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Mumtaz S, Akhtar N, Ahmed A, Qazi AS. Dietary Pattern and Cancer. Cancer Treat Res 2024; 191:191-216. [PMID: 39133409 DOI: 10.1007/978-3-031-55622-7_8] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 08/13/2024]
Abstract
Diet play an important role in the development of cancer. A lot of research has been done on the role of individual nutrients or phytochemicals and cancer risk. Both harmful and beneficial associations of this nutrient have been observed with cancer. However, there is an interaction of individual dietary constituents to influence disease risk. On the other hand, examining the diet as a whole as is done in dietary patterns research may produce more accurate estimates and data that can be more easily translated into dietary recommendations. Dietary patterns and cancer research are becoming increasingly common in the epidemiology literature, and novel dietary patterns are being generated at a rapid pace. However, major issues remain over whether one general "healthy" dietary pattern can be suggested for cancer prevention or whether several diets should be advocated for different forms of cancer protection. It is challenging to study typical human diet in animal model that is appropriate for cancer prevention. Some dietary patterns, such as the ketogenic diet or macronutrient composition alteration, have been investigated more extensively in animal models than in humans in terms of cancer prevention, and bigger human observational studies are now needed to advise dietary guidelines. The question of whether to adapt nutritional guidelines to population subgroups based on susceptibility factors (for example, family history, sex, age, other lifestyle factors or comorbidities, metabolomics signatures, or microbiota-based profiles) is still open and will be crucial in moving the field forward.
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Affiliation(s)
- Sara Mumtaz
- National University of Medical Sciences (NUMS), Rawalpindi, Pakistan.
| | - Nosheen Akhtar
- National University of Medical Sciences (NUMS), Rawalpindi, Pakistan
| | | | - Asma Saleem Qazi
- National University of Medical Sciences (NUMS), Rawalpindi, Pakistan
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2
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Zou M, Liang Q, Zhang W, Zhu Y, Xu Y. Causal association between dietary factors and esophageal diseases: A Mendelian randomization study. PLoS One 2023; 18:e0292113. [PMID: 38019753 PMCID: PMC10686502 DOI: 10.1371/journal.pone.0292113] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/15/2023] [Accepted: 10/17/2023] [Indexed: 12/01/2023] Open
Abstract
BACKGROUND Using Mendelian randomization (MR) approach, our objective was to determine whether there was a causal association between dietary factors and gastroesophageal reflux disease (GERD), Barrett's esophagus (BE), or esophageal cancer (EC). METHODS Genome-wide association study (GWAS) data for eighteen types of dietary intake were obtained from the UK Biobank. GWAS data for GERD, BE, and EC were sourced from the FinnGen consortium. We performed univariable and multivariable MR analysis to assess the cause effect between dietary factors and esophageal diseases. MR results were expressed as odds ratios (OR) with 95% confidence intervals (CI). RESULTS Raw vegetable intake was associated with a lower risk of GERD (OR = 0.478; P = 0.011). On the contrary, cooked vegetable intake increased the risk of GERD (OR = 1.911; P = 0.024). Bread intake was associated with increased odds of BE (OR = 6.754; P = 0.007), while processed meat intake was associated with reduced risk of BE (OR = 0.210; P = 0.035). We also observed evidence that increased consumption of dried fruit (OR = 0.087; P = 0.022) and salt added to food (OR = 0.346; P = 0.045) could prevent EC. The results of multivariable MR showed that the protective effect of consumption of salt added to food on EC was no longer significant after adjusting for the consumption of dried fruit. CONCLUSION Vegetable consumption was associated with GERD, whereas consumption of bread and processed meat was associated with BE. Dried fruit intake was associated with a lower risk of EC, and the protective effect of consumption of salt added food on EC may also be mediated by consumption of dried fruit. Future research should be performed to investigate the mechanisms behind these cause-and-effect relationships to reduce the burden of disease caused by dietary habits.
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Affiliation(s)
- Menglong Zou
- The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, China
- Graduate School of Hunan University of Chinese Medicine, Changsha, Hunan, China
| | - Qiaoli Liang
- Zhuhai Second Hospital of Chinese Medicine, Zhuhai, Guangdong, China
| | - Wei Zhang
- The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, China
- Graduate School of Hunan University of Chinese Medicine, Changsha, Hunan, China
| | - Ying Zhu
- The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, China
| | - Yin Xu
- The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, China
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3
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Nakauchi M, Vos EL, Carr RA, Barbetta A, Tang LH, Gonen M, Russo A, Janjigian YY, Yoon SS, Sihag S, Rusch VW, Bains MS, Jones DR, Coit DG, Molena D, Strong VE. Distinct Differences in Gastroesophageal Junction and Gastric Adenocarcinoma in 2194 Patients: In Memory of Rebecca A. Carr, February 24, 1988-January 19, 2021. Ann Surg 2023; 277:629-636. [PMID: 34845172 PMCID: PMC9148370 DOI: 10.1097/sla.0000000000005320] [Citation(s) in RCA: 9] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
Abstract
OBJECTIVE We sought to compare gastroesophageal junction (GEJ) cancer and gastric cancer (GC) and identify clinicopathological and oncological differences. SUMMARY BACKGROUND DATA GEJ cancer and GC are frequently studied together. Although the treatment approach for each often differs, clinico-pathological and oncological differences between the 2 have not been fully evaluated. METHODS We retrospectively identified patients with GEJ cancer or GC who underwent R0 resection at our center between January 2000 and December 2016. Clinicopathological characteristics, disease-specific survival (DSS), and site of first recurrence were compared. RESULTS In total, 2194 patients were analyzed: 1060 (48.3%) with GEJ cancer and 1134 (51.7%) with GC. Patients with GEJ cancer were younger (64 vs 66 years; P < 0.001), more often received neoadjuvant treatment (70.9% vs 30.2%; P < 0.001), and had lower pathological T and N status. Five-year DSS was 62.2% in patients with GEJ cancer and 74.6% in patients with GC ( P < 0.001). After adjustment for clinicopathological factors, DSS remained worse in patients with GEJ cancer (hazard ratio, 1.78; 95% confidence interval, 1.40-2.26; P < 0.001). The cumulative incidence of recurrence was approximately 10% higher in patients with GEJ cancer ( P < 0.001). The site of first recurrence was more likely to be hematogenous in patients with GEJ cancer (60.1% vs 31.4%; P < 0.001) and peritoneal in patients with GC (52.9% vs 12.5%; P < 0.001). CONCLUSIONS GEJ adenocarcinoma is more aggressive, with a higher incidence of recurrence and worse DSS, compared with gastric adenocarcinoma. Distinct differences between GEJ cancer and GC, especially in patterns of recurrence, may affect evaluation of optimal treatment strategies.
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Affiliation(s)
- Masaya Nakauchi
- Gastric and Mixed Tumor Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY
| | - Elvira L. Vos
- Gastric and Mixed Tumor Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY
| | - Rebecca A. Carr
- Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY
| | - Arianna Barbetta
- Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY
| | - Laura H. Tang
- Gastrointestinal Pathology Service, Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY
| | - Mithat Gonen
- Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY
| | - Ashley Russo
- Gastric and Mixed Tumor Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY
| | - Yelena Y. Janjigian
- Gastrointestinal Oncology Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY
| | - Sam S. Yoon
- Gastric and Mixed Tumor Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY
| | - Smita Sihag
- Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY
| | - Valerie W. Rusch
- Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY
| | - Manjit S. Bains
- Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY
| | - David R. Jones
- Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY
| | - Daniel G. Coit
- Gastric and Mixed Tumor Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY
| | - Daniela Molena
- Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY
| | - Vivian E. Strong
- Gastric and Mixed Tumor Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY
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4
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Teufel A, Quante M, Kandulski A, Hirth M, Zhan T, Eckardt M, Thieme R, Kusnik A, Yesmembetov K, Wiest I, Riemann JF, Schlitt HJ, Gockel I, Malfertheiner P, Ebert MP. [Prevention of gastrointestinal cancer]. ZEITSCHRIFT FUR GASTROENTEROLOGIE 2021; 59:964-982. [PMID: 34507375 DOI: 10.1055/a-1540-7539] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 10/20/2022]
Abstract
Throughout the past decades, considerable progress has been made in the (early) diagnosis and treatment of gastrointestinal cancers. However, the prognosis for advanced stages of gastrointestinal tumors remains limited for many patients and approximately one third of all tumor patients die as a result of gastrointestinal tumors. The prevention and early detection of gastrointestinal tumors is therefore of great importance.For this reason, we summarize the current state of knowledge and recommendations for the primary, secondary and tertiary prevention of esophageal, stomach, pancreas, liver and colorectal cancer in the following.
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Affiliation(s)
- Andreas Teufel
- II. Medizinische Klinik, Sektion Hepatologie, Medizinische Fakultät Mannheim, Universität Heidelberg, Universitätsklinikum Mannheim, Mannheim.,Klinische Kooperationseinheit Healthy Metabolism, Zentrum für Präventivmedizin und Digitale Gesundheit Baden-Württemberg, Medizinische Fakultät Mannheim, Universität Heidelberg, Mannheim
| | - Michael Quante
- Klinik für Innere Medizin II, Medizinische Universitätsklinik, Universitätsklinikum Freiburg, Freiburg im Breisgau
| | - Arne Kandulski
- Klinik und Poliklinik für Innere Medizin I, Universitätsklinikum Regensburg, Regensburg
| | - Michael Hirth
- II. Medizinische Klinik, Medizinische Fakultät Mannheim, Universität Heidelberg, Mannheim, Universitätsklinikum Mannheim, Mannheim
| | - Tianzuo Zhan
- II. Medizinische Klinik, Medizinische Fakultät Mannheim, Universität Heidelberg, Mannheim, Universitätsklinikum Mannheim, Mannheim
| | - Maximilian Eckardt
- II. Medizinische Klinik, Medizinische Fakultät Mannheim, Universität Heidelberg, Mannheim, Universitätsklinikum Mannheim, Mannheim
| | - René Thieme
- Klinik und Poliklinik für Viszeral-, Transplantations-, Thorax- und Gefäßchirurgie, Department für Operative Medizin (DOPM), Universitatsklinikum Leipzig, Leipzig
| | - Alexander Kusnik
- II. Medizinische Klinik, Medizinische Fakultät Mannheim, Universität Heidelberg, Mannheim, Universitätsklinikum Mannheim, Mannheim
| | - Kakharman Yesmembetov
- Klinik für Gastroenterologie, Stoffwechselerkrankungen und Internistische Intensivmedizin (Med. III), RWTH Universitätsklinikum Aachen, Aachen
| | - Isabella Wiest
- II. Medizinische Klinik, Medizinische Fakultät Mannheim, Universität Heidelberg, Mannheim, Universitätsklinikum Mannheim, Mannheim
| | | | - Hans Jürgen Schlitt
- Klinik und Poliklinik für Chirurgie, Universitatsklinikum Regensburg, Regensburg
| | - Ines Gockel
- Klinik und Poliklinik für Viszeral-, Transplantations-, Thorax- und Gefäßchirurgie, Department für Operative Medizin (DOPM), Universitatsklinikum Leipzig, Leipzig
| | - Peter Malfertheiner
- Klinik für Gastroenterologie, Hepatologie und Infektiologie, Medizinische Fakultät Magdeburg, Magdeburg
| | - Matthias Philip Ebert
- II. Medizinische Klinik, Medizinische Fakultät Mannheim, Universität Heidelberg, Mannheim, Universitätsklinikum Mannheim, Mannheim.,Klinische Kooperationseinheit Healthy Metabolism, Zentrum für Präventivmedizin und Digitale Gesundheit Baden-Württemberg, Medizinische Fakultät Mannheim, Universität Heidelberg, Mannheim
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Heavy Alcohol Use Is Associated With Gastric Cancer: Analysis of the National Health and Nutrition Examination Survey From 1999 to 2010. Am J Gastroenterol 2021; 116:1083-1086. [PMID: 33625123 PMCID: PMC9354725 DOI: 10.14309/ajg.0000000000001166] [Citation(s) in RCA: 22] [Impact Index Per Article: 5.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/09/2020] [Accepted: 12/29/2020] [Indexed: 12/11/2022]
Abstract
INTRODUCTION Evidence regarding the association between alcohol use and gastric cancer (GC) has been inconsistent. METHODS Adults who participated in the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2010 were included. Multivariable regression was used to assess the association between GC and heavy alcohol use (≥5 alcoholic drinks daily). RESULTS Of 470,168 individuals surveyed, 342 had a history of GC. Heavy alcohol use was associated with GC (odds ratio 3.13, 95% confidence interval 1.15-8.64) on multivariable analysis. DISCUSSION This is the largest study to our knowledge to demonstrate an association between heavy alcohol use and GC in the United States.
