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Ilic M, Milicic B, Ilic I. Association between oral contraceptive use and pancreatic cancer risk: A systematic review and meta-analysis. World J Gastroenterol 2021; 27:2643-2656. [PMID: 34092981 PMCID: PMC8160625 DOI: 10.3748/wjg.v27.i20.2643] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/06/2021] [Revised: 03/13/2021] [Accepted: 04/23/2021] [Indexed: 02/06/2023] Open
Abstract
BACKGROUND Studies on the association of oral contraceptive (OC) use and pancreatic cancer showed inconsistent findings.
AIM To evaluate the relationship between OC use and pancreatic cancer risk.
METHODS A literature search for observational studies (case-control and cohort studies) was conducted up to December 2020. A meta-analysis was performed by calculating pooled relative risks (RRs) and 95% confidence intervals (CIs). Heterogeneity was assessed using Cochran’s chi-square test and I2 statistic. Subgroup analyses were performed by study design, source of controls in case-control studies, number of cases of pancreatic cancers, study quality according to Newcastle-Ottawa Scale score, geographical region and menopausal status. All analyses were performed using Review Manager 5.3 (RevMan 5.3).
RESULTS A total of 21 studies (10 case-control studies and 11 cohort studies) were finally included in the present meta-analysis, comprising 7700 cases of pancreatic cancer in total. A significant association was observed between the ever use of OC and pancreatic cancer risk in the overall analysis (RR = 0.85; 95%CI = 0.73-0.98; P = 0.03). Duration of OC use (< 1 year, < 5 years, 5-10 years, > 10 years) was not significantly associated with the risk of pancreatic cancer. Subgroup analyses revealed a statistically significant subgroup difference for the geographic region in which the study was conducted (Europe vs Americas vs Asia; P = 0.07). Subgroup analyses showed a statistically significant decrease in pancreatic cancer risk and OC use in high-quality studies, studies conducted in Europe, and in postmenopausal women.
CONCLUSION Despite the suggested protective effects of OC use in this meta-analysis, further epidemiological studies are warranted to fully elucidate the association between the use of OC and pancreatic cancer risk.
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Affiliation(s)
- Milena Ilic
- Department of Epidemiology, Faculty of Medical Sciences, University of Kragujevac, Kragujevac 34000, Serbia
| | - Biljana Milicic
- Department of Medical Statistics and Informatics, Faculty of Dental Medicine, University of Belgrade, Belgrade 11000, Serbia
| | - Irena Ilic
- Faculty of Medicine, University of Belgrade, Belgrade 11000, Serbia
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Monroy-Iglesias MJ, Dolly S, Sarker D, Thillai K, Van Hemelrijck M, Santaolalla A. Pancreatic Cancer Exposome Profile to Aid Early Detection and Inform Prevention Strategies. J Clin Med 2021; 10:1665. [PMID: 33924591 PMCID: PMC8069449 DOI: 10.3390/jcm10081665] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/28/2021] [Revised: 03/19/2021] [Accepted: 04/08/2021] [Indexed: 12/12/2022] Open
Abstract
Pancreatic cancer (PCa) is associated with a poor prognosis and high mortality rate. The causes of PCa are not fully elucidated yet, although certain exposome factors have been identified. The exposome is defined as the sum of all environmental factors influencing the occurrence of a disease during a life span. The development of an exposome approach for PCa has the potential to discover new disease-associated factors to better understand the carcinogenesis of PCa and help with early detection strategies. Our systematic review of the literature identified several exposome factors that have been associated with PCa alone and in combination with other exposures. A potential inflammatory signature has been observed among the interaction of several exposures (i.e., smoking, alcohol consumption, diabetes mellitus, obesity, and inflammatory markers) that further increases the incidence and progression of PCa. A large number of exposures have been identified such as genetic, hormonal, microorganism infections and immune responses that warrant further investigation. Future early detection strategies should utilize this information to assess individuals' risk for PCa.
