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Long Y, Zhai W. Evaluation of Football Teaching Quality Based on Big Data. COMPUTATIONAL AND MATHEMATICAL METHODS IN MEDICINE 2022; 2022:7174246. [PMID: 35799663 PMCID: PMC9256316 DOI: 10.1155/2022/7174246] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 04/27/2022] [Revised: 05/21/2022] [Accepted: 05/24/2022] [Indexed: 11/17/2022]
Abstract
The arrival of the big data era has opened up new avenues for assessing the quality of physical education instruction. Using big data to explore these systems may help improve the quality of physical education itself, in addition to assisting schools in developing quality assessment systems for physical education. More and more schools are making football a compulsory part of their physical education and wellness curriculum. Therefore, this study used the methods of literature materials, expert interviews, questionnaires, and Delphi method to determine the evaluation indicators and index weight coefficients of football teaching and borrowed the application background of big data to initially explore the construction of a football teaching quality evaluation system. To this end, this paper completes the following tasks: (1) The current state of football teaching quality evaluation studies in the United States and internationally is summarized. (2) A football teaching quality evaluation system based on the background of big data is constructed. (3) Our experiments show that the assessment approach described in this study is scientifically and rationally distributed and can accurately represent all components of physical education. As a result, evaluating football instruction using big data is a possibility.
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Affiliation(s)
- Yue Long
- Football College, Wuhan Sports University, Wuhan Hubei 430077, China
| | - Wei Zhai
- Football College, Wuhan Sports University, Wuhan Hubei 430077, China
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2
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Kumar S, Metz DC, Kaplan DE, Goldberg DS. The association of Helicobacter pylori with pancreatic cancer. ACTA ACUST UNITED AC 2020; 2:157-164. [PMID: 33692655 DOI: 10.1002/ygh2.398] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/24/2022]
Abstract
Background & Aims Infection with Helicobacter pylori (HP) affects 50% of the world. Previous studies have suggested an association between HP and pancreatic adenocarcinoma (PC). These association studies have been limited in their ability to identify the incidence and risk factors of PC among HP infected individuals and the impact of HP eradication on PC. Methods Retrospective cohort study within the Veterans Administration of 103,595 patients (median age 62.3; 92.0% male) with HP diagnosis based on pathology, stool antigen, urea breath test, or serum antibody between 1/1/1994-12/31/2018. Primary outcome was future PC diagnosis. A time to event with competing risk analysis was performed, evaluating patient demographics and history, method of HP diagnosis, and whether the patient received HP treatment. Secondary analysis of those treated evaluated whether confirmed eradication was associated with PC. Results The cumulative incidence of PC at 5 and 10 years was 0.37% and 0.54%, respectively. Patients who developed PC were older, male, reside in areas with higher poverty. Preceding diabetes and chronic pancreatitis were strongly associated with PC. Factors not associated with PC included receiving an eradication regimen, diagnosis of an active infection (versus prior exposure alone), and eradication of HP. Conclusions PC after HP is rare. Chronic pancreatitis is the main risk factor for PC. Active HP infection, treatment of HP infection, or eradication of HP are not associated with future PC. This study calls into question the association between PC and HP.
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Affiliation(s)
- Shria Kumar
- Division of Gastroenterology, Perelman School of Medicine at the University of Pennsylvania
| | - David C Metz
- Division of Gastroenterology, Perelman School of Medicine at the University of Pennsylvania
| | - David E Kaplan
- Division of Gastroenterology, Perelman School of Medicine at the University of Pennsylvania.,Division of Gastroenterology, Veterans Health Administration
| | - David S Goldberg
- Division of Digestive Health and Liver Diseases, Department of Medicine, University of Miami Miller School of Medicine
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Barone E, Corrado A, Gemignani F, Landi S. Environmental risk factors for pancreatic cancer: an update. Arch Toxicol 2016; 90:2617-2642. [PMID: 27538405 DOI: 10.1007/s00204-016-1821-9] [Citation(s) in RCA: 67] [Impact Index Per Article: 7.4] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/21/2016] [Accepted: 08/04/2016] [Indexed: 02/07/2023]
Abstract
Pancreatic cancer (PC) is one of the most aggressive diseases. Only 10 % of all PC cases are thought to be due to genetic factors. Here, we analyzed the most recently published case-control association studies, meta-analyses, and cohort studies with the aim to summarize the main environmental factors that could have a role in PC. Among the most dangerous agents involved in the initiation phase, there are the inhalation of cigarette smoke, and the exposure to mutagenic nitrosamines, organ-chlorinated compounds, heavy metals, and ionizing radiations. Moreover, pancreatitis, high doses of alcohol drinking, the body microbial infections, obesity, diabetes, gallstones and/or cholecystectomy, and the accumulation of asbestos fibers seem to play a crucial role in the progression of the disease. However, some of these agents act both as initiators and promoters in pancreatic acinar cells. Protective agents include dietary flavonoids, marine omega-3, vitamin D, fruit, vegetables, and the habit of regular physical activity. The identification of the factors involved in PC initiation and progression could be of help in establishing novel therapeutic approaches by targeting the molecular signaling pathways responsive to these stimuli. Moreover, the identification of these factors could facilitate the development of strategies for an early diagnosis or measures of risk reduction for high-risk people.