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6
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Yu X, Chen J, Jiang W, Zhang D. Alcohol, Alcoholic Beverages and Risk of Esophageal Cancer by Histological Type: A Dose–Response Meta-Analysis of Observational Studies. Alcohol Alcohol 2020; 55:457-467. [DOI: 10.1093/alcalc/agaa047] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 08/30/2023] Open
Abstract
Abstract
Aims
We conducted a dose–response meta-analysis to explore the association between alcohol and particular alcoholic beverages with risk of esophageal cancer (EC) by histological type [esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC)] and whether the association differs according to gender.
Methods
PubMed and Web of Science databases were searched for relevant articles published between January 1960 and December 2019. The pooled relative ratios (RRs) and 95% confidence interval (CI) were calculated with the fixed or random effect model. The dose–response relationship was assessed by restricted cubic spline.
Results
A total of 74 published articles involving 31,105 cases among 3,369,024 participants were included in this meta-analysis. The pooled RRs of the highest versus lowest alcohol intake were 3.67 (95% CI, 2.89,4.67) for EC, 5.11 (95% CI, 3.60,7.25) for ESCC and 0.96 (95% CI, 0.79,1.16) for EAC. The above-mentioned associations were observed in cohort design, for different alcoholic beverages (beer, wine and liquor/spirits) and gender. Evidence of a nonlinear dose–response relationship for EC risk with alcohol intake was found (Pnon-linearity < 0.001), and a linear relationship (Pnon-linearity = 0.216) suggested that the risk of ESCC increased by 33% for every 12.5 g/day increment of alcohol intake.
Conclusions
This meta-analysis suggests that alcohol intake might significantly increase the incidence of EC, especially for ESCC.
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Affiliation(s)
- Xiaohui Yu
- Department of Epidemiology and Health Statistics, The School of Public Health of Qingdao University, 308 Ningxia Road, Qingdao, Shandong 266071, People’s Republic of China
| | - Jiahao Chen
- Department of Epidemiology and Health Statistics, The School of Public Health of Qingdao University, 308 Ningxia Road, Qingdao, Shandong 266071, People’s Republic of China
| | - Wenjie Jiang
- Department of Epidemiology and Health Statistics, The School of Public Health of Qingdao University, 308 Ningxia Road, Qingdao, Shandong 266071, People’s Republic of China
| | - Dongfeng Zhang
- Department of Epidemiology and Health Statistics, The School of Public Health of Qingdao University, 308 Ningxia Road, Qingdao, Shandong 266071, People’s Republic of China
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7
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Zhang YJ, Wang YY, Yang Q, Li JB. Scaphoid metastasis as the first sign of occult gastroesophageal junction cancer: A case report. World J Clin Cases 2020; 8:1287-1294. [PMID: 32337204 PMCID: PMC7176614 DOI: 10.12998/wjcc.v8.i7.1287] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/20/2019] [Revised: 01/13/2020] [Accepted: 03/09/2020] [Indexed: 02/05/2023] Open
Abstract
BACKGROUND Metastatic tumors of the hand are very rare. They are usually late manifestations of massive advanced malignancies. However, a small portion of acrometastases are indications of occult primary cancer. Here, we report an extremely rare case in which a scaphoid bone lesion was the initial manifestation and was found to be a metastasis from gastroesophageal junction (GEJ) cancer.
CASE SUMMARY A 57-year-old male patient presented with ongoing left wrist pain and swelling after trauma. He was initially misdiagnosed with infection of the scaphoid bone and treated with antibiotics and anti-inflammatory drugs. Further radiographic investigations showed a scaphoid pathological fracture, indicating a metastatic tumor derived from the GEJ and/or right lung malignancies. Gastroscopy failed to identify the pathology of the mass at the GEJ, which grew in an exophytic pattern. A lung puncture biopsy was not performed because the patient refused the procedure. To relieve his wrist pain and obtain a definite pathology, we resected the scaphoid lesion. Based on the clinical and pathological results, the patient was finally diagnosed with multiple metastases of advanced GEJ adenocarcinoma. He underwent chemotherapy and died 6 mo after his initial presentation.
CONCLUSION Despite the rareness of the disease, orthopedic surgeons should consider the possibility of metastasis to the bones of the hand when patients complain of persistent and progressive pain in the hand.
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Affiliation(s)
- Yu-Jie Zhang
- Department of Orthopedic Surgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, Zhejiang Province, China
| | - Yan-Yan Wang
- Department of Oncology Surgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, Zhejiang Province, China
| | - Qi Yang
- Department of Pathology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, Zhejiang Province, China
| | - Jian-Bing Li
- Department of Orthopedic Surgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, Zhejiang Province, China
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8
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Ma JL, Zhao Y, Guo CY, Hu HT, Zheng L, Zhao EJ, Li HL. Dietary vitamin B intake and the risk of esophageal cancer: a meta-analysis. Cancer Manag Res 2018; 10:5395-5410. [PMID: 30464635 PMCID: PMC6225909 DOI: 10.2147/cmar.s168413] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/23/2022] Open
Abstract
BACKGROUND Several epidemiology studies have explored the association between dietary B vitamins' intake and the risk of esophageal cancer (EC). However, the results remain inconclusive. Thus, we conducted a systematic review with meta-analysis to evaluate such association. METHODS Literature retrieval was performed using PubMed (Medline), ScienceDirect, and Cochrane Library electronic databases for all studies published from database inception to December 2017. RESULTS The meta-analysis included 19 studies and showed an overall decreased risk of EC (OR=0.77, 95% CI: 0.68-0.87) in association with multivitamin B (ie, B1, B2, B3, B5, B6, B9, and B12) dietary intake. In a subgroup analysis based on vitamin B subclass, B1, B3, B6, and B9 vitamins were associated with decreased EC risk (vitamin B1: OR=0.68, 95% CI: 0.56-0.82; vitamin B3: OR=0.70, 95% CI: 0.53-0.94; vitamin B6: OR=0.64, 95% CI: 0.49-0.83; and vitamin B9: OR=0.69, 95% CI: 0.55-0.86). By contrast, no association was detected between dietary vitamin B2 and vitamin B5 intake and EC risk (vitamin B2: OR=0.86, 95% CI: 0.64-1.16; vitamin B5: OR=0.49, 95% CI: 0.20-1.20), whereas a potential non-linear dose-response association was found between dietary vitamin B12 intake and EC risk. A statistically significant, inverse association was observed for an increase of 100 µg/day in supplemental vitamin B6 and B9 and EC risk (vitamin B6: OR=0.98, 95% CI: 0.98-0.99; vitamin B9: OR= 0.89; 95% CI: 0.86-0.94). CONCLUSION These findings support that vitamin B may have an influence on carcinogenesis of the esophagus. Vitamin B1, B3, B6, B9 showed a decreased risk of EC, and vitamin B12 showed an increased risk of EC.
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Affiliation(s)
- Jun-Li Ma
- Department of Radiology Intervention, Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou 450003, China,
| | - Yan Zhao
- Department of Radiology Intervention, Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou 450003, China,
| | - Chen-Yang Guo
- Department of Radiology Intervention, Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou 450003, China,
| | - Hong-Tao Hu
- Department of Radiology Intervention, Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou 450003, China,
| | - Lin Zheng
- Department of Radiology Intervention, Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou 450003, China,
| | - Er-Jiang Zhao
- Department of Epidemiology and Biostatistics, Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou 450003, China
| | - Hai-Liang Li
- Department of Radiology Intervention, Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou 450003, China,
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Wang QL, Xie SH, Li WT, Lagergren J. Smoking Cessation and Risk of Esophageal Cancer by Histological Type: Systematic Review and Meta-analysis. J Natl Cancer Inst 2017; 109. [DOI: 10.1093/jnci/djx115] [Citation(s) in RCA: 51] [Impact Index Per Article: 6.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 08/30/2023] Open
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10
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He D, Huang X, Wang ZP, Chen D, Chen J, Duan CY. Dietary fat intake and risk of esophageal carcinoma: a meta-analysis of observational studies. Oncotarget 2017; 8:99049-99056. [PMID: 29228750 PMCID: PMC5716790 DOI: 10.18632/oncotarget.21462] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/27/2017] [Accepted: 09/21/2017] [Indexed: 01/02/2023] Open
Abstract
Dietary fat intake is potentially associated with the onset of esophageal carcinoma (EC), but evidence from observational studies has remained unclear. This study aimed to evaluate the role of fat intake in the development of esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma (ESCC). A systematic search was conducted in PubMed and Web of Science to identify all relevant studies. Study-specific relative risks (RR) for the highest versus the lowest intake categories and 95% confidence intervals (CI) were pooled using a random-effects model. Seventeen case-control studies (2058 EAC cases, 1581 ESCC cases and 11696 controls) and two prospective cohort studies (494, 978 participants and 630 EAC cases and 215 ESCC cases) were identified. In EAC, the RRs (95% CI) were 1.69 (1.14–2.50) for total fat intake, 1.88 (1.28–2.77) for saturated fat (SFA) intake, 1.04 (0.86–1.27) for polyunsaturated fat (PUFA) intake and 1.70 (1.01–2.84) for monounsaturated fat (MUFA) intake. In ESCC, the RRs (95% CI) were 1.12 (0.84–1.51) for total fat, 1.38 (0.91–2.08) for SFA, 0.95 (0.55–1.62) for PUFA and 1.04 (0.65–1.66) for MUFA. In conclusion, total fat, SFA and MUFA intake were associated with EAC risk, but fat intake showed no significant association with ESCC risk. Large-scale prospective cohort studies are needed to confirm our findings.
