norwegian women. Cancer Causes Control 2013; 24:1347-56. [PMID: 23633026 PMCID: PMC3675272 DOI: 10.1007/s10552-013-0213-1] [Citation(s) in RCA: 44] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/30/2012] [Accepted: 04/13/2013] [Indexed: 12/19/2022]
Abstract
PURPOSE Recently, The International Agency for Research on Cancer classified cigarette smoking as possibly carcinogenic to the human breast. Since some new cohort studies have suggested that this risk is confined to women who started to smoke before first childbirth, we wanted to examine the association between smoking and breast cancer, with a focus on time of smoking initiation in relation to the first childbirth. METHODS We followed 302,865 Norwegian women born between 1899 and 1975, recruited from 1974 to 2003, by linkage to national registries through December 2007. We used Cox proportional hazard models to estimate hazard ratios (HR) and 95% confidence intervals (CI). RESULTS During more than 4.1 million person-years of follow-up, we ascertained 7,490 cases of primary invasive breast cancer. Compared with never smokers, ever smokers had a 15% (HR = 1.15, 95% CI 1.10-1.21) increased risk of breast cancer overall and also a significantly increased risk of breast cancer in the three most exposed categories of age at smoking initiation (parous women), number of cigarettes smoked per day, years of smoking duration and number of pack-years. Ever smokers who started to smoke more than 1 year after the first childbirth had not an increased risk (HR = 0.93, 95% CI 0.86-1.02), while those who initiated smoking more than 10 years before their first childbirth had a 60% (HR = 1.60, 95% CI 1.42-1.80) increased risk of breast cancer, compared with never smokers. CONCLUSION Smoking initiation before the first childbirth increases the risk of breast cancer.
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Parajuli R, Bjerkaas E, Tverdal A, Selmer R, Le Marchand L, Weiderpass E, Gram IT. The increased risk of colon cancer due to cigarette smoking may be greater in women than men. Cancer Epidemiol Biomarkers Prev 2013; 22:862-71. [PMID: 23632818 DOI: 10.1158/1055-9965.epi-12-1351] [Citation(s) in RCA: 38] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2022] Open
Abstract
BACKGROUND Smoking is a recently established risk factor for colon cancer. We wanted to explore the hypothesis that women may be more susceptible to smoking-attributed colon cancer than men as one of the possible explanations for the high colon cancer risk of Norwegian women. METHODS We followed 602,242 participants aged 19 to 67 years at enrollment in 1972-2003, by linkage to national registries through December 2007. We used Cox proportional hazard models to estimate HRs and 95% confidence intervals (CI). RESULTS During a mean follow-up of 14 years, altogether 3,998 (46% women) subjects developed colon cancer. Female ever-smokers had a 19% (HR = 1.19, 95% CI = 1.09-1.32) and male ever-smokers an 8% (HR = 1.08, CI = 0.97-1.19) increased risk of colon cancer compared with never smokers. For all the four dose-response variables examined, female ever-smokers in the most exposed category of smoking initiation, (HR = 1.48, 95% CI = 1.21-1.81), of daily cigarette consumption (HR = 1.28, 95% CI = 1.06-1.55), of smoking duration (HR = 1.47, 95% CI = 1.11-1.95), and of pack-years of smoking (HR = 1.33, 95% CI = 1.11-1.57) had a significantly increased risk of more than 20% for colon cancer overall and of more than 40% for proximal colon cancer, compared with never smokers. A test for heterogeneity by gender was statistically significant only for ever smoking and risk of proximal colon cancer (Wald χ(2), P = 0.02). CONCLUSIONS Female smokers may be more susceptible to colon cancer and especially to proximal colon cancer than male smokers. IMPACT Women who smoke are more vulnerable to colon cancer than men.
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Affiliation(s)
- Ranjan Parajuli
- Department of Community Medicine, University of Tromsø, N-9037 Tromsø, Norway
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Abstract
The growing epidemic of obesity has resulted in a large increase in multiple related diseases. Recent evidence has strengthened the proposed synergistic relationship between obesity-related insulin resistance (IR) and/or diabetes mellitus (DM) and cancer. Within the past year, many studies have examined this relationship. Although the precise mechanisms and pathways are uncertain, it is becoming clear that hyperinsulinemia and possibly sustained hyperglycemia are important regulators of not only the development of cancer but also of treatment outcome. Further, clinical decision-making regarding the treatment of choice for DM will likely be impacted as we learn more about the non-metabolic effects of the available hyperglycemic agents. In our review, we endeavored to synthesize the recent literature and provide a concise view of the journey from macro-level clinical associations to specific mechanistic relationships being elucidated in cell lines and animal models.