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Affiliation(s)
- Elisa Barone
- Genetic Unit, Department of Biology, University of Pisa, Via Derna, 1, 56121, Pisa, Italy
| | - Alda Corrado
- Genetic Unit, Department of Biology, University of Pisa, Via Derna, 1, 56121, Pisa, Italy
| | - Federica Gemignani
- Genetic Unit, Department of Biology, University of Pisa, Via Derna, 1, 56121, Pisa, Italy
| | - Stefano Landi
- Genetic Unit, Department of Biology, University of Pisa, Via Derna, 1, 56121, Pisa, Italy.
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Risch HA, Lu L, Kidd MS, Wang J, Zhang W, Ni Q, Gao YT, Yu H. Helicobacter pylori seropositivities and risk of pancreatic carcinoma. Cancer Epidemiol Biomarkers Prev 2014; 23:172-8. [PMID: 24234587 PMCID: PMC3947155 DOI: 10.1158/1055-9965.epi-13-0447] [Citation(s) in RCA: 56] [Impact Index Per Article: 5.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/24/2022] Open
Abstract
BACKGROUND Pathophysiologic actions of Helicobacter pylori colonization on gastric acidity have been hypothesized to modulate the effect of pancreatic carcinogens, through CagA-negative organism strain type, hyperchlorhydria and increased risk of pancreatic cancer, or CagA-positive strain, hypochlorhydria and decreased risk of pancreatic cancer. We aimed to determine H. pylori strain-specific associations with pancreatic cancer in a population in which colonization by CagA-positive strains is common. METHODS We carried out a large population-based case-control study of pancreatic carcinoma in Shanghai, China. Venipuncture specimens were obtained from a representative sample of 761 case patients and 794 randomly selected control subjects matched by category of age and gender. Antibody seropositivity for H. pylori and its virulence protein CagA were determined by commercial enzyme-linked immunosorbent IgG assays. RESULTS Compared with individuals seronegative for both H. pylori and CagA, decreased pancreas-cancer risk was seen for CagA seropositivity [adjusted OR, 0.68; 95% confidence interval (CI), 0.54-0.84], whereas some increased risk was suggested for CagA-negative H. pylori seropositivity (OR, 1.28; 95% CI, 0.76-2.13). No risk interactions were observed between CagA seropositivity and gender, cigarette smoking, or age-21 body mass index. CONCLUSIONS Similar to what has been seen in animal models, our results provide suggestive evidence in humans for the involvement of gastric acidity, through its bidirectional modification according to colonization by H. pylori CagA strain type, in the risk of pancreatic carcinoma. IMPACT H. pylori colonization may have diverse effects on cancer risk, depending on the organism strain type as well as on the particular cancer site.