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Affiliation(s)
- Maria J. Monroy-Iglesias
- Translational Oncology & Urology Research (TOUR), School of Cancer and Pharmaceutical Sciences, King’s College London, London SE1 9RT, UK; (M.J.M.-I.); (M.V.H.)
| | - Saoirse Dolly
- Department of Medical Oncology, Guy’s and St Thomas’ NHS Foundation Trust, London SE1 9RT, UK; (S.D.); (D.S.); (K.T.)
| | - Debashis Sarker
- Department of Medical Oncology, Guy’s and St Thomas’ NHS Foundation Trust, London SE1 9RT, UK; (S.D.); (D.S.); (K.T.)
- School of Cancer and Pharmaceutical Sciences, King’s College London, London SE1 9RT, UK
| | - Kiruthikah Thillai
- Department of Medical Oncology, Guy’s and St Thomas’ NHS Foundation Trust, London SE1 9RT, UK; (S.D.); (D.S.); (K.T.)
| | - Mieke Van Hemelrijck
- Translational Oncology & Urology Research (TOUR), School of Cancer and Pharmaceutical Sciences, King’s College London, London SE1 9RT, UK; (M.J.M.-I.); (M.V.H.)
| | - Aida Santaolalla
- Translational Oncology & Urology Research (TOUR), School of Cancer and Pharmaceutical Sciences, King’s College London, London SE1 9RT, UK; (M.J.M.-I.); (M.V.H.)
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Andersson G, Lundgren S, Heby M, Nodin B, Elebro J, Jirström K. Clinical significance of stromal ER and PR expression in periampullary adenocarcinoma. Biomark Res 2019; 7:26. [PMID: 31827798 PMCID: PMC6862740 DOI: 10.1186/s40364-019-0176-9] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/03/2019] [Accepted: 10/25/2019] [Indexed: 02/06/2023] Open
Abstract
BACKGROUND Tamoxifen treatment has previously been reported to confer life-prolonging effects in patients with advanced pancreatic cancer, and most evidently so in women. None of these trials did however include biomarkers, and the relevance of female hormone signaling in pancreatic or other periampullary adenocarcinoma remains largely unexplored. The aim of this study was to examine the extent and potential clinical significance of estrogen receptor-α (ER) and progesterone receptor (PR) expression in pancreatic and other periampullary cancers. METHODS ER and PR expression was examined using immunohistochemistry on tissue microarrays with primary tumors from a retrospective consecutive cohort of 175 patients with resected periampullary adenocarcinoma, with long-term clinical follow-up. Non-parametric and Chi square tests were applied to examine the associations of stromal ER and PR expression with patient and tumor characteristics. Kaplan-Meier analysis and log rank test were applied to illustrate survival differences in relation to ER and PR expression. Cox regression proportional hazards models were applied to examine the associations between investigative factors and risk of death and recurrence, and to test for interactions between KRAS mutation status and hormone receptor expression in relation to survival. RESULTS Expression of both ER and PR was more frequent in the tumor-associated stroma than in the epithelium. A significant prognostic interaction, independent of tumor morphology, was found between stromal PR expression and KRAS mutation status in relation to both overall and recurrence-free survival (pinteraction = 0.026 and pinteraction = 0.005), in particular in women (pinteraction = 0.002 and pinteraction = 0.005). Specifically, stromal PR expression was associated with a prolonged survival in patients with KRAS-mutated tumors, whereas the opposite was seen for KRAS wild-type tumors. The prognostic value of ER positivity was limited to the subgroup of women with tumors of pancreatic origin. CONCLUSIONS These results demonstrate that stromal PR rather than ER expression, together with KRAS mutation status, provides long-term prognostic information in patients with periampullary adenocarcinoma. Further study into the mechanistic basis for these observations may unveil important clues to the pathogenesis of these cancers and open up for the discovery of novel treatment options.