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Affiliation(s)
- Du He
- Department of Oncology, The Central Hospital of Enshi Autonomous Prefecture, Enshi 445000, China.,Enshi Clinical College of Wuhan University, Enshi 445000, China
| | - Xue Huang
- Department of Oncology, The Central Hospital of Enshi Autonomous Prefecture, Enshi 445000, China.,Enshi Clinical College of Wuhan University, Enshi 445000, China
| | - Zai-Ping Wang
- Department of Oncology, The Central Hospital of Enshi Autonomous Prefecture, Enshi 445000, China.,Enshi Clinical College of Wuhan University, Enshi 445000, China
| | - Dian Chen
- Department of Oncology, The Central Hospital of Enshi Autonomous Prefecture, Enshi 445000, China.,Enshi Clinical College of Wuhan University, Enshi 445000, China
| | - Jun Chen
- Department of Oncology, The Central Hospital of Enshi Autonomous Prefecture, Enshi 445000, China.,Enshi Clinical College of Wuhan University, Enshi 445000, China
| | - Chun-Yan Duan
- Department of Oncology, The Central Hospital of Enshi Autonomous Prefecture, Enshi 445000, China.,Enshi Clinical College of Wuhan University, Enshi 445000, China
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11
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Filiberti RA, Fontana V, De Ceglie A, Blanchi S, Grossi E, Della Casa D, Lacchin T, De Matthaeis M, Ignomirelli O, Cappiello R, Rosa A, Foti M, Laterza F, D'Onofrio V, Iaquinto G, Conio M. Alcohol consumption pattern and risk of Barrett's oesophagus and erosive oesophagitis: an Italian case-control study. Br J Nutr 2017; 117:1151-1161. [PMID: 28478792 DOI: 10.1017/s0007114517000940] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
Knowledge about the association between alcohol and Barrett's oesophagus and reflux oesophagitis is conflicting. In this case-control study we evaluated the role of specific alcoholic beverages (red and white wine, beer and liquors) in 339 Barrett's oesophagus and 462 oesophagitis patients compared with 619 endoscopic controls with other disorders, recruited in twelve Italian endoscopic units. Data on alcohol and other individual characteristics were obtained from structured questionnaires. No clear, monotonic significant dose-response relationship was pointed out for red wine. However, a generalised U-shaped trend of Barrett's oesophagus/oesophagitis risk due to red wine consumption particularly among current drinkers was found. Similar results were also found for white wine. Liquor/spirit consumption seemed to bring about a 1·14-2·30 risk excess, although statistically non-significant, for current Barrett's oesophagus/oesophagitis drinkers. Statistically significant decreasing dose-response relationships were found in Barrett's oesophagus for frequency and duration of beer consumption. Similar, but less clear downward tendencies were also found for oesophagitis patients. In conclusion, although often not statistically significant, our data suggested a reduced risk of Barrett's oesophagus and oesophagitis with a low/moderate intake of wine and beer consumption. A non-significant increased risk of Barrett's oesophagus/oesophagitis was observed with a higher intake of any type of heavy alcohol consumption, but no conclusion can be drawn owing to the high number of non-spirit drinkers and to the small number of drinkers at higher alcohol intake levels.
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Affiliation(s)
- Rosa A Filiberti
- 1Clinical Epidemiology,IRCCS AOU San Martino-IST,Largo R Benzi 10,16132 Genova,Italy
| | - Vincenzo Fontana
- 1Clinical Epidemiology,IRCCS AOU San Martino-IST,Largo R Benzi 10,16132 Genova,Italy
| | - Antonella De Ceglie
- 2Gastroenterology,General Hospital,Via G Borea 56,18038 Sanremo,Imperia,Italy
| | - Sabrina Blanchi
- 2Gastroenterology,General Hospital,Via G Borea 56,18038 Sanremo,Imperia,Italy
| | - Enzo Grossi
- 3Medical Department,Bracco Spa,Via E Folli 50,20134 Milan,Italy
| | - Domenico Della Casa
- 4Digestive Endoscopic Surgery,Spedali Civili di Brescia,Piazzale Spedali Civili 1,25123 Brescia,Italy
| | - Teresa Lacchin
- 5Endoscopy,Policlinico San Giorgio,Via Gemelli 10,33170 Pordenone,Italy
| | - Marina De Matthaeis
- 6Gastroenterology and Digestive Endoscopy,Ospedale di Lavagna,ASL 4 Chiavarese,Via Don Bobbio 25,16033 Lavagna,Italy
| | - Orazio Ignomirelli
- 7Endoscopy,IIRCCS,Centro di Riferimento Oncologico di Basilicata,Via Padre Pio 1,85028 Rionero in Vulture,Potenza,Italy
| | - Roberta Cappiello
- 8Gastroenterology,S. Maria degli Angeli Hospital,Via Piave 54,33170 Pordenone,Italy
| | - Alessandra Rosa
- 1Clinical Epidemiology,IRCCS AOU San Martino-IST,Largo R Benzi 10,16132 Genova,Italy
| | - Monica Foti
- 9Gastroenterology,LARC Private Clinic,Cso Venezia 10,10155 Torino,Italy
| | - Francesco Laterza
- 10Department of Internal Medicine,Unit of Endoscopy and Gastroenterology,University Hospital SS.Annunziata, G.D'Annunzio University,Via dei Vestini,66100 Chieti,Italy
| | - Vittorio D'Onofrio
- 11Gastroenterology and Digestive Endoscopy,S. G. Moscati Hospital,Via San Giuseppe Moscati,83100 Avellino,Italy
| | - Gaetano Iaquinto
- 11Gastroenterology and Digestive Endoscopy,S. G. Moscati Hospital,Via San Giuseppe Moscati,83100 Avellino,Italy
| | - Massimo Conio
- 2Gastroenterology,General Hospital,Via G Borea 56,18038 Sanremo,Imperia,Italy
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Abstract
Gastroesophageal junction tumors have been increasing in incidence over time, with most tumors presenting at a locally advanced stage. The treatment plan depends on the stage at diagnosis. PET-CT and endoscopic ultrasound are used to determine clinical stage. Depending on the location of the tumor in the esophagus and stomach, treatment can include chemotherapy with or without radiation, followed by surgery if there is no disease progression. Prognosis is related to stage at diagnosis and response to preoperative treatment. Most surgery for gastroesophageal junction tumors can be performed minimally invasively, which helps decrease postoperative length of stay and morbidity from surgery.
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Affiliation(s)
- Ikenna C Okereke
- Thoracic Surgery, Division of Cardiothoracic Surgery, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555, USA.
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13
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Zhang LQ, Song X, Zhao XK, Huang J, Zhang P, Wang LW, Meng H, Ku JW, Kong GQ, Jiang T, Li XM, Lv XL, Ma T, Yuan G, Wu MJ, Hu SJ, Lv S, Zhang TJ, Ji LF, Fan ZM, Wang NC, Zhang YW, Zhou FY, Wang LD. Association of genotypes of rs671 within ALDH2 with risk for gastric cardia adenocarcinoma in the Chinese Han population in high- and low-incidence areas. Cancer Biol Med 2017; 14:60-65. [PMID: 28443204 PMCID: PMC5365177 DOI: 10.20892/j.issn.2095-3941.2016.0089] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022] Open
Abstract
OBJECTIVE : This study aimed to determine if gastric cardia adenocarcinoma (GCA) risk was associated with the lys (A or *2) allele at the rs671 (glu504lys) polymorphism within the aldehyde dehydrogenase 2 (ALDH2) gene in a Chinese Han population. We also aimed to investigateALDH2 genotypic distributions between subjects from high- and low-incidence areas for both GCA and esophageal squamous cell carcinoma (ESCC). METHODS : We designed a case-control study including 2,686 patients with GCA and 3,675 control subjects from high- and low-incidence areas for both GCA and ESCC in China. TaqMan allele discrimination assay was used to genotype the rs671 polymorphism.χ2 test and binary logistic regression analysis were used to estimate the odds ratios for the development of GCA, and multivariate ordinal logistic regression was used to analyzeALDH2 genotypic distributions among different groups. RESULTS : Compared withALDH2*1/*1 homozygotes,ALDH2*1/*2 andALDH2*2/*2 carriers did not increase the risk for GCA in the Chinese Han population (P>0.05). Interestingly, the ratio of homozygous or heterozygousALDH2 *2 carriers in high-incidence areas for both GCA and ESCC was lower than that in low-incidence areas (P<0.001). CONCLUSIONS : Genotypes of rs671 atALDH2 may not increase GCA susceptibility in Chinese Han populations. In addition, theALDH2 genotypic distribution differs between Chinese Han populations from high- and low-incidence areas for both GCA and ESCC. Our findings may shed light on the possible genetic mechanism for the dramatic geographic differences of GCA occurrence in China.
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Affiliation(s)
- Lian-Qun Zhang
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China.,Anyang Tumor Hospital, Anyang 455000, China
| | - Xin Song
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Xue-Ke Zhao
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Jia Huang
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Peng Zhang
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Lu-Wen Wang
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Hui Meng
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Jian-Wei Ku
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Guo-Qiang Kong
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Tao Jiang
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Xin-Min Li
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Xiao-Long Lv
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Teng Ma
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Guo Yuan
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Min-Jie Wu
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Shou-Jia Hu
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Shuang Lv
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China.,Cancer Research Center, Xinxiang Medical University, Xinxiang 453003, China
| | - Tang-Juan Zhang
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Ling-Fen Ji
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | - Zong-Min Fan
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
| | | | | | | | - Li-Dong Wang
- Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
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14
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Sun L, Zhang Z, Xu J, Xu G, Liu X. Dietary fiber intake reduces risk for Barrett's esophagus and esophageal cancer. Crit Rev Food Sci Nutr 2015; 57:2749-2757. [PMID: 26462851 DOI: 10.1080/10408398.2015.1067596] [Citation(s) in RCA: 32] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/11/2023]
Affiliation(s)
- Lingli Sun
- Department of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing Jiangsu Province, China
| | - Zhizhong Zhang
- Department of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing Jiangsu Province, China
| | - Jian Xu
- Molecular Oncology Research Institute, Tufts Medical Center, Tufts University, Boston, Massachusetts, USA
| | - Gelin Xu
- Department of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing Jiangsu Province, China
| | - Xinfeng Liu
- Department of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing Jiangsu Province, China
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15
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Han J, Jiang Y, Liu X, Meng Q, Xi Q, Zhuang Q, Han Y, Gao Y, Ding Q, Wu G. Dietary Fat Intake and Risk of Gastric Cancer: A Meta-Analysis of Observational Studies. PLoS One 2015; 10:e0138580. [PMID: 26402223 PMCID: PMC4581710 DOI: 10.1371/journal.pone.0138580] [Citation(s) in RCA: 35] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/04/2015] [Accepted: 09/01/2015] [Indexed: 12/12/2022] Open
Abstract
BACKGROUND AND OBJECTIVES Consumption of dietary fat has been reported to be associated with gastric cancer risk, but the results of epidemiologic studies remain inconsistent. We conducted a meta-analysis to summarize the evidence regarding the association between dietary fat intake and gastric cancer risk. METHODS A comprehensive search of PubMed and EMBASE was performed to identify observational studies providing quantitative estimates between dietary fat and gastric cancer risk. Random effects model was used to calculate the summary relative risk(SRR) in the highest versus lowest analysis. Categorical dose-response analysis was conducted to quantify the association between dietary fat intake and gastric cancer risk. Heterogeneity among studies was evaluated using I2 and tau2(between study variance)statistics. Subgroup analysis and publication bias analysis were also performed. RESULTS Twenty-two articles were included in the meta-analysis. The SRR for gastric cancer was 1.18 for individuals with highest intake versus lowest intake of total fat (95% confidence interval [CI]: 0.999-1.39; n = 28; P< 0.001; tau2 = 0.12; I2 = 69.5%, 95% CI: 55%-79%) and 1.08 with a daily increase in total fat intake (20 g/d) (95%CI: 1.02-1.14; n = 6; P = 0.09; tau2 = 0.002; I2 = 46.8%, 95% CI: 0%-79%). Positive association between saturated fat intake (SRR = 1.31; 95%CI: 1.09-1.58;n = 18;P<0.001; tau2 = 0.08; I2 = 60.6%, 95% CI: 34%-76%), inverse association between polyunsaturated fat intake (SRR = 0.77; 95%CI: 0.65-0.92; n = 16; P = 0.003; tau2 = 0.06; I2 = 56.2%, 95% CI: 23%-75%) and vegetable fat intake (SRR = 0.55; 95%CI: 0.41-0.74; n = 4;P = 0.12; tau2 = 0.04; I2 = 48.6%, 95% CI: 0%-83%), and no association between monounsaturated fat intake (SRR = 1.00; 95%CI: 0.79-1.25; n = 14; P< 0.001; tau2 = 0.10; I2 = 63.0%, 95% CI: 34%-79%) and animal fat intake (SRR = 1.10; 95%CI: 0.90-1.33; n = 6; P = 0.13;tau2 = 0.02; I2 = 42.0%, 95% CI: 0%-70%) and gastric cancer risk were observed. CONCLUSIONS Our results suggest that intake of total fat is potentially positively associated with gastric cancer risk, and specific subtypes of fats account for different effects. However, these findings should be confirmed by further well-designed cohort studies with detailed dietary assessments and strict control of confounders.