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Affiliation(s)
- Harvey A. Risch
- Department of Chronic Disease Epidemiology, Yale School of Public Health, Yale School of Medicine, New Haven, Connecticut
| | - Lingeng Lu
- Department of Chronic Disease Epidemiology, Yale School of Public Health, Yale School of Medicine, New Haven, Connecticut
| | - Mark S. Kidd
- Department of Surgery, Yale School of Medicine, New Haven, Connecticut
| | - Jing Wang
- Department of Epidemiology, Shanghai Cancer Institute and Jiao Tong University, Shanghai, China
| | - Wei Zhang
- Department of Epidemiology, Shanghai Cancer Institute and Jiao Tong University, Shanghai, China
| | - Quanxing Ni
- Department of Pancreas and Hepatobiliary Surgery, Shanghai Medical College, Fudan University, Shanghai, China
| | - Yu-Tang Gao
- Department of Epidemiology, Shanghai Cancer Institute and Jiao Tong University, Shanghai, China
| | - Herbert Yu
- Epidemiology Program, University of Hawaii Cancer Center, Honolulu, Hawaii
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Michaud DS, Izard J, Wilhelm-Benartzi CS, You DH, Grote VA, Tjønneland A, Dahm CC, Overvad K, Jenab M, Fedirko V, Boutron-Ruault MC, Clavel-Chapelon F, Racine A, Kaaks R, Boeing H, Foerster J, Trichopoulou A, Lagiou P, Trichopoulos D, Sacerdote C, Sieri S, Palli D, Tumino R, Panico S, Siersema PD, Peeters PHM, Lund E, Barricarte A, Huerta JM, Molina-Montes E, Dorronsoro M, Quirós JR, Duell EJ, Ye W, Sund M, Lindkvist B, Johansen D, Khaw KT, Wareham N, Travis RC, Vineis P, Bueno-de-Mesquita HB, Riboli E. Plasma antibodies to oral bacteria and risk of pancreatic cancer in a large European prospective cohort study. Gut 2013; 62:1764-70. [PMID: 22990306 PMCID: PMC3815505 DOI: 10.1136/gutjnl-2012-303006] [Citation(s) in RCA: 302] [Impact Index Per Article: 25.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
Abstract
OBJECTIVE Examine the relationship between antibodies to 25 oral bacteria and pancreatic cancer risk in a prospective cohort study. DESIGN We measured antibodies to oral bacteria in prediagnosis blood samples from 405 pancreatic cancer cases and 416 matched controls, nested within the European Prospective Investigation into Cancer and Nutrition study. Analyses were conducted using conditional logistic regression and additionally adjusted for smoking status and body mass index. RESULTS Individuals with high levels of antibodies against Porphyromonas gingivalis ATTC 53978, a pathogenic periodontal bacteria, had a twofold higher risk of pancreatic cancer than individuals with lower levels of these antibodies (OR 2.14; 95% CI 1.05 to 4.36; >200 ng/ml vs ≤200 ng/ml). To explore the association with commensal (non-pathogenic) oral bacteria, we performed a cluster analysis and identified two groups of individuals, based on their antibody profiles. A cluster with overall higher levels of antibodies had a 45% lower risk of pancreatic cancer than a cluster with overall lower levels of antibodies (OR 0.55; 95% CI 0.36 to 0.83). CONCLUSIONS Periodontal disease might increase the risk for pancreatic cancer. Moreover, increased levels of antibodies against specific commensal oral bacteria, which can inhibit growth of pathogenic bacteria, might reduce the risk of pancreatic cancer. Studies are needed to determine whether oral bacteria have direct effects on pancreatic cancer pathogenesis or serve as markers of the immune response.
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Affiliation(s)
- Dominique S Michaud
- Department of Epidemiology, Division of Biology and Medicine, Brown University, Providence, Rhode Island, USA
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Takayama S, Wakasugi T, Funahashi H, Takeyama H. Strategies for gastric cancer in the modern era. World J Gastrointest Oncol 2010; 2:335-41. [PMID: 21160804 PMCID: PMC2999138 DOI: 10.4251/wjgo.v2.i9.335] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/13/2010] [Revised: 08/09/2010] [Accepted: 08/16/2010] [Indexed: 02/05/2023] Open
Abstract
Gastric cancer is one of the most common neoplasms in Japan, and it is also the second leading cause of cancer-related deaths worldwide. Nowadays, infection with Helicobacter pylori (H. pylori) is a known risk factor for the development of gastric cancer. Therefore, gastric cancer should be considered as an infectious disease, and in fact, prophylactic eradication of H. pylori may prevent the development of metachronous gastric carcinoma. Before the role of H. pylori was understood, a different approach was used. Recently even after the cancer has developed, some newer therapeutic approaches have been pursued. These newer treatments have been summarized as “minimally invasive therapies” and use endoscopic or laparoscopic techniques. In addition, robotic approaches are being developed that seem to hold a great potential to change the surgical approach. Since basic understanding and treatment of the disease have both changed significantly over the last decade, we present a review of current advances in gastric cancer research and therapy.