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Affiliation(s)
- Etan Orgel
- Jonathan Jaques Children’s Cancer Center, Keck School of Medicine, University of Southern California, Miller Children’s Hospital, 2801 Atlantic Avenue, Long Beach, CA 90806, 562-933-8600 phone
| | - Steven D. Mittelman
- Children’s Hospital Los Angeles, Keck School of Medicine, University of Southern California, 4650 Sunset Blvd., MS #93, Los Angeles, CA 90027, 323-361-7653 phone
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Häggström C, Rapp K, Stocks T, Manjer J, Bjørge T, Ulmer H, Engeland A, Almqvist M, Concin H, Selmer R, Ljungberg B, Tretli S, Nagel G, Hallmans G, Jonsson H, Stattin P. Metabolic factors associated with risk of renal cell carcinoma. PLoS One 2013; 8:e57475. [PMID: 23468995 PMCID: PMC3585341 DOI: 10.1371/journal.pone.0057475] [Citation(s) in RCA: 53] [Impact Index Per Article: 4.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/17/2012] [Accepted: 01/21/2013] [Indexed: 01/20/2023] Open
Abstract
Previous studies have shown that obesity and hypertension are associated with increased risk of renal cell carcinoma (RCC), but less is known about the association to other metabolic factors. In the Metabolic Syndrome and Cancer project (Me-Can) data on body mass index (BMI, kg/m2), blood pressure, and circulating levels of glucose, cholesterol, and triglycerides were collected from 560,388 men and women in cohorts from Norway, Austria, and Sweden. By use of Cox proportional hazard models, hazard ratios (HR) were calculated for separate and composite metabolic exposures. During a median follow-up of 10 years, 592 men and 263 women were diagnosed with RCC. Among men, we found an increased risk of RCC for BMI, highest vs. lowest quintile, (HR = 1.51, 95% CI 1.13–2.03), systolic blood pressure, (HR = 3.40, 95% CI 1.91–6.06), diastolic blood pressure, (HR = 3.33, 95% CI 1.85–5.99), glucose, (HR = 3.75, 95% CI 1.46–9.68), triglycerides, (HR = 1.79, 95% CI 1.00–3.21) and a composite score of these metabolic factors, (HR = 2.68, 95% CI 1.75–4.11). Among women we found an increased risk of RCC for BMI, highest vs. lowest quintile, (HR = 2.21, 95% CI 1.32–3.70) and the composite score, (HR = 2.29, 95% CI 1.12–4.68). High levels of the composite score were also associated with risk of death from RCC among both men and women. No multiplicative statistical or biological interactions between metabolic factors on risk of RCC were found. High levels of BMI, blood pressure, glucose and triglycerides among men and high BMI among women were associated with increased risk of RCC.
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Affiliation(s)
- Christel Häggström
- Department of Surgical and Perioperative sciences, Urology and Andrology, Umeå University, Umeå, Sweden.
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Strohmaier S, Edlinger M, Manjer J, Stocks T, Bjørge T, Borena W, Häggström C, Engeland A, Nagel G, Almquist M, Selmer R, Tretli S, Concin H, Hallmans G, Jonsson H, Stattin P, Ulmer H. Total serum cholesterol and cancer incidence in the Metabolic syndrome and Cancer Project (Me-Can). PLoS One 2013; 8:e54242. [PMID: 23372693 PMCID: PMC3553083 DOI: 10.1371/journal.pone.0054242] [Citation(s) in RCA: 98] [Impact Index Per Article: 8.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/03/2012] [Accepted: 12/10/2012] [Indexed: 12/13/2022] Open
Abstract
OBJECTIVE To investigate the association between total serum cholesterol (TSC) and cancer incidence in the Metabolic syndrome and Cancer project (Me-Can). METHODS Me-Can consists of seven cohorts from Norway, Austria, and Sweden including 289,273 male and 288,057 female participants prospectively followed up for cancer incidence (n = 38,978) with a mean follow-up of 11.7 years. Cox regression models with age as the underlying time metric were used to estimate hazard ratios (HR) and their 95% confidence intervals (CI) for quintiles of cholesterol levels and per 1 mmol/l, adjusting for age at first measurement, body mass index (BMI), and smoking status. Estimates were corrected for regression dilution bias. Furthermore, we performed lag time analyses, excluding different times of follow-up, in order to check for reverse causation. RESULTS In men, compared with the 1st quintile, TSC concentrations in the 5th quintile were borderline significantly associated with decreasing risk of total cancer (HR = 0.94; 95%CI: 0.88, 1.00). Significant inverse associations were observed for cancers of the liver/intrahepatic bile duct (HR = 0.14; 95%CI: 0.07, 0.29), pancreas cancer (HR = 0.52, 95% CI: 0.33, 0.81), non-melanoma of skin (HR = 0.67; 95%CI: 0.46, 0.95), and cancers of the lymph-/hematopoietic tissue (HR = 0.68, 95%CI: 0.54, 0.87). In women, hazard ratios for the 5th quintile were associated with decreasing risk of total cancer (HR = 0.86, 95%CI: 0.79, 0.93) and for cancers of the gallbladder (HR = 0.23, 95%CI: 0.08, 0.62), breast (HR = 0.70, 95%CI: 0.61, 0.81), melanoma of skin (HR = 0.61, 95%CI: 0.42, 0.88), and cancers of the lymph-/hematopoietic tissue (HR = 0.61, 95%CI: 0.44, 0.83). CONCLUSION TSC was negatively associated with risk of cancer overall in females and risk of cancer at several sites in both males and females. In lag time analyses some associations persisted, suggesting that for these cancer sites reverse causation did not apply.
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Affiliation(s)
- Susanne Strohmaier
- Department of Medical Statistics, Informatics and Health Economics, Innsbruck Medical University, Innsbruck, Austria
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Prospective cohort study of metabolic risk factors and gastric adenocarcinoma risk in the Metabolic Syndrome and Cancer Project (Me-Can). Cancer Causes Control 2012; 24:107-16. [DOI: 10.1007/s10552-012-0096-6] [Citation(s) in RCA: 28] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/24/2012] [Accepted: 11/02/2012] [Indexed: 01/04/2023]
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