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Affiliation(s)
- Jun Han
- The Clinical Nutrition Center of Shanghai, Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai, China
| | - Yi Jiang
- The Clinical Nutrition Center of Shanghai, Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai, China
| | - Xiao Liu
- Nursing Department, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Nanjing, Jiangsu Province, China
| | - Qingyang Meng
- The Clinical Nutrition Center of Shanghai, Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai, China
| | - Qiulei Xi
- The Clinical Nutrition Center of Shanghai, Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai, China
| | - Qiulin Zhuang
- The Clinical Nutrition Center of Shanghai, Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai, China
| | - Yusong Han
- The Clinical Nutrition Center of Shanghai, Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai, China
| | - Ying Gao
- Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China
| | - Qiurong Ding
- Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China
| | - Guohao Wu
- The Clinical Nutrition Center of Shanghai, Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai, China
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16
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Kong P, Cai Q, Geng Q, Wang J, Lan Y, Zhan Y, Xu D. Vitamin intake reduce the risk of gastric cancer: meta-analysis and systematic review of randomized and observational studies. PLoS One 2014; 9:e116060. [PMID: 25549091 PMCID: PMC4280145 DOI: 10.1371/journal.pone.0116060] [Citation(s) in RCA: 47] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/04/2014] [Accepted: 12/01/2014] [Indexed: 02/07/2023] Open
Abstract
AIM The association between vitamin intake and gastric cancer (GC) has been widely debated due to the relatively weak evidence. In this study, a meta-analysis of prospective and well designed observational studies were performed to explore this association. METHODS MEDLINE, Cochrane Library, and Sciencedirect were searched for studies of vitamin consumption and gastric cancer. This produced 47 relevant studies covering 1,221,392 human subjects. Random effects models were used to estimate summary relative risk (RR). Dose-response, subgroup, sensitivity, meta-regression, and publication bias analyses were conducted. RESULTS The RR of gastric cancer in the group with the highest vitamin intake was compared to that of the lowest intake group. Total vitamin intake was 0.78 (95% CI, 0.71-0.83). In 9 studies that individuals were given doses at least 4 times above the tolerable upper intake (UL) vitamins, the RR was 1.20 (95% CI, 0.99-1.44). However, in 17 studies that individuals received doses below the UL, the RR was 0.76 (95% CI, 0.68-0.86). Dose-response analysis was conducted on different increments in different types of vitamins (vitamin A: 1.5 mg/day, vitamin C: 100 mg/day, vitamin E: 10 mg/day) intake with a significant reduction in the risk of gastric cancer, respectively, 29% in vitamin A, 26% in vitamin C, and 24% in vitamin E. CONCLUSION This meta-analysis clearly demonstrated that low doses of vitamins can significantly reduce the risk of GC, especially vitamin A, vitamin C, vitamin E.
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Affiliation(s)
- Pengfei Kong
- State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
- Department of Gastric and Pancreatic Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China
| | - Qingqing Cai
- State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
- Department of Medical Oncology, Sun Yat-sen University Cancer Center, Guangzhou, China
| | - Qirong Geng
- State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
- Department of Hematology Oncology, Sun Yat-sen University Cancer Center, Guangzhou, China
| | - Jing Wang
- State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
- Department of Molecular Diagnosis, Sun Yat-sen University Cancer Center, Guangzhou, China
| | - Yadong Lan
- Department of Oncological Surgery, the first affiliated hospital of Bengbu medical college, Bengbu, China
| | - Youqing Zhan
- State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
- Department of Gastric and Pancreatic Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China
| | - Dazhi Xu
- State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
- Department of Gastric and Pancreatic Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China
- * E-mail:
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18
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Wu Y, Ye Y, Shi Y, Li P, Xu J, Chen K, Xu E, Yang J. Association between vitamin A, retinol intake and blood retinol level and gastric cancer risk: A meta-analysis. Clin Nutr 2014; 34:620-6. [PMID: 25008141 DOI: 10.1016/j.clnu.2014.06.007] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/21/2013] [Revised: 05/15/2014] [Accepted: 06/17/2014] [Indexed: 01/11/2023]
Abstract
BACKGROUND & AIMS The association between dietary vitamin A, retinol intake and blood retinol level and gastric cancer risk has been investigated by many studies. However, the results of these studies were controversial. The aim of our study was to systematically assess this issue. METHODS PUBMED and EMBASE were searched, supplemented with manual-screening for relevant publications. Meta-analyses were performed to evaluate the association between vitamin A, retinol dietary intake or blood retinol level and gastric cancer risk. RESULTS Thirty-one studies were included in this meta-analysis. Comparing the highest with the lowest categories, vitamin A intake significantly reduced gastric cancer risk (pooled RR = 0.66, 95% CI: 0.52-0.84), whereas a marginally inverse association was found between retinol intake (pooled RR = 0.94, 95% CI: 0.87-1.03) or blood retinol level (pooled RR = 0.87, 95% CI: 0.73-1.05) and gastric cancer risk. Interestingly, the results of subgroup analysis indicated that high vitamin A intake and blood retinol level were associated with reduced gastric cancer risk in Western countries, while a marginally inverse association was found between retinol and gastric cancer risk in Western countries. CONCLUSIONS Vitamin A intake was inversely associated with gastric cancer risk, while no significant association was found with retinol intake or blood retinol level.
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Affiliation(s)
- Yihua Wu
- Zhejiang University School of Medicine, Hangzhou 310058, China; Department of Epidemiology and Health Statistics, Zhejiang University School of Public Health, Hangzhou 310058, China
| | - Yao Ye
- Zhejiang University School of Medicine, Hangzhou 310058, China; Department of Epidemiology and Health Statistics, Zhejiang University School of Public Health, Hangzhou 310058, China
| | - Yu Shi
- State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China
| | - Peiwei Li
- Zhejiang University School of Medicine, Hangzhou 310058, China; Department of Epidemiology and Health Statistics, Zhejiang University School of Public Health, Hangzhou 310058, China
| | - Jinming Xu
- Zhejiang University School of Medicine, Hangzhou 310058, China; Department of Epidemiology and Health Statistics, Zhejiang University School of Public Health, Hangzhou 310058, China
| | - Kun Chen
- Zhejiang University School of Medicine, Hangzhou 310058, China; Department of Epidemiology and Health Statistics, Zhejiang University School of Public Health, Hangzhou 310058, China
| | - Enping Xu
- Zhejiang University School of Medicine, Hangzhou 310058, China; Department of Pathology, Zhejiang University School of Medicine, Hangzhou 310058, China.
| | - Jun Yang
- Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital of Zhejiang University, Hangzhou 310003, China; Department of Medicine, Hangzhou Normal University, 16, Xuelin Str., Xiasha High Education Zone, Hangzhou, Zhejiang 310036, China.
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19
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Influence of Life Style Factors on Barrett's Oesophagus. Gastroenterol Res Pract 2014; 2014:408470. [PMID: 24971090 PMCID: PMC4058172 DOI: 10.1155/2014/408470] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/07/2014] [Accepted: 03/23/2014] [Indexed: 01/10/2023] Open
Abstract
Background. Since the incidence of adenocarcinoma of the oesophagus is rising, the prognosis is poor, and surveillance programs are expensive and mostly cost ineffective, there is a need to increase the knowledge of risk factors in Barrett's oesophagus and oesophageal cancer in order to be able to give attention to medical prevention and/or surveillance programs. Aim. To study if there is a correlation between the development of Barrett's oesophagus and GOR (gastro oesophageal reflux), family history of GOR, and life style factors, such as alcohol, smoking habits, and mental stress. Methods. Fifty-five consecutively selected patients with Barrett's oesophagus (BO) examined at Linköping University Hospital's Oesophageal Laboratory were matched by sex, age, and duration of reflux symptoms with 55 GOR patients without Barrett's oesophagus at the Oesophageal Laboratory. The medical charts in respective groups were examined for comparison of life style factors, mental stress, medication, duration of gastroesophageal acid reflux at 24 hr-pH-metry, and incidence of antireflux surgery and of adenocarcinoma of the oesophagus (ACO). Also, potential gender differences and diagnosis of ACO were studied. Results. Mean percentage reflux time on 24 hr-pH-metry was higher for the Barrett's oesophagus group, 18% for women and 17% for men compared to 4% for women and 4% for men in the control group (P < 0.05). Family history of GOR was more frequent in Barrett's oesophagus patients (62%) than in the control group (35%) (P < 0.05). Male patients with Barrett's oesophagus had medical therapy for their GOR symptoms to a higher extent (38%) than male controls (65%) (P < 0.05). No difference was found in the number of tobacco users or former tobacco users between Barrett's oesophagus patients and controls. Barrett's oesophagus patients had the same level of alcohol consumption and the same average BMI as the control subjects. Female patients with Barrett's oesophagus rated themselves as more mentally stressed (67%) than the female controls (38%) (P < 0.05). In the five-year medical chart follow-up, five of 55 patients developed adenocarcinoma among the Barrett's oesophagus patients, none in the control group. Conclusions. Long reflux time and family clustering of GOR seem to influence the development of Barrett's oesophagus. Smoking habits, alcohol consumption and BMI do not seem to have any impact on the development of Barrett's oesophagus.
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20
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Baroudi O, Chaaben AB, Mezlini A, Moussa A, Omrane I, Jilson I, Benammar-Elgaaied A, Chabchoub S. Impact of lifestyle factors and nutrients intake on occurrence of gastrointestinal cancer in Tunisian population. Tumour Biol 2014; 35:5815-22. [DOI: 10.1007/s13277-014-1771-x] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/08/2013] [Accepted: 02/18/2014] [Indexed: 01/24/2023] Open
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21
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Li P, Zhang H, Chen J, Shi Y, Cai J, Yang J, Wu Y. Association between dietary antioxidant vitamins intake/blood level and risk of gastric cancer. Int J Cancer 2014; 135:1444-53. [PMID: 24510802 DOI: 10.1002/ijc.28777] [Citation(s) in RCA: 38] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/20/2013] [Accepted: 01/27/2014] [Indexed: 12/31/2022]
Abstract
We aimed to systematically evaluate the association between dietary intake/blood levels of antioxidant vitamins (vitamin C, vitamin E, β-carotene, and α-carotene) and gastric cancer risk. Systematic literature searches were conducted until April 2013 in Pubmed and Embase to identify relevant studies. Either a fixed- or a random-effects model was adopted to estimate overall odds ratios (ORs). Dose-response, meta-regression, subgroup, and publication bias analyses were applied. Forty articles were finally included in the present study. Higher dietary intake of vitamin C, vitamin E, β-carotene, and α-carotene was inversely associated with gastric cancer risk (for vitamin C, pooled OR=0.58, 95% CI 0.51-0.65; for vitamin E, pooled OR=0.65, 95% CI 0.57-0.74; for β-carotene, pooled OR=0.59, 95% CI 0.49-0.70; for α-carotene, pooled OR=0.69, 95% CI 0.52-0.93). Subgroup analyses suggested the effects of these antioxidant vitamins were different in gastric cancer subtypes. As indicated by dose-response analysis, a 100 mg/day increment of vitamin C intake conferred an OR of 0.78 (95% CI 0.67-0.90); a 15 mg/day increment of vitamin E intake conferred an OR of 0.79 (95% CI 0.66-0.94); and a 5 mg/day increment in β-carotene intake conferred an OR of 0.80 (95% CI 0.60-1.04). No significant association was observed between blood vitamin C, α-tocopherol, γ- tocopherol, β-carotene and α-carotene levels and gastric cancer risk. In conclusion, dietary intake of vitamin C, vitamin E, β-carotene and α-carotene was inversely associated with gastric cancer risk while no such association was observed for blood levels of these antioxidant vitamins, thus the results should be interpreted cautiously.