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Affiliation(s)
- Satoru Takayama
- Satoru Takayama, Takehiro Wakasugi, Hitoshi Funahashi, Hiromitsu Takeyama, Department of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-ku, Nagoya 467-8601, Japan
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Jesnowski R, Isaksson B, Möhrcke C, Bertsch C, Bulajic M, Schneider-Brachert W, Klöppel G, Lowenfels AB, Maisonneuve P, Löhr JM. Helicobacter pylori in autoimmune pancreatitis and pancreatic carcinoma. Pancreatology 2010; 10:462-6. [PMID: 20720447 DOI: 10.1159/000264677] [Citation(s) in RCA: 47] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/09/2009] [Accepted: 10/16/2009] [Indexed: 12/11/2022]
Abstract
BACKGROUND Helicobacter pylori has been suggested to be involved in pancreatic diseases, namely autoimmune pancreatitis and pancreatic carcinoma. We investigated the presence of conserved sequences of Helicobacter in pancreatic tissue and pancreatic juice from patients with chronic nonautoimmune and autoimmune pancreatitis as well as pancreatic ductal adenocarcinoma (PDAC). METHODS 35 pancreatic juices collected during routine endoscopic retrograde cholangiopancreatography and 30 pancreatic tissues were studied. Nested PCR was used to detect H. pylori in the isolated DNA samples. In order to exclude a methodological bias, the samples were analyzed blindly in 2 different laboratories using either conventional or LightCycler PCR for H. pylori urease A and 16S ribosomal DNA. RESULTS In the pancreas of 11 patients with autoimmune pancreatitis, no H. pylori DNA could be detected. Further, in none of the other tissue samples of chronic pancreatitis or PDAC could we detect any Helicobacter sequences. Out of the pancreatic juice samples, none demonstrated either of the 2 Helicobacter gene sequences investigated. CONCLUSION Despite good scientific reasoning for an involvement of Helicobacter in pancreatic diseases, a direct infection of the microbial agent seems unlikely. Rather, the pathomechanism must involve molecular mimicry in autoimmune pancreatitis, or the transformation of nitric food constituents to nitrosamines in pancreatic cancer. and IAP.
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Affiliation(s)
- Ralf Jesnowski
- Molecular Gastroenterology G350, DKFZ Heidelberg, Heidelberg, Germany
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Laiyemo AO, Kamangar F, Marcus PM, Taylor PR, Virtamo J, Albanes D, Stolzenberg-Solomon RZ. Serum pepsinogen level, atrophic gastritis and the risk of incident pancreatic cancer--a prospective cohort study. Cancer Epidemiol 2009; 33:368-73. [PMID: 19800305 DOI: 10.1016/j.canep.2009.09.001] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/10/2009] [Revised: 09/04/2009] [Accepted: 09/07/2009] [Indexed: 02/06/2023]
Abstract
BACKGROUND Pancreatic cancer is a highly fatal disease without screening tests. Studies have suggested possible etiologic similarities between gastric and pancreatic cancers. Atrophic gastritis, a pre-malignant condition for gastric cancer, is characterized by low serum pepsinogen I (SPGI) level. We hypothesized that low SPGI level may be associated with an increased risk of pancreatic cancer and be a useful biomarker for the disease. METHODS Our analytic cohort included 20,962 participants in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC) who had SPGI level measured. Of these, 1663 (7.9%) subjects had low SPGI levels (<25 microg/l) and were invited for gastroscopy which was completed in 1059 (63.7%) participants. Atrophic gastritis was histologically confirmed in 1006 (95.0%) subjects. We used Cox proportional hazards regression to calculate the hazard ratios (HR) and 95% confidence intervals (CI) for pancreatic cancer. RESULTS During follow-up of up to 16.3 years (mean=10.8 years; 226,325 person-years), 227 incident pancreatic cancers were diagnosed. The incidence rates were 9.9, 11.3, and 12.7 per 10,000 person-years of follow-up for participants with normal pepsinogen level (> or = 25 microg/l), low pepsinogen level and histologically confirmed atrophic gastritis, respectively. Compared to subjects with normal pepsinogen levels, there was no statistically significant increased risk of pancreatic cancer among subjects with low pepsinogen level (adjusted HR=1.01; 95% CI: 0.63-1.62) or those with histologically confirmed atrophic gastritis (adjusted HR=1.13; 95% CI: 0.66-1.95). CONCLUSIONS Atrophic gastritis, serological or histological, is not associated with increased risk of pancreatic cancer. These findings do not provide any evidence for potential usefulness of SPGI for pancreatic cancer screening.