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Affiliation(s)
- Gustav Andersson
- Division of Oncology and Pathology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden
| | - Sebastian Lundgren
- Division of Oncology and Pathology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden
| | - Margareta Heby
- Division of Oncology and Pathology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden
| | - Björn Nodin
- Division of Oncology and Pathology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden
| | - Jacob Elebro
- Division of Oncology and Pathology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden
| | - Karin Jirström
- Division of Oncology and Pathology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden
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Andersson G, Borgquist S, Jirström K. Hormonal factors and pancreatic cancer risk in women: The Malmö Diet and Cancer Study. Int J Cancer 2018; 143:52-62. [PMID: 29424426 PMCID: PMC5969235 DOI: 10.1002/ijc.31302] [Citation(s) in RCA: 32] [Impact Index Per Article: 4.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/30/2017] [Revised: 12/13/2017] [Accepted: 02/05/2018] [Indexed: 12/30/2022]
Abstract
The incidence of pancreatic cancer is leveling between sexes. Smoking, high age and heredity are established risk factors, but evidence regarding the influence of hormonal factors is unclear. In this study, we investigated the associations of reproductive factors, use of oral contraceptives (OC) and hormone replacement therapy (HRT) with pancreatic cancer risk in the Malmö Diet and Cancer Study, a prospective, population‐based cohort encompassing 17,035 women. Up until 31 December 2015, 110 women were identified with incident pancreatic cancer through the Swedish Cancer Registry. Higher age at menarche was significantly associated with pancreatic cancer risk (age‐adjusted [hazard ratio] HR = 1.17; 95% confidence interval [CI] 1.04–1.32, and fully adjusted HR = 1.17; 95% CI 1.04–1.32). Ever use of OC was not significantly associated with pancreatic cancer risk but ever use of HRT was significantly associated with a decreased risk of pancreatic cancer (age‐adjusted HR = 0.47, 95% CI 0.23–0.97, and fully adjusted HR = 0.48, 95% CI 0.23–1.00), in particular use of estrogen‐only regimen (age‐adjusted HR = 0.21; 95% CI 0.05–0.87 and fully adjusted HR = 0.22; 95% CI 0.05–0.90). Age at menopause or first childbirth, parity and breastfeeding history were not significantly associated with pancreatic cancer risk. Collectively, these findings suggest a protective role of female hormones against pancreatic cancer. Further studies are needed, and potential modifying genetic factors and indirect hazardous effects of smoking should also be considered. What's new? Female hormones appear to protect against pancreatic cancer, at least in Sweden. Numerous studies have investigated the relationship between the two, but no clear picture has yet emerged. These authors used data from the Malmö Diet and Cancer study, looking for correlations between hormone levels and cancer risk. They found that a younger start to menstruation—indicating an earlier boost in estrogen—correlated with less chance of developing pancreatic cancer. Use of hormone replacement therapy, particularly estrogen‐only therapy, significantly reduced risk among postmenopausal women. Breastfeeding, oral contraceptive use and parity did not appear to affect pancreatic cancer risk.