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Affiliation(s)
- Peiwei Li
- Department of Epidemiology and Health Statistics, Zhejiang University School of Public Health, Hangzhou, China
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22
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Connor CA, Adriaens M, Pierini R, Johnson IT, Belshaw NJ. Procyanidin induces apoptosis of esophageal adenocarcinoma cells via JNK activation of c-Jun. Nutr Cancer 2014; 66:335-41. [PMID: 24471892 DOI: 10.1080/01635581.2014.868914] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/16/2023]
Abstract
Procyanidins are polymeric flavanols found in fruits and vegetables and have shown anticarcinogenic/chemopreventive properties. We previously showed that oligomeric procyanidin extracted from apples induced cell cycle arrest and apoptosis in esophageal adenocarcinoma (OA) cells. To understand the mechanism of action, we determined transcriptomic changes induced by procyanidin in OA cells. Pathway analysis implicated mitogen-activated protein kinase signaling pathways in eliciting these responses. Procyanidin induced the activation of JNK and p38 and the phosphorylation and expression of c-Jun. Inhibition of JNK but not p38 kinase activity prevented the procyanidin-induced phosphorylation and expression of c-Jun. Knockdown of the expression of JNK1, JNK2, or JUN diminished procyanidin-induced effects on cell proliferation and apoptosis. c-Jun is a component of the transcription factor AP-1 and AP-1 binding sites are overrepresented in the promoters of procyanidin-induced genes. This indicates that JNK activation of c-Jun by procyanidin leads to the induction of apoptosis of OA cells and suggests a role for a c-Jun-mediated transcriptional program. These data provide a mechanistic understanding of how procyanidin specifically targets a distinct pathway involved in the induction of apoptosis in OA cells and will inform future studies investigating its use as a chemopreventive/therapeutic agent.
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Abstract
Esophageal cancer is a highly lethal disease, with most patients presenting with unresectable or metastatic disease. Since metastatic esophageal cancer is an incurable disease, the goals for chemotherapy are to palliate symptoms and improve survival. Although some patients may achieve symptomatic improvement with the use of standard first-line chemotherapy regimens, response rates are usually low and short lasting. Virtually all patients with metastatic esophageal cancer will develop progressive disease following front-line therapy. With the availability of several chemotherapeutic agents with more tolerable side effects, a number of patients who retain a good performance status after the initial treatment remain candidates for additional therapy. This review summarizes the recent advances in second-line therapy for esophageal cancer.
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Affiliation(s)
- Mike G Martin
- Hematology-Oncology, Washington University School of Medicine, St Louis, MO 63110, USA.
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24
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Esophageal cancer. Mol Oncol 2013. [DOI: 10.1017/cbo9781139046947.045] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/06/2022] Open
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Coleman HG, Murray LJ, Hicks B, Bhat SK, Kubo A, Corley DA, Cardwell CR, Cantwell MM. Dietary fiber and the risk of precancerous lesions and cancer of the esophagus: a systematic review and meta-analysis. Nutr Rev 2013; 71:474-82. [PMID: 23815145 DOI: 10.1111/nure.12032] [Citation(s) in RCA: 40] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022] Open
Abstract
Dietary fiber has several anticarcinogenic effects and is thought to be protective against esophageal cancer. The aim of this systematic review was to quantify the association between dietary fiber and the risk of esophageal cancer by investigating histological subtypes of esophageal cancer and the stage at which fiber may influence the carcinogenic pathway. Systematic search strategies were used to identify relevant studies, and adjusted odds ratios (ORs) were combined using random-effects meta-analyses to assess the risk of cancer when comparing extreme categories of fiber intake. Ten relevant case-control studies were identified within the timeframe searched. Pooled estimates from eight studies of esophageal adenocarcinoma revealed a significant inverse association with the highest fiber intakes (OR 0.66; 95% confidence interval [CI] 0.44-0.98). Two studies also identified protective effects of dietary fiber against Barrett's esophagus. Similar, though nonsignificant, associations were observed when results from five studies of fiber intake and risk of squamous cell carcinoma were combined (OR 0.61; 95%CI 0.31-1.20). Dietary fiber is associated with protective effects against esophageal carcinogenesis, most notably esophageal adenocarcinoma. Potential methods of action include modification of gastroesophageal reflux and/or weight control.
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Affiliation(s)
- Helen G Coleman
- Cancer Epidemiology & Health Services Research Group, Centre for Public Health, Queen's University Belfast, Belfast, Northern Ireland.
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Zhang Z, Xu G, Ma M, Yang J, Liu X. Dietary fiber intake reduces risk for gastric cancer: a meta-analysis. Gastroenterology 2013; 145:113-120.e3. [PMID: 23567349 DOI: 10.1053/j.gastro.2013.04.001] [Citation(s) in RCA: 82] [Impact Index Per Article: 6.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/20/2012] [Revised: 03/18/2013] [Accepted: 04/01/2013] [Indexed: 01/11/2023]
Abstract
BACKGROUND & AIMS The association between dietary fiber intake and gastric cancer risk has been investigated by many studies, with inconclusive results. We conducted a meta-analysis of case-control and cohort studies to analyze this association. METHODS Relevant studies were identified by searching PubMed and Embase through October 2012. We analyzed 21 articles, which included 580,064 subjects. Random-effects models were used to estimate summary relative risks. Dose-response, subgroup, sensitivity, meta-regression, and publication bias analyses were performed. RESULTS The summary odds ratios of gastric cancer for the highest, compared with the lowest, dietary fiber intake was 0.58 (95% confidence interval, 0.49-0.67) with significant heterogeneity among studies (P < .001, I(2) = 62.2%). Stratified analysis for study design, geographic area, source and type of fiber, Lauren's classification, publication year, sample size, and quality score of study yielded consistent results. Dose-response analysis associated a 10-g/day increment in fiber intake with a significant (44%) reduction in gastric cancer risk. Sensitivity analysis restricted to studies with control for conventional risk factors produced similar results, and omission of any single study had little effect on the combined risk estimate. CONCLUSIONS In a meta-analysis, we show that dietary fiber intake is associated inversely with gastric cancer risk; the effect probably is independent of conventional risk factors. The direction of the protective association of dietary fiber was consistent among all studies, but the absolute magnitude was less certain because of heterogeneity among the studies. Further studies therefore are required to establish this association.
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Affiliation(s)
- Zhizhong Zhang
- Department of Neurology, Jinling Hospital, Nanjing University School of Medicine, Jiangsu Province, China
| | - Gelin Xu
- Department of Neurology, Jinling Hospital, Nanjing University School of Medicine, Jiangsu Province, China
| | - Minmin Ma
- Department of Neurology, Jinling Hospital, Nanjing University School of Medicine, Jiangsu Province, China
| | - Jie Yang
- Department of Neurology, Nanjing First Hospital, Nanjing, China
| | - Xinfeng Liu
- Department of Neurology, Jinling Hospital, Nanjing University School of Medicine, Jiangsu Province, China.
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Argos M, Melkonian S, Parvez F, Rakibuz-Zaman M, Ahmed A, Chen Y, Ahsan H. A population-based prospective study of energy-providing nutrients in relation to all-cause cancer mortality and cancers of digestive organs mortality. Int J Cancer 2013; 133:2422-8. [PMID: 23650102 DOI: 10.1002/ijc.28250] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/04/2013] [Accepted: 04/15/2013] [Indexed: 12/30/2022]
Abstract
The effect of dietary composition on mortality in low-income countries is largely unknown. We evaluated whether percentages of dietary energy derived from protein, fat and carbohydrates were associated with all-cause and cancer mortalities in a Bangladeshi population. Data from a prospective population-based cohort study of 17,244 men and women were used. Percentages of dietary energy derived from protein, fat and carbohydrates, assessed using a validated food-frequency questionnaire at baseline, were analyzed in relation to mortality over an average of 9 years (155,126 person-years) of follow-up. Cox proportional hazards regression models were used to estimate hazard ratios for all cause, all cancer and cancers of the digestive organs mortalities. Percentage of dietary energy from protein appeared to be significantly associated with cancer mortality. Fully adjusted hazard ratios for cancer mortality in increasing tertiles of percentage of dietary energy from protein were 1.0 (reference), 1.21 (0.73, 2.00) and 1.84 (1.08, 3.15) (p for trend = 0.023). These associations were much stronger for deaths from cancers of the digestive organs with fully adjusted hazard ratios in increasing tertiles of percentage of dietary energy from protein being 1.0 (reference), 2.25 (0.91, 5.59) and 4.85 (1.88, 12.51) (p for trend = 0.001). No significant associations in relation to cancer-related mortality were observed for percentage of dietary energy from fat. Novel findings from this prospective study show protein is an important risk factor or proxy to an important risk factor for cancer mortality especially from digestive organ cancers in Bangladesh.
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Affiliation(s)
- Maria Argos
- Department of Health Studies, The University of Chicago, Chicago, IL
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Godoy MCB, Bruzzi JF, Viswanathan C, Truong MT, Guimarães MD, Hofstetter WL, Erasmus JJ, Marom EM. Multimodality imaging evaluation of esophageal cancer: staging, therapy assessment, and complications. ACTA ACUST UNITED AC 2013; 38:974-93. [DOI: 10.1007/s00261-013-9986-7] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
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Buas MF, Vaughan TL. Epidemiology and risk factors for gastroesophageal junction tumors: understanding the rising incidence of this disease. Semin Radiat Oncol 2013; 23:3-9. [PMID: 23207041 PMCID: PMC3535292 DOI: 10.1016/j.semradonc.2012.09.008] [Citation(s) in RCA: 219] [Impact Index Per Article: 18.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/23/2022]
Abstract
Gastroesophageal (GE) junction carcinoma is a rare but often lethal condition with increasing importance as a public health problem in recent decades. Whereas diagnosis of this disease has been complicated historically by the lack of uniform classification standards, available data from the Surveillance, Epidemiology, and End Results cancer registry program in the United States show an approximate 2.5-fold increase in the incidence of GE junction adenocarcinoma from 1973 to 1992, with rates stabilizing in the past 2 decades. Similar proportional trends are observed among subgroups defined by race and gender, but rates are significantly higher in males relative to females, and in white males relative to black males. Smoking, obesity, and GE reflux disease are significant risk factors for GE junction adenocarcinoma, and may account for a substantial fraction of total disease burden. Infection with Helicobacter pylori has been associated with reduced incidence, and high dietary fiber intake has also been linked to lower disease risk. Ongoing studies continue to explore a potential role for nonsteroidal anti-inflammatory drugs in chemoprevention.