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Affiliation(s)
- Adeyinka O Laiyemo
- Cancer Prevention Fellowship Program, Office of Preventive Oncology, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD 20892, USA.
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de Martel C, Llosa AE, Friedman GD, Vogelman JH, Orentreich N, Stolzenberg-Solomon RZ, Parsonnet J. Helicobacter pylori infection and development of pancreatic cancer. Cancer Epidemiol Biomarkers Prev 2008; 17:1188-94. [PMID: 18483341 DOI: 10.1158/1055-9965.epi-08-0185] [Citation(s) in RCA: 61] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/25/2022] Open
Abstract
BACKGROUND Infection with Helicobacter pylori is an established risk factor for gastric cancer. Results from two studies suggest that it may also be a risk factor for pancreatic cancer. METHODS We conducted a nested case control study among 128,992 adult subscribers to the Kaiser Permanente Medical Care Program who had been enrolled in a multiphasic health checkup from 1964 to 1969. Serum collected during the checkup was maintained frozen, and subjects were followed for cancer. Cases consisted of 104 randomly selected subjects among 507 who developed pancreatic cancer in the cohort. Controls consisted of 262 pancreatic cancer-free subjects from a pool of 730 controls previously tested for studies conducted on this cohort. Controls were individually matched to cases on age, gender, race, site, and date of multiphasic health checkup. Control sera were compared with cases for antibodies to H. pylori and the CagA protein. The effects of smoking, alcohol consumption, obesity, and years of education were also investigated. RESULTS Neither H. pylori [odds ratio (OR), 0.85; 95% confidence interval (95% CI), 0.49-1.48] nor its CagA protein (OR, 0.96; 95% CI, 0.48-1.92) was associated with subsequent development of pancreatic cancer. Smoking (OR, 2.09; 95% CI, 1.17-3.74) and greater number of years of education (OR, 2.13; 95% CI, 1.23-3.69) were risk factors for pancreatic cancer, whereas alcohol consumption and obesity were not. CONCLUSION Our results suggest that H. pylori infection is not associated with development of pancreatic cancer.
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Affiliation(s)
- Catherine de Martel
- Department of Health Research and Policy, Stanford University School of Medicine, 300 Pasteur Road, Stanford, CA 94305, USA.
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Abstract
Pancreatic cancer kills more than 250,000 people each year worldwide and has a poor prognosis. The aim of this article is to critically review the epidemiologic evidence for exposures that may either increase or decrease the risk. A Medline search was performed for epidemiologic studies and reviews published up to April 2007. Consistent evidence of a positive association was found for family history and cigarette smoking. Many studies documented a positive association with diabetes mellitus and chronic pancreatitis, although the etiologic mechanisms are unclear. Other associations were detected, but the results were either inconsistent or from few studies. These included positive associations with red meat, sugar, fat, body mass index, gallstones, and Helicobacter pylori, and protective effects of increasing parity, dietary folate, aspirin, and statins. There was no evidence linking alcohol or coffee consumption with an increased risk of pancreatic cancer. The associations with many exposures need to be clarified from further epidemiologic work in which there is both precise measurement of risk factors, adjustment for potential confounders, and, for dietary studies, information recorded on the method of food preparation and pattern of consumption. Such work is important to reduce the incidence of this fatal disease.