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Affiliation(s)
- Gustav Andersson
- Division of Oncology and Pathology, Department of Clinical Sciences, Lund University, Lund, Sweden
| | - Signe Borgquist
- Division of Oncology and Pathology, Department of Clinical Sciences, Lund University, Lund, Sweden.,Clinical Trial Unit, Skåne University Hospital, Lund, Sweden
| | - Karin Jirström
- Division of Oncology and Pathology, Department of Clinical Sciences, Lund University, Lund, Sweden
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Lujan-Barroso L, Zhang W, Olson SH, Gao YT, Yu H, Baghurst PA, Bracci PM, Bueno-de-Mesquita HB, Foretová L, Gallinger S, Holcatova I, Janout V, Ji BT, Kurtz RC, La Vecchia C, Lagiou P, Li D, Miller AB, Serraino D, Zatonski W, Risch HA, Duell EJ. Menstrual and Reproductive Factors, Hormone Use, and Risk of Pancreatic Cancer: Analysis From the International Pancreatic Cancer Case-Control Consortium (PanC4). Pancreas 2016; 45:1401-1410. [PMID: 27088489 PMCID: PMC5065728 DOI: 10.1097/mpa.0000000000000635] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
OBJECTIVES We aimed to evaluate the relation between menstrual and reproductive factors, exogenous hormones, and risk of pancreatic cancer (PC). METHODS Eleven case-control studies within the International Pancreatic Cancer Case-control Consortium took part in the present study, including in total 2838 case and 4748 control women. Pooled estimates of odds ratios (ORs) and their 95% confidence intervals (CIs) were calculated using a 2-step logistic regression model and adjusting for relevant covariates. RESULTS An inverse OR was observed in women who reported having had hysterectomy (ORyesvs.no, 0.78; 95% CI, 0.67-0.91), remaining significant in postmenopausal women and never-smoking women, adjusted for potential PC confounders. A mutually adjusted model with the joint effect for hormone replacement therapy (HRT) and hysterectomy showed significant inverse associations with PC in women who reported having had hysterectomy with HRT use (OR, 0.64; 95% CI, 0.48-0.84). CONCLUSIONS Our large pooled analysis suggests that women who have had a hysterectomy may have reduced risk of PC. However, we cannot rule out that the reduced risk could be due to factors or indications for having had a hysterectomy. Further investigation of risk according to HRT use and reason for hysterectomy may be necessary.
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Affiliation(s)
- Leila Lujan-Barroso
- From the *Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO), Bellvitge Biomedical Research Institute (IDIBELL), Barcelona, Spain; †Department of Epidemiology, Shanghai Cancer Institute and Jiao Tong University, Shanghai, China; ‡Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY; §Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI; ∥Public Health, Women's and Children's Hospital, Adelaide, SA, Australia; ¶University of California, San Francisco, San Francisco, CA; #National Institute for Public Health and the Environment (RIVM), Bilthoven; **Department of Gastroenterology and Hepatology, University Medical Center Utrecht, Utrecht, The Netherlands; ††Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK; ‡‡Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; §§Department of Cancer Epidemiology and Genetics, Masaryk Memorial Cancer Institute, Institute and MF MU, Brno, Czech Republic; ∥∥University Health Network, Department of Surgery, University of Toronto, Toronto, Canada; ¶¶Institute of Hygiene and Epidemiology, 1st Faculty of Medicine, Charles University in Prague, Prague; ##Department of Preventive Medicine, Faculty of Medicine, Palacky University, Olomouc, Czech Republic; ***National Cancer Institute, Bethesda, MD; †††Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY; ‡‡‡Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy; §§§Department of Hygiene, Epidemiology and Medical Statistics, School of Medicine, University of Athens, Greece; ∥∥∥Department of Epidemiology, Harvard School of Public Health, Boston, MA; ¶¶¶M.D. Anderson Cancer Center, University of Texas, Houston, TX; ###Dalla Lana School of Public Health, University of Toronto, Toronto, Canada; ****Unit of Epidemiology and Biostatistics, CRO Aviano, National Cancer Institute, IRCCS, Aviano, Italy; ††††Cancer Center and Institute of Oncology, Warsaw, Poland; and ‡‡‡‡Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT
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Luo AJ, Feng RH, Wang XW, Wang FZ. Older age at first birth is a risk factor for pancreatic cancer: a meta-analysis. Hepatobiliary Pancreat Dis Int 2016; 15:125-30. [PMID: 27020627 DOI: 10.1016/s1499-3872(16)60063-2] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
BACKGROUND Some studies found that age at first birth is associated with pancreatic cancer; others did not. The present meta-analysis was to evaluate the relationship between age at first birth and pancreatic cancer in women. DATA SOURCES We searched PubMed, Embase, and the Cochrane Library for relevant publications on age at first birth and pancreatic cancer up to April, 2014. The eligible studies (six cohorts and five case-controls) were independently selected by two authors. Pooled relative risk (RR) estimates and corresponding 95% confidence interval (95% CI) were calculated using the inverse-variance method. RESULTS The pooled RR of pancreatic cancer risk for the highest versus lowest categories of age at first birth was 1.21 (95% CI: 1.01-1.45, P=0.314, I2=13.7%). Consistent relationships were also observed within subgroup analyses stratified by study design, geographic region, and whether the studies included adjustment for cigarette smoking, diabetes, or all of the confounders. In this meta-analysis, no publication bias among studies was observed using Egger's test (P=0.383) or Begg's test (P=0.436). CONCLUSION Our findings suggest that older age at first birth is associated with an increased risk of pancreatic cancer in women and the exact functional mechanism needs further investigation.