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Affiliation(s)
- Matthew F. Buas
- Program in Epidemiology, Fred Hutchinson Cancer Research Center, Seattle Washington
- Department of Epidemiology, University of Washington School of Public Health, Seattle, WA
| | - Thomas L. Vaughan
- Program in Epidemiology, Fred Hutchinson Cancer Research Center, Seattle Washington
- Department of Epidemiology, University of Washington School of Public Health, Seattle, WA
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O'Doherty MG, Freedman ND, Hollenbeck AR, Schatzkin A, Murray LJ, Cantwell MM, Abnet CC. Association of dietary fat intakes with risk of esophageal and gastric cancer in the NIH-AARP diet and health study. Int J Cancer 2012; 131:1376-87. [PMID: 22116732 PMCID: PMC3346853 DOI: 10.1002/ijc.27366] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/30/2011] [Accepted: 11/15/2011] [Indexed: 12/19/2022]
Abstract
The aim of our study was to investigate whether intakes of total fat and fat subtypes were associated with esophageal adenocarcinoma (EAC), esophageal squamous cell carcinoma (ESCC), gastric cardia or gastric noncardia adenocarcinoma. From 1995-1996, dietary intake data was reported by 494,978 participants of the NIH-AARP cohort. The 630 EAC, 215 ESCC, 454 gastric cardia and 501 gastric noncardia adenocarcinomas accrued to the cohort. Cox proportional hazards regression was used to examine the association between the dietary fat intakes, whilst adjusting for potential confounders. Although apparent associations were observed in energy-adjusted models, multivariate adjustment attenuated results to null [e.g., EAC energy adjusted hazard ratio (HR) and 95% confidence interval (95% CI) 1.66 (1.27-2.18) p for trend <0.01; EAC multivariate adjusted HR (95% CI) 1.17 (0.84-1.64) p for trend = 0.58]. Similar patterns were also observed for fat subtypes [e.g., EAC saturated fat, energy adjusted HR (95% CI) 1.79 (1.37-2.33) p for trend <0.01; EAC saturated fat, multivariate adjusted HR (95% CI) 1.27 (0.91-1.78) p for trend = 0.28]. However, in multivariate models an inverse association for polyunsaturated fat (continuous) was seen for EAC in subjects with a body mass index (BMI) in the normal range (18.5-<25 kg/m(2)) [HR (95% CI) 0.76 (0.63-0.92)], that was not present in overweight subjects [HR (95% CI) 1.04 (0.96-1.14)], or in unstratified analysis [HR (95% CI) 0.97 (0.90-1.05)]. p for interaction = 0.02. Overall, we found null associations between the dietary fat intakes with esophageal or gastric cancer risk; although a protective effect of polyunsaturated fat intake was seen for EAC in subjects with a normal BMI.
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Affiliation(s)
- Mark G O'Doherty
- Cancer Epidemiology Health Services Research Group, Centre for Public Health, Queens University Belfast, Belfast, Northern Ireland, United Kingdom.
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Lubin JH, Cook MB, Pandeya N, Vaughan TL, Abnet CC, Giffen C, Webb PM, Murray LJ, Casson AG, Risch HA, Ye W, Kamangar F, Bernstein L, Sharp L, Nyrén O, Gammon MD, Corley DA, Wu AH, Brown LM, Chow WH, Ward MH, Freedman ND, Whiteman DC. The importance of exposure rate on odds ratios by cigarette smoking and alcohol consumption for esophageal adenocarcinoma and squamous cell carcinoma in the Barrett's Esophagus and Esophageal Adenocarcinoma Consortium. Cancer Epidemiol 2012; 36:306-16. [PMID: 22504051 PMCID: PMC3489030 DOI: 10.1016/j.canep.2012.03.001] [Citation(s) in RCA: 55] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/31/2011] [Revised: 02/06/2012] [Accepted: 03/07/2012] [Indexed: 12/16/2022]
Abstract
BACKGROUND Cigarette smoking is associated with esophageal adenocarcinoma (EAC), esophagogastric junctional adenocarcinoma (EGJA) and esophageal squamous cell carcinoma (ESCC), and alcohol consumption with ESCC. However, no analyses have examined how delivery rate modifies the strength of odds ratio (OR) trends with total exposure, i.e., the impact on the OR for a fixed total exposure of high exposure rate for short duration compared with low exposure rate for long duration. METHODS The authors pooled data from 12 case-control studies from the Barrett's Esophagus and Esophageal Adenocarcinoma Consortium (BEACON), including 1242 (EAC), 1263 (EGJA) and 954 (ESCC) cases and 7053 controls, modeled joint ORs for cumulative exposure and exposure rate for cigarette smoking and alcohol consumption, and evaluated effect modification by sex, body mass index (BMI), age and self-reported acid reflux. RESULTS For smoking, all sites exhibited inverse delivery rate effects, whereby ORs with pack-years increased, but trends weakened with increasing cigarettes/day. None of the examined factors modified associations, except for ESCC where younger ages at diagnosis enhanced smoking effects (P<0.01). For EAC and EGJA, ORs with drink-years exhibited inverse associations in <5 drinks/day consumers and no association in heavier consumers. For ESCC, ORs with drink-years increased, with trends strengthening with greater drinks/day. There was no significant effect modification, except for EAC and EGJA where acid reflux mitigated the inverse associations (P=0.02). For ESCC, younger ages at diagnosis enhanced drinking-related ORs (P<0.01). CONCLUSIONS Patterns of ORs by pack-years and drink-years, delivery rate effects and effect modifiers revealed common as well as distinct etiologic elements for these diseases.
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Affiliation(s)
- Jay H Lubin
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH/DHHS, Bethesda, MD 20892, USA.
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Cook MB, Shaheen NJ, Anderson LA, Giffen C, Chow WH, Vaughan TL, Whiteman DC, Corley DA. Cigarette smoking increases risk of Barrett's esophagus: an analysis of the Barrett's and Esophageal Adenocarcinoma Consortium. Gastroenterology 2012; 142:744-53. [PMID: 22245667 PMCID: PMC3321098 DOI: 10.1053/j.gastro.2011.12.049] [Citation(s) in RCA: 119] [Impact Index Per Article: 9.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/11/2011] [Revised: 12/07/2011] [Accepted: 12/31/2011] [Indexed: 12/17/2022]
Abstract
BACKGROUND & AIMS Cigarette smoking has been implicated in the etiology of esophageal adenocarcinoma, but it is not clear if smoking is a risk factor for Barrett's esophagus. We investigated whether tobacco smoking and other factors increase risk for Barrett's esophagus. METHODS We analyzed data from 5 case-control studies included in the international Barrett's and Esophageal Adenocarcinoma Consortium. We compared data from subjects with Barrett's esophagus (n = 1059) with those from subjects with gastroesophageal reflux disease (gastroesophageal reflux disease controls, n = 1332), and population-based controls (n = 1143), using multivariable logistic regression models to test associations with cigarette smoking. We also tested whether cigarette smoking has synergistic effects with other exposures, which might further increase risk for Barrett's esophagus. RESULTS Subjects with Barrett's esophagus were significantly more likely to have ever smoked cigarettes than the population-based controls (odds ratio [OR] = 1.67; 95% confidence interval [CI]: 1.04-2.67) or gastroesophageal reflux disease controls (OR = 1.61; 95% CI: 1.33-1.96). Increasing pack-years of smoking increased the risk for Barrett's esophagus. There was evidence of a synergy between ever-smoking and heartburn or regurgitation; the attributable proportion of disease among individuals who ever smoked and had heartburn or regurgitation was estimated to be 0.39 (95% CI: 0.25-0.52). CONCLUSIONS Cigarette smoking is a risk factor for Barrett's esophagus. The association was strengthened with increased exposure to smoking until ∼20 pack-years, when it began to plateau. Smoking has synergistic effects with heartburn or regurgitation, indicating that there are various pathways by which tobacco smoking might contribute to development of Barrett's esophagus.
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Affiliation(s)
| | | | | | | | - Wong-Ho Chow
- Division of Cancer Epidemiology and Genetics, NCI
| | - Thomas L. Vaughan
- Program in Epidemiology, Fred Hutchinson Cancer Research Center, Seattle, WA
| | | | - Douglas A. Corley
- Division of Research and Oakland Medical Center, Kaiser Permanente, CA
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Jessri M, Rashidkhani B, Hajizadeh B, Jessri M, Gotay C. Macronutrients, vitamins and minerals intake and risk of esophageal squamous cell carcinoma: a case-control study in Iran. Nutr J 2011; 10:137. [PMID: 22185224 PMCID: PMC3260093 DOI: 10.1186/1475-2891-10-137] [Citation(s) in RCA: 56] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/16/2011] [Accepted: 12/20/2011] [Indexed: 12/17/2022] Open
Abstract
Background Although Iran is a high-risk region for esophageal squamous cell carcinoma (ESCC), dietary factors that may contribute to this high incidence have not been thoroughly studied. The aim of this study was to evaluate the effect of macronutrients, vitamins and minerals on the risk of ESCC. Methods In this hospital-based case-control study, 47 cases with incident ESCC and 96 controls were interviewed and usual dietary intakes were collected using a validated food frequency questionnaire. Data were modeled through unconditional multiple logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI), controlling for age, sex, gastrointestinal reflux, body mass index, smoking history (status, intensity and duration), physical activity, and education. Results ESCC cases consumed significantly more hot foods and beverages and fried and barbecued meals, compared to the controls (p < 0.05). After adjusting for potential confounders, the risk of ESCC increased significantly in the highest tertiles of saturated fat [OR:2.88,95%CI:1.15-3.08], cholesterol [OR:1.53, 95%CI: 1.41-4.13], discretionary calorie [OR:1.51, 95%CI: 1.06-3.84], sodium [OR:1.49,95%CI:1.12-2.89] and total fat intakes [OR:1.48, 95%CI:1.09-3.04]. In contrast, being in the highest tertile of carbohydrate, dietary fiber and (n-3) fatty acid intake reduced the ESCC risk by 78%, 71% and 68%, respectively. The most cancer-protective effect was observed for the combination of high folate and vitamin E intakes (OR: 0.02, 95%CI: 0.00-0.87; p < 0.001). Controls consumed 623.5 times higher selenium, 5.48 times as much β-carotene and 1.98 times as much α-tocopherol as the amount ESCC cases consumed. Conclusion This study suggests that high intake of nutrients primarily found in plant-based foods is associated with a reduced esophageal cancer risk. Some nutrients such as folate, vitamin E and selenium might play major roles in the etiology of ESCC and their status may eventually be used as an epidemiological marker for esophageal cancer in Iran, and perhaps other high-risk regions.
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Affiliation(s)
- Mahsa Jessri
- Human Nutrition Division, Department of Agricultural, Food and Nutritional Sciences, Edmonton Clinic Health Academy, University of Alberta, Edmonton, Canada
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O'Doherty MG, Cantwell MM, Murray LJ, Anderson LA, Abnet CC. Dietary fat and meat intakes and risk of reflux esophagitis, Barrett's esophagus and esophageal adenocarcinoma. Int J Cancer 2011; 129:1493-502. [PMID: 21455992 DOI: 10.1002/ijc.26108] [Citation(s) in RCA: 59] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/12/2023]
Abstract
The aim of our study was to investigate whether dietary fat and meat intakes are associated with reflux esophagitis (RE), Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). In this all-Ireland case-control study, dietary intake data were collected using a food frequency questionnaire in 219 RE patients, 220 BE patients, 224 EAC patients and 256 frequency-matched controls between 2002 and 2005. Unconditional multiple logistic regression analysis was used to examine the association between dietary variables and disease risk using quartiles of intake, to attain odds ratios (ORs) and 95% confidence intervals (95% CIs), while adjusting for potential confounders. Patients in the highest quartile of total fat intake had a higher risk of RE (OR = 3.54; 95% CI = 1.32-9.46) and EAC (OR = 5.44; 95% CI = 2.08-14.27). A higher risk of RE and EAC was also reported for patients in the highest quartile of saturated fat intake (OR = 2.79; 95% CI = 1.11-7.04; OR = 2.41; 95% CI = 1.14-5.08, respectively) and monounsaturated fat intake (OR = 2.63; 95% CI = 1.01-6.86; OR = 5.35; 95% CI = 2.14-13.34, respectively). Patients in the highest quartile of fresh red meat intake had a higher risk of EAC (OR = 3.15; 95% CI = 1.38-7.20). Patients in the highest category of processed meat intake had a higher risk of RE (OR = 4.67; 95% CI = 1.71-12.74). No consistent associations were seen for BE with either fat or meat intakes. Further studies investigating the association between dietary fat and food sources of fat are needed to confirm these results.
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Affiliation(s)
- Mark G O'Doherty
- Cancer Epidemiology Health Services Research Group, Centre for Public Health, Queens University Belfast, Belfast, Northern Ireland, United Kingdom.