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Luo J, Nordenvall C, Nyrén O, Adami HO, Permert J, Ye W. The risk of pancreatic cancer in patients with gastric or duodenal ulcer disease. Int J Cancer 2007; 120:368-72. [PMID: 17044024 DOI: 10.1002/ijc.22123] [Citation(s) in RCA: 40] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2022]
Abstract
Although Helicobacter pylori (H. pylori) seropositivity is linked to an excess risk of pancreatic cancer, the biologic mechanism is unknown. Gastric ulcer is primarily associated with corpus colonization of H. pylori, atrophic gastritis and formation of N-nitrosamines. Duodenal ulcer is a marker of antral colonization, hyperacidity and uninhibited secretin release. We estimated relative risks for pancreatic cancer among patients with gastric or duodenal ulcer, based on a register-based retrospective cohort study with 88,338 patients hospitalized for gastric ulcer and 70,516 patients for duodenal ulcer recorded in the Swedish Inpatient Register between 1965 and 2003. Following operation, the 14,887 patients who underwent gastric resection and 8,205 with vagotomy were analyzed separately. Multiple record-linkages allowed complete follow-up and identification of all incident cases of pancreatic cancer until December 31, 2003. Standardized incidence ratios (SIRs) estimated relative risks. During years 3-38 of follow-up, we observed a 20% excess risk (95% confidence interval [CI] 10-40%) for pancreatic cancer among unoperated gastric ulcer patients. The excess increased to 50% (95% CI 10-110%) 15 years after first hospitalization (p for trend = 0.03). SIR was 2.1 (95% CI 1.4-3.1) 20 years after gastric resection. Unoperated duodenal ulcer was not associated with pancreatic cancer risk, nor was vagotomy. Our results lend indirect support to the nitrosamine hypothesis, but not to the hyperacidity hypothesis in the etiology of pancreatic cancer.
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Affiliation(s)
- Juhua Luo
- Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
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Nilsson HO, Stenram U, Ihse I, Wadstrom T. Helicobacter species ribosomal DNA in the pancreas, stomach and duodenum of pancreatic cancer patients. World J Gastroenterol 2006; 12:3038-43. [PMID: 16718784 PMCID: PMC4124378 DOI: 10.3748/wjg.v12.i19.3038] [Citation(s) in RCA: 79] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023] Open
Abstract
AIM: To determine whether gastric and enteric Helicobacter species are associated with pancreatic cancer.
METHODS: Patients with exocrine pancreatic cancer (n = 40), neuroendocrine cancer (n = 14), multiple endocrine neoplasia type 1 (n = 8), and chronic pancreatitis (n = 5) were studied. Other benign pancreatic diseases (n = 10) and specimens of normal pancreas (n = 7) were included as controls. Pancreatic tissue specimens were analyzed by Helicobacter-specific PCR-assay and products were characterized by denaturing gradient electrophoresis and DNA-sequencing. From a subset of the pancreatic cancer patients, gastric and/or duodenal tissue as well as gallbladder and ductus choledochus tissue were analyzed. Gallbladder and choledochus samples were included as controls. Stomach and duodenum samples were investigated to analyze whether a gastric helicobacter might disseminate to the pancreas in pancreatic cancer patients. Pancreatic specimens were analyzed by Bacteroides-specific PCR for detecting the translocation of indigenous gut microbes to the diseased pancreas.
RESULTS: Helicobacter DNA was detected in pancreas (tumor and/or surrounding tissue) of 75% of patients with exocrine cancer, 57% of patients with neuroendocrine cancer, 38% of patients with multiple endocrine neoplasia, and 60% of patients with chronic pancreatitis. All samples from other benign pancreatic diseases and normal pancreas were negative. Thirty-three percent of the patients were helicobacter-positive in gastroduodenal specimens. Surprisingly, H. bilis was identified in 60% of the positive gastroduodenal samples. All gallbladder and ductus choledochus specimens were negative for helicobacter. Bacteroides PCR-assay was negative for all pancreatic samples.
CONCLUSION: Helicobacter DNA commonly detected in pancreatic cancer suggests a possible role of the emerging pathogens in the development of chronic pancreatitis and pancreatic cancer.
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Affiliation(s)
- Hans-Olof Nilsson
- Department of Laboratory Medicine, Division of Medical Microbiology, Lund University, Solvegatan 23, S-223 62 Lund, Sweden.