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Affiliation(s)
- Ai-Jing Luo
- School of Public Health, Central South University, Changsha 410078, China.
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Tang B, Lv J, Li Y, Yuan S, Wang Z, He S. Relationship between female hormonal and menstrual factors and pancreatic cancer: a meta-analysis of observational studies. Medicine (Baltimore) 2015; 94:e177. [PMID: 25700305 PMCID: PMC4554173 DOI: 10.1097/md.0000000000000177] [Citation(s) in RCA: 20] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
The objective of this study was to assess the relationship between female hormone and menstrual factors and pancreatic cancer (PC) through a meta-analysis of observational studies. We undertook a systematic literature search up to July 10, 2014 in PubMed and EMBASE databases. Combined relative risks (RRs) were estimated by random-effects models. Subgroup analysis was performed by study design, source of control, and geographic regions. Sensitivity analyses and publication bias were utilized to evaluate the robustness of our results. A total of 27 case-control and cohort studies were retrieved for this meta-analysis. No significant associations were observed between the risk of PC and age at menarche (RR = 0.94, 95% confidence interval [CI] 0.83-1.07), age at menopause (RR = 0.98, 95% CI 0.85-1.13), hysterectomy (RR = 0.97, 95% CI 0.84-1.11), oophorectomy (RR = 1.02, 95% CI 0.82-1.26), hormone replacement therapy (RR = 0.97, 95% CI 0.87-1.08), and oral contraceptives (RR = 1.09, 95% CI 0.96-1.23). This meta-analysis of observational studies does not support the hypothesis that exogenous hormone use and menstrual factors are associated with PC.
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Affiliation(s)
- Bo Tang
- From the Department of Hepatobiliary Surgery (BT, SY, ZW, SH), Affiliated Hospital of Guilin Medical University; Laboratory of Liver Injury and Repair Molecular Medicine (BT, SH), Guilin Medical University, Guilin; Department of Infectious Diseases (JL), People's Hospital of Beihai, Beihai; and Department of Medical Oncology (YL), Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, People's Republic of China
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Zhu B, Zou L, Han J, Chen W, Shen N, Zhong R, Li J, Chen X, Liu C, Shi Y, Miao X. Parity and pancreatic cancer risk: evidence from a meta-analysis of twenty epidemiologic studies. Sci Rep 2014; 4:5313. [PMID: 24936955 PMCID: PMC4060503 DOI: 10.1038/srep05313] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/17/2014] [Accepted: 04/11/2014] [Indexed: 12/20/2022] Open
Abstract
Multiple studies have hypothesized parity is associated with pancreatic cancer risk but obtained conflicting results. We conducted a meta-analysis (including a dose-response approach) of current available epidemiologic studies to investigate the association between parity and risk of pancreatic cancer. Ten cohort studies and ten case-control studies including 8205 cases were eligible for inclusion. The combined RR (relative risk) of pancreatic cancer for the parous vs. nulliparous was 0.91 (95% CI, confidence interval = 0.85–0.97, I2 = 39.0%, Ph = 0.01). We observed an inverse association between giving birth to two children pancreatic cancer risk with RR of 0.86 (95% CI = 0.80–0.93, I2 = 8.7%, Ph = 0.36). And no evidence supported there was non-linear (P = 0.33) or linear relationship (P = 0.14) between number of parity and risk of pancreatic cancer. Findings from this meta-analysis indicate that giving birth to two children has the lowest pancreatic cancer risk, mechanism of this protective effect needs further investigation.