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Wiseman EF, Ang YS. Risk factors for neoplastic progression in Barrett’s esophagus. World J Gastroenterol 2011; 17:3672-83. [PMID: 21990948 PMCID: PMC3181452 DOI: 10.3748/wjg.v17.i32.3672] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/21/2010] [Revised: 10/11/2010] [Accepted: 10/18/2010] [Indexed: 02/06/2023] Open
Abstract
Barrett’s esophagus (BE) confers a significant increased risk for development of esophageal adenocarcinoma (EAC), with the pathogenesis appearing to progress through a “metaplasia-dysplasia-carcinoma” (MDC) sequence. Many of the genetic insults driving this MDC sequence have recently been characterized, providing targets for candidate biomarkers with potential clinical utility to stratify risk in individual patients. Many clinical risk factors have been investigated, and associations with a variety of genetic, specific gastrointestinal and other modifiable factors have been proposed in the literature. This review summarizes the current understanding of the mechanisms involved in neoplastic progression of BE to EAC and critically appraises the relative roles and contributions of these putative risk factors from the published evidence currently available.
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Lahmann PH, Pandeya N, Webb PM, Green AC, Whiteman DC. Body mass index, long-term weight change, and esophageal squamous cell carcinoma. Cancer 2011; 118:1901-9. [DOI: 10.1002/cncr.26455] [Citation(s) in RCA: 36] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/05/2011] [Revised: 06/20/2011] [Accepted: 06/22/2011] [Indexed: 11/11/2022]
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Abstract
BACKGROUND Smoking has been related to esophageal and gastric cardia adenocarcinoma, but the magnitude of the association is uncertain. METHODS We conducted a meta-analysis of 33 studies published up to January 2010. We derived summary estimates using random-effects models. RESULTS Compared with never-smokers, the pooled relative risk (RR) was 1.76 (95% confidence interval = 1.54-2.01) for ever-smokers, 2.32 (1.96-2.75) for current smokers, and 1.62 (1.40-1.87) for ex-smokers. There was no important difference between esophageal (RR = 1.85 for ever- vs. never-smokers) and gastric cardia (RR = 1.76) adenocarcinoma. We found a direct association with dose (RR = 2.48 [2.14-2.86] for ≥ 20 cigarettes/d) and duration (RR = 2.32 [1.92-2.82] for ≥ 40 years) of cigarette consumption. CONCLUSIONS This meta-analysis estimates the excess of esophageal and gastric cardia adenocarcinoma risk for smokers. This risk was similar for the 2 cancer sites.
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Thrift AP, Pandeya N, Smith KJ, Mallitt KA, Green AC, Webb PM, Whiteman DC. Lifetime alcohol consumption and risk of Barrett's Esophagus. Am J Gastroenterol 2011; 106:1220-30. [PMID: 21427711 DOI: 10.1038/ajg.2011.89] [Citation(s) in RCA: 25] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
OBJECTIVES Alcohol is a carcinogen that may increase the risk of Barrett's esophagus (BE) through direct contact with esophageal mucosa. However, few studies have investigated this association and findings have been inconsistent. We sought to examine the association between measures of total and beverage-specific alcohol consumption and BE risk. METHODS We conducted a large population-based case-control study that collected information on lifetime alcohol consumption and other exposures from 285 patients with nondysplastic BE, 108 patients with dysplastic BE, and two separate control groups: 313 endoscopy patients with acute inflammatory changes ("inflammation controls") and 644 population controls. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) for categories of average alcohol consumption using unconditional multivariate logistic regression. RESULTS Relative to life-long nondrinkers and consumption of <1 drink/week, consumption of 7-20 drinks/week (OR=0.53, 95% CI: 0.31-0.91) and 21-41 drinks/week (OR=0.37, 95% CI: 0.19-0.73) of total alcohol throughout the life was inversely associated with nondysplastic BE, for comparisons with population controls. Lifetime total alcohol consumption was also inversely associated with dysplastic BE (7-20 drinks/week OR=0.52, 95% CI: 0.19-1.43; 21-41 drinks/week OR=0.22, 95% CI: 0.07-0.73). Similarly, reduced risk estimates were found for comparisons with inflammation controls. The inverse associations were observed separately for beer and wine consumption, with a significant linear trend observed with beer consumption. The risks associated with liquor consumption were up to twofold higher; however, they were not statistically significant. We found no evidence for effect modification by factors known (or suspected) to cause BE. CONCLUSIONS Overall, alcohol consumption does not increase the risk of BE. Significant inverse associations were observed for beer consumption, the underlying reasons for which remain unclear.
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Affiliation(s)
- Aaron P Thrift
- School of Population Health, The University of Queensland, Brisbane, Australia
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Jacobson BC, Giovannucci EL, Fuchs CS. Smoking and Barrett's esophagus in women who undergo upper endoscopy. Dig Dis Sci 2011; 56:1707-17. [PMID: 21448698 PMCID: PMC3100531 DOI: 10.1007/s10620-011-1672-4] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/26/2010] [Accepted: 03/08/2011] [Indexed: 01/11/2023]
Abstract
BACKGROUND Cigarette use is associated with esophageal adenocarcinoma, and cross-sectional studies suggest an association between smoking and Barrett's esophagus. AIMS We sought to examine prospectively the effect of smoking on the risk for Barrett's esophagus. METHODS This was a prospective cohort study among 20,863 women within the Nurses' Health Study who underwent upper gastrointestinal endoscopy for any reason between 1980 and 2006. We assessed the association between smoking and pathologically-confirmed Barrett's esophagus (n = 377). Self-reported data on smoking and potential confounding variables were collected from biennial questionnaires. RESULTS Compared with women who never smoked, former smokers of 1-24 cigarettes/day had a multivariate odds ratio for Barrett's esophagus of 1.25 (95% CI 0.99-1.59), former smokers of ≥ 25 cigarettes/day had a multivariate odds ratio of 1.52 (95% CI 1.04-2.22), current smokers of 1-24 cigarettes/day had a multivariate odds ratio of 0.89 (95% CI 0.54-1.45), and current smokers of ≥ 25 cigarettes/day had a multivariate odds ratio of 0.92 (95% CI 0.34-2.54). The risk for Barrett's esophagus increased significantly with increasing pack-years smoked among former (P = 0.008) but not current smokers (P = 0.99), especially when considering exposure ≥ 25 years before index endoscopy. Results were similar among women reporting regular heartburn/acid-reflux one or more times a week, and were not accounted for by changes in weight. CONCLUSIONS Heavy, remote smoking is associated with an increased risk for Barrett's esophagus. This finding suggests a long latency period between exposure and development of the disease, even after discontinuation of smoking.
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Tramacere I, Pelucchi C, Bagnardi V, Rota M, Scotti L, Islami F, Corrao G, Boffetta P, La Vecchia C, Negri E. A meta-analysis on alcohol drinking and esophageal and gastric cardia adenocarcinoma risk. Ann Oncol 2011; 23:287-97. [PMID: 21551004 DOI: 10.1093/annonc/mdr136] [Citation(s) in RCA: 67] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022] Open
Abstract
BACKGROUND In order to provide a precise quantification of the association between alcohol drinking and esophageal and gastric cardia adenocarcinoma risk, we conducted a meta-analysis of available data. PATIENTS AND METHODS We identified 20 case-control and 4 cohort studies, including a total of 5500 cases. We derived meta-analytic estimates using random-effects models, taking into account correlation between estimates, and we carried out a dose-risk analysis using nonlinear random-effects meta-regression models. RESULTS The relative risk (RR) for drinkers versus nondrinkers was 0.96 [95% confidence interval (CI) 0.85-1.09] overall, 0.87 (95% CI 0.74-1.01) for esophageal adenocarcinoma and 0.89 (95% CI 0.76-1.03) for gastric cardia adenocarcinoma. Compared with nondrinkers, the pooled RRs were 0.86 for light (≤ 1 drink per day), 0.90 for moderate (1 to < 4 drinks per day), and 1.16 for heavy (≥ 4 drinks per day) alcohol drinking. The dose-risk model found a minimum at 25 g/day, and the curve was < 1 up to 70 g/day. CONCLUSIONS This meta-analysis provides definite evidence of an absence of association between alcohol drinking and esophageal and gastric cardia adenocarcinoma risk, even at higher doses of consumption.
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Affiliation(s)
- I Tramacere
- Department of Epidemiology, Mario Negri Institute for Pharmacological Research, Milan, Italy
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41
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Islami F, Fedirko V, Tramacere I, Bagnardi V, Jenab M, Scotti L, Rota M, Corrao G, Garavello W, Schüz J, Straif K, Negri E, Boffetta P, La Vecchia C. Alcohol drinking and esophageal squamous cell carcinoma with focus on light-drinkers and never-smokers: a systematic review and meta-analysis. Int J Cancer 2011; 129:2473-84. [PMID: 21190191 DOI: 10.1002/ijc.25885] [Citation(s) in RCA: 111] [Impact Index Per Article: 7.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/14/2010] [Accepted: 11/17/2010] [Indexed: 12/11/2022]
Abstract
Quantification of the association between alcohol drinking and risk of esophageal squamous cell carcinoma (ESCC) is an open issue, particularly among light alcohol drinkers, never-smokers, and Asian populations, in which some high-risk polymorphisms in alcohol metabolizing genes are more prevalent. To address these issues, we conducted a systematic review and meta-analysis using 40 case-control and 13 cohort studies that reported on the risk associated with alcohol drinking for at least three levels of consumption. In studies adjusted for age, sex, and tobacco smoking, the relative risk (RR) and 95% confidence interval (CI) for the association between light alcohol drinking (≤ 12.5 g/d) and risk of ESCC was 1.38 (1.14-1.67). The association was slightly stronger in Asian countries than in other populations. The adjusted RRs (95% CIs) were 2.62 (2.07-3.31) for moderate drinking (>12.5-<50 g/d) and 5.54 (3.92-7.28) for high alcohol intake (≥50 g/d); the RRs were slightly higher in non-Asian populations. In prospective studies, the RR (95% CI) was 1.35 (0.92-1.98) for light, 2.15 (1.55-2.98) for moderate, and 3.35 (2.06-5.46) for high alcohol intakes; light drinking showed an association with ESCC in Asia (five studies) but not in other regions (three studies). Among never-smokers (nine studies), the RR (95% CI) was 0.74 (0.47-1.16) for light, 1.54 (1.09-2.17) for moderate, and 3.09 (1.75-5.46) for high intakes. This meta-analysis further corroborates the association of moderate and high alcohol intake with risk of ESCC and provides risk estimates based on multiple prospective studies. Light alcohol intake appears to be associated to ESCC mainly in studies in Asia, which suggests a possible role of genetic susceptibility factors.
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Affiliation(s)
- Farhad Islami
- International Agency for Research on Cancer, Lyon, France.
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42
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De Ceglie A, Fisher DA, Filiberti R, Blanchi S, Conio M. Barrett's esophagus, esophageal and esophagogastric junction adenocarcinomas: the role of diet. Clin Res Hepatol Gastroenterol 2011; 35:7-16. [PMID: 20970272 DOI: 10.1016/j.gcb.2010.08.015] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/27/2010] [Revised: 08/20/2010] [Accepted: 08/27/2010] [Indexed: 02/04/2023]
Abstract
Identification of modifiable risk factors is an attractive approach to primary prevention of esophageal adenocarcinoma (EAC) and esophagogastric junction adenocarcinoma (EGJAC). We conducted a review of the literature to investigate the association between specific dietary components and the risk of Barrett’s esophagus (BE), EAC and EGJAC, supposing diet might be a risk factor for these tumors. Consumption of meat and high-fat meals has been found positively associated with EAC and EGJAC. An inverse association with increased intake of fruit, vegetables and antioxidants has been reported but this association was not consistent across all studies reviewed. Few studies have examined the association between diet and BE. Additional research is needed to confirm the aforementioned association and clarify the mechanisms by which dietary components affect the risk of developing EAC and EGJAC. Future studies could advance our knowledge by emphasizing prospective designs to reduce recall bias, by using validated dietary intake questionnaires and biological measures and by considering important confounders such as gastro-esophageal reflux disease (GERD) symptoms, tobacco and alcohol use, biometrics, physical activity, and socioeconomic factors.