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Abstract
Pancreas cancer is considered an 'orphan' cancer because of its relative low incidence. Unfortunately even with early diagnosis, mortality rates are high, explaining why, despite the low incidence, it ranks eighth in a world listing of cancer mortality. International incidence rates vary in different countries, implying that environmental factors are important. Of these factors, smoking is the most well documented etiologic agent, explaining about 25% of all cases. Dietary factors may be important, but it has been difficult to define specific items which either increase or decrease the risk of pancreatic cancer. Since the incidence of pancreas cancer is so strongly age-dependent, we can anticipate an increasing number of patients as the population of most Western countries ages.
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Affiliation(s)
- Albert B Lowenfels
- Department of Surgery, New York Medical College, Munger Pavilion, Valhalla, NY 10595, USA.
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Nilsson I, Kornilovs'ka I, Lindgren S, Ljungh Å, Wadström T. Increased prevalence of seropositivity for non-gastric Helicobacter species in patients with autoimmune liver disease. J Med Microbiol 2004; 52:949-953. [PMID: 14532338 DOI: 10.1099/jmm.0.05344-0] [Citation(s) in RCA: 44] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022] Open
Abstract
Various Helicobacter species have been isolated from the stomach, intestinal tract and liver of a variety of mammalian and some avian species, and Helicobacter DNA has been detected in human bile and liver samples. An immunoblot assay was established to analyse serum antibody responses to non-gastric Helicobacter species in patients with autoimmune liver diseases, in comparison with healthy individuals. Sera from 36 patients with primary sclerosing cholangitis (PSC), 21 with primary biliary cirrhosis, 19 with autoimmune chronic hepatitis and 80 blood donors were analysed by immunoblot, using cell-surface proteins from Helicobacter pullorum, Helicobacter bilis and Helicobacter hepaticus as antigens. Prior to testing, sera were cross-absorbed with a whole-cell lysate of Helicobacter pylori. Antibody reactivity to various proteins of these three Helicobacter species was measured by densitometric scanning and results were processed by computer software to estimate antigenic specificity. Results were also compared with antibody response to H. pylori. For H. pullorum, reactivity to at least two of the proteins with molecular masses of 48, 45, 37, 20 and 16 kDa, for H. hepaticus, reactivity to the 76, 30 and 21 kDa proteins and for H. bilis, reactivity to the 22 and 20 kDa proteins, seemed to have high specificity. Positive immunoblot results with sera from patients with PSC to antigens of H. pullorum, H. bilis and H. hepaticus were found in 38, 22 and 25 % of cases, respectively, and from patients with other autoimmune liver diseases, in 30, 22 and 22 % of cases, respectively. Prevalence of serum antibodies to non-gastric Helicobacter species was significantly higher in patients with autoimmune chronic liver diseases than in healthy blood donors (P < 0.001). Increased antibody levels to enterohepatic Helicobacter species raise questions concerning an infectious role of these emerging bacterial pathogens in human autoimmune liver diseases.
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Affiliation(s)
- Ingrid Nilsson
- Department of Medical Microbiology, Dermatology and Infection, Division of Bacteriology, Lund University, Sölvegatan 23, S-223 62, Lund, Sweden 2Gastroenterology-Hepatology Division, Department of Medicine, University Hospital of Malmö, Sweden
| | - Iryna Kornilovs'ka
- Department of Medical Microbiology, Dermatology and Infection, Division of Bacteriology, Lund University, Sölvegatan 23, S-223 62, Lund, Sweden 2Gastroenterology-Hepatology Division, Department of Medicine, University Hospital of Malmö, Sweden
| | - Stefan Lindgren
- Department of Medical Microbiology, Dermatology and Infection, Division of Bacteriology, Lund University, Sölvegatan 23, S-223 62, Lund, Sweden 2Gastroenterology-Hepatology Division, Department of Medicine, University Hospital of Malmö, Sweden
| | - Åsa Ljungh
- Department of Medical Microbiology, Dermatology and Infection, Division of Bacteriology, Lund University, Sölvegatan 23, S-223 62, Lund, Sweden 2Gastroenterology-Hepatology Division, Department of Medicine, University Hospital of Malmö, Sweden
| | - Torkel Wadström
- Department of Medical Microbiology, Dermatology and Infection, Division of Bacteriology, Lund University, Sölvegatan 23, S-223 62, Lund, Sweden 2Gastroenterology-Hepatology Division, Department of Medicine, University Hospital of Malmö, Sweden
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15
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Risch HA. Etiology of pancreatic cancer, with a hypothesis concerning the role of N-nitroso compounds and excess gastric acidity. J Natl Cancer Inst 2003; 95:948-60. [PMID: 12837831 DOI: 10.1093/jnci/95.13.948] [Citation(s) in RCA: 118] [Impact Index Per Article: 5.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
In the United States, pancreatic cancer is the fourth most frequent cause of cancer death in males as well as females, after lung, prostate or breast, and colorectal cancer. Each year, approximately 30 000 Americans are diagnosed with pancreatic cancer and about the same number die of it. Germline mutations in a few genes including p16 and BRCA2 have been implicated in a small fraction of cases, as has chronic pancreatitis. The one established risk factor for pancreatic cancer is cigarette smoking: current smokers have two to three times the risk of nonsmokers. Studies of dietary factors have not been entirely consistent but do suggest associations of higher risk with consumption of smoked or processed meats or with animal foods in general and lower risk with consumption of fruits and vegetables. Colonization by Helicobacter pylori appears to increase risk, and a history of diabetes mellitus may also increase risk. The purpose of this epidemiologic review is to consider the possibility that risk of pancreatic cancer is increased by factors associated with pancreatic N-nitrosamine or N-nitrosamide exposures and with chronic excess gastric or duodenal acidity. Host genetic variation in inflammatory cytokine mechanisms may also be involved in this process. Many features of the evidence bearing on the pathophysiology of pancreatic cancer appear to support connections with N-nitroso compounds and with gastric acidity.
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Affiliation(s)
- Harvey A Risch
- Department of Epidemiology and Public Health, Yale University School of Medicine, 60 College St., P.O. Box 208034, New Haven, CT 06520-8034, USA.
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16
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Zalatnai A. Pancreatic cancer - a continuing challenge in oncology. Pathol Oncol Res 2003; 9:252-63. [PMID: 14688834 DOI: 10.1007/bf02893388] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/12/2003] [Accepted: 11/26/2003] [Indexed: 12/15/2022]
Abstract
Pancreatic cancer is still one of the major health problems because of its rising incidence and the modest therapeutic results. The paper surveys the statistical data, the risk factors, the preneoplastic ductal lesions, the hormonal sensitivity, the possible transdifferentiation in the endocrine and exocrine parts and the possibilities for chemoprevention. Hungary is peculiar among the European countries because during the last 50 years the incidence of pancreatic cancer has displayed a 15-fold increase. Apart from smoking, additional risk factors seem to be important, and recently a puzzling association between Helicobacter pylori seropositivity and pancreatic cancer was found. First-degree relatives of patients with pancreatic cancer are also at increased risk of this tumor. The term pancreatic intraepithelial neoplasia (PanIN) seems yet to be established, but the dynamics of these lesions needs to be further elucidated. Several lines of firmly established data indicate the hormonal sensitivity of this tumor, but still an unexplained discrepancy exists between the experimental and the clinical results. In addition to the somatostatin analogs, anti-gastrin vaccine is being tested. The mixed exocrine-endocrine tumors might suggest a real possibility of transdifferentiation between different compartments of the pancreas. Finally, the paper outlines the available data about the possibility of chemoprevention, including the role of cyclooxygenase inhibitors.
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Affiliation(s)
- Attila Zalatnai
- 1st Department of Pathology and Experimental Cancer Research, Faculty of Medicine Semmelweis University, H-1085 Budapest, Hungary.
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Abstract
The genus Helicobacter has expanded at a rapid pace and no fewer than 31 species have been named since the proposal of the genus in 1989. Of these 31 species, 22 are principally associated with extragastric niches and there is increasing interest in the role of these taxa in diseases of humans and animals. Substantial evidence attests to certain species playing a role in the pathogenesis of enteric, hepatic and biliary disorders and some taxa demonstrate zoonotic potential. The importance of extragastric Helicobacters is likely to be an important topic for research in the near future. Here, important papers published in the field this last year are reviewed.
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Affiliation(s)
- Stephen L W On
- Danish Veterinary Institute, Bülowsvej 27, Copenhagen, Denmark.
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