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Affiliation(s)
- A De Ceglie
- Department of Gastroenterology and Digestive Endoscopy, Cancer Institute Giovanni Paolo II, Bari, Italy
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43
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Murphy SJ, Anderson LA, Ferguson HR, Johnston BT, Watson PR, McGuigan J, Comber H, Reynolds JV, Murray LJ, Cantwell MM. Dietary antioxidant and mineral intake in humans is associated with reduced risk of esophageal adenocarcinoma but not reflux esophagitis or Barrett's esophagus. J Nutr 2010; 140:1757-63. [PMID: 20702746 DOI: 10.3945/jn.110.124362] [Citation(s) in RCA: 50] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/23/2022] Open
Abstract
The role of antioxidants in the pathogenesis of reflux esophagitis (RE), Barrett's esophagus (BE), and esophageal adenocarcinoma (EAC) remains unknown. We evaluated the associations among dietary antioxidant intake and these diseases. We performed an assessment of dietary antioxidant intake in a case control study of RE (n = 219), BE (n = 220), EAC (n = 224), and matched population controls (n = 256) (the Factors Influencing the Barrett's Adenocarcinoma Relationship study) using a modification of a validated FFQ. We found that overall antioxidant index, a measure of the combined intake of vitamin C, vitamin E, total carotenoids, and selenium, was associated with a reduced risk of EAC [odds ratio (OR) = 0.57; 95% CI = 0.33-0.98], but not BE (OR = 0.95; 95% CI = 0.53-1.71) or RE (OR = 1.60; 95% CI = 0.86-2.98), for those in the highest compared with lowest category of intake. Those in the highest category of vitamin C intake had a lower risk of EAC (OR = 0.37; 95% CI = 0.21-0.66; P-trend = 0.001) and RE (OR = 0.46; 95% CI = 0.24-0.90; P-trend = 0.03) compared with those in the lowest category. Vitamin C intake was not associated with BE, and intake of vitamin E, total carotenoids, zinc, copper, or selenium was not associated with EAC, BE, or RE. In conclusion, the overall antioxidant index was associated with a reduced risk of EAC. Higher dietary intake of vitamin C was associated with a reduced risk of EAC and RE. These results suggest that antioxidants may play a role in the pathogenesis of RE and EAC and may be more important in terms of progression rather than initiation of the disease process.
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Affiliation(s)
- Seamus J Murphy
- Centre for Public Health, Queen's University Belfast, Belfast BT12 6BJ, Northern Ireland.
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44
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Rota M, Bellocco R, Scotti L, Tramacere I, Jenab M, Corrao G, La Vecchia C, Boffetta P, Bagnardi V. Random-effects meta-regression models for studying nonlinear dose-response relationship, with an application to alcohol and esophageal squamous cell carcinoma. Stat Med 2010; 29:2679-87. [DOI: 10.1002/sim.4041] [Citation(s) in RCA: 63] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]
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Abstract
Incidence rates for oesophageal adenocarcinoma have increased by over 500% during the past few decades without clear reasons. Gastro-oesophageal reflux disease, obesity and smoking have been identified as risk factors, although the demographic distribution of these risk factors is not consistent with the demographic distribution of oesophageal adenocarcinoma, which is substantially more common among whites and males than any other demographic groups. Numerous epidemiological studies have suggested associations between dietary factors and the risks of oesophageal adenocarcinoma and its precursor, Barrett's oesophagus, though a comprehensive review is lacking. The main aim of the present review is to consider the evidence linking dietary factors with the risks of oesophageal adenocarcinoma, Barrett's oesophagus, and the progression from Barrett's oesophagus to oesophageal adenocarcinoma. The existing epidemiological evidence is strongest for an inverse relationship between intake of vitamin C, β-carotene, fruits and vegetables, particularly raw fruits and vegetables and dark green, leafy and cruciferous vegetables, carbohydrates, fibre and Fe and the risk of oesophageal adenocarcinoma and Barrett's oesophagus. Patients at higher risk for Barrett's oesophagus and oesophageal adenocarcinoma may benefit from increasing their consumption of fruits and vegetables and reducing their intake of red meat and other processed food items. Further research is needed to evaluate the relationship between diet and the progression of Barrett's oesophagus to oesophageal adenocarcinoma. Evidence from cohort studies will help determine whether randomised chemoprevention trials are warranted for the primary prevention of Barrett's oesophagus or its progression to cancer.
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46
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Whiteman DC, Parmar P, Fahey P, Moore SP, Stark M, Zhao ZZ, Montgomery GW, Green AC, Hayward NK, Webb PM. Association of Helicobacter pylori infection with reduced risk for esophageal cancer is independent of environmental and genetic modifiers. Gastroenterology 2010; 139:73-83; quiz e11-2. [PMID: 20399210 DOI: 10.1053/j.gastro.2010.04.009] [Citation(s) in RCA: 102] [Impact Index Per Article: 6.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/13/2009] [Revised: 03/21/2010] [Accepted: 04/01/2010] [Indexed: 02/08/2023]
Abstract
BACKGROUND & AIMS Infection with Helicobacter pylori is associated with reduced risk of esophageal adenocarcinoma (EAC), but it is not clear whether this reduction is modified by genotype, other host characteristics, or environmental factors. Furthermore, little is known about the association between H pylori and adenocarcinomas of the esophagogastric junction (EGJAC) or squamous cell carcinomas (ESCC). We sought to measure the association between H pylori infection and esophageal cancer and identify potential modifiers. METHODS In an Australian, population-based, case-control study, we compared the prevalence of H pylori seropositivity and single nucleotide polymorphisms in interleukin (IL)-1B (-31, -511) and tumor necrosis factor (TNF)-alpha (-308, -238) among 260 EAC, 298 EGJAC, and 208 ESCC patients and 1346 controls. To estimate relative risks, we calculated odds ratios (OR) and 95% confidence intervals (CI) using multivariable logistic regression in the entire sample and within strata of phenotypic and genotypic risk factors. RESULTS H pylori infection was associated with significantly reduced risks of EAC (OR, 0.45; 95% CI: 0.30-0.67) and EGJAC (OR, 0.41; 95% CI: 0.27-0.60) but not ESCC (OR, 1.04; 95% CI: 0.71-1.50). For each cancer subtype, risks were of similar magnitude across strata of reflux frequency and smoking status. We found no evidence that polymorphisms in IL-1B or TNF-alpha modified the association between H pylori and EAC or EGJAC. CONCLUSIONS H pylori infection is inversely associated with risks of EAC and EGJAC (but not ESCC); the reduction in risk is similar across subgroups of potential modifiers.
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Abstract
Barrett's esophagus (BE) increases the risk for development of esophageal adenocarcinoma. Because of the rapid rise in incidence of esophageal adenocarcinoma, screening for BE with subsequent surveillance when found has been proposed as a method of early detection. Sedated endoscopy, however, is too expensive for wide spread screening. As a result, other techniques including unsedated transnasal esophagoscopy and capsule esophagoscopy have been proposed to expand screening programs.
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48
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Dietary patterns and risk of oesophageal squamous cell carcinoma: a case–control study. Public Health Nutr 2010; 13:1107-12. [DOI: 10.1017/s1368980010000145] [Citation(s) in RCA: 32] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/30/2023]
Abstract
AbstractObjectiveWe conducted a hospital-based, case–control study to examine the association between dietary patterns and the risk of oesophageal squamous cell carcinoma in Iran.DesignA total of forty-seven patients with oesophageal squamous cell carcinoma and ninety-six controls underwent face-to-face interviews. Factor analysis was used to detect dietary patterns. Multivariate logistic regression was used to estimate OR and 95 % CI.ResultsWe defined two major dietary patterns in this population: ‘healthy diet’ (high in vegetables, nuts, fruits, low-fat dairy and fish) and ‘western diet’ (high in solid oil, sugar, sweets, tea, eggs, pickles and processed meat). Both healthy and western pattern scores were divided into two categories (based on medians). Higher healthy pattern scores were significantly associated with decreased risk of oesophageal squamous cell carcinoma (high: second median v. low: first median, OR = 0·17, 95 % CI 0·19, 0·98). An increased risk of oesophageal squamous cell carcinoma was observed with the western pattern (high: second median v. low: first median, OR = 10·13, 95 % CI 8·45, 43·68).ConclusionsThe results of the present study suggested that diet might be associated with oesophageal carcinoma.
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Ansary-Moghaddam A, Huxley RR, Lam TH, Woodward M. The risk of upper aero digestive tract cancer associated with smoking, with and without concurrent alcohol consumption. ACTA ACUST UNITED AC 2010; 76:392-403. [PMID: 19642154 DOI: 10.1002/msj.20125] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
BACKGROUND Smoking and alcohol are major causal factors for upper aerodigestive tract cancer, but reliable quantification of the combined impact of smoking and alcohol on this cancer and its major subtypes has not been performed. METHODS A meta-analysis of studies that had published quantitative estimates of smoking and upper aerodigestive tract cancer by January 2007 was performed. Pooled estimates of relative risks were obtained. Publication bias was investigated through funnel plots and corrected if found to be present. RESULTS Overall, 85 studies with information on 53,940 individuals with upper aerodigestive tract cancer were included. The pooled estimate for the association between smoking and the risk of this cancer was 3.47 (95% confidence interval, 3.06-3.92). The risk remained elevated for a decade after smoking cessation but declined thereafter. Individuals who both smoked and consumed alcohol had double the risk of upper aerodigestive tract cancer in comparison with those who only smoked: the relative risk was 6.93 (95% confidence interval, 4.99-9.62) for the former and 2.56 (95% confidence interval, 2.20-2.97) for the latter (P < 0.001). CONCLUSIONS Public health interventions that simultaneously discourage smoking and heavy drinking would have greater benefits than would be expected from those that target only one of these risk factors.
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50
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Kubo A, Block G, Quesenberry CP, Buffler P, Corley DA. Effects of dietary fiber, fats, and meat intakes on the risk of Barrett's esophagus. Nutr Cancer 2010; 61:607-16. [PMID: 19838934 DOI: 10.1080/01635580902846585] [Citation(s) in RCA: 43] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/26/2022]
Abstract
Animal and human models suggest associations between fat intake, fiber intake, and the risk of esophageal adenocarcinoma. We evaluated whether these factors may act early in the carcinogenic pathway as a risk factor for Barrett's esophagus, a potentially premalignant precursor to esophageal adenocarcinoma using a case-control design within the Kaiser Permanente, Northern California population. Incident Barrett's esophagus cases (n = 296) were matched to persons with gastroesophageal reflux disease (GERD) (n = 308) and to population controls (n = 309). Higher intakes of omega-3-fatty-acids [cases vs. population controls; OR = 0.46, 95% CI = 0.22-0.97, 4th vs. 1st quartiles of intake], polyunsaturated fat, total fiber (OR = 0.34, 95% CI = 0.15-0.76), and fiber from fruits and vegetables (OR = 0.47 95% CI = 0.25-0.88) were associated with a lower risk of Barrett's esophagus. Higher meat intakes were associated with a lower risk of long-segment Barrett's esophagus (OR = 0.25, 95% CI = 0.09-0.72). In contrast, higher trans-fat intakes were associated with increased risk (OR = 1.11; 95% CI = 1.03-1.21 per g/day). Total fat intake, barbecued foods, and fiber intake from sources other than fruits and vegetables were not associated with Barrett's esophagus. Future studies to evaluate whether dietary interventions might influence the risk of Barrett's esophagus or esophageal adenocarcinoma in high risk persons are needed.
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Affiliation(s)
- Ai Kubo
- Northern California Kaiser Permanente, Oakland, California 94612, USA.
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