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Affiliation(s)
- Beibei Zhu
- State Key Laboratory of Environment Health (Incubation), MOE (Ministry of Education) Key Laboratory of Environment & Health, Ministry of Environmental Protection Key Laboratory of Environment and Health (Wuhan),and Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Li Zou
- State Key Laboratory of Environment Health (Incubation), MOE (Ministry of Education) Key Laboratory of Environment & Health, Ministry of Environmental Protection Key Laboratory of Environment and Health (Wuhan),and Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Juan Han
- Department of biliary and pancreatic surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Wei Chen
- State Key Laboratory of Environment Health (Incubation), MOE (Ministry of Education) Key Laboratory of Environment & Health, Ministry of Environmental Protection Key Laboratory of Environment and Health (Wuhan),and Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Na Shen
- State Key Laboratory of Environment Health (Incubation), MOE (Ministry of Education) Key Laboratory of Environment & Health, Ministry of Environmental Protection Key Laboratory of Environment and Health (Wuhan),and Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Rong Zhong
- State Key Laboratory of Environment Health (Incubation), MOE (Ministry of Education) Key Laboratory of Environment & Health, Ministry of Environmental Protection Key Laboratory of Environment and Health (Wuhan),and Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Jiaoyuan Li
- State Key Laboratory of Environment Health (Incubation), MOE (Ministry of Education) Key Laboratory of Environment & Health, Ministry of Environmental Protection Key Laboratory of Environment and Health (Wuhan),and Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Xueqin Chen
- State Key Laboratory of Environment Health (Incubation), MOE (Ministry of Education) Key Laboratory of Environment & Health, Ministry of Environmental Protection Key Laboratory of Environment and Health (Wuhan),and Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Cheng Liu
- State Key Laboratory of Environment Health (Incubation), MOE (Ministry of Education) Key Laboratory of Environment & Health, Ministry of Environmental Protection Key Laboratory of Environment and Health (Wuhan),and Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Yang Shi
- State Key Laboratory of Environment Health (Incubation), MOE (Ministry of Education) Key Laboratory of Environment & Health, Ministry of Environmental Protection Key Laboratory of Environment and Health (Wuhan),and Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Xiaoping Miao
- State Key Laboratory of Environment Health (Incubation), MOE (Ministry of Education) Key Laboratory of Environment & Health, Ministry of Environmental Protection Key Laboratory of Environment and Health (Wuhan),and Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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Guan HB, Wu L, Wu QJ, Zhu J, Gong T. Parity and pancreatic cancer risk: a dose-response meta-analysis of epidemiologic studies. PLoS One 2014; 9:e92738. [PMID: 24658609 PMCID: PMC3962437 DOI: 10.1371/journal.pone.0092738] [Citation(s) in RCA: 36] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/31/2013] [Accepted: 02/24/2014] [Indexed: 02/07/2023] Open
Abstract
Background Previous epidemiologic studies have reported inconsistent results between parity and pancreatic cancer (PC) risk. To our knowledge, a comprehensive and quantitative assessment of this association has not been conducted. Methods Relevant published studies of parity and PC were identified using MEDLINE (PubMed) and Web of Science databases until November 2013. Two authors (H-BG and LW) independently assessed eligibility and extracted data. Eleven prospective and 11 case-control studies reported relative risk (RR) estimates and 95% confidence intervals (CIs) of PC associated with parity. Fixed- and random-effects models were used to estimate the summary RR depending on the heterogeneity of effects. Results The summary RR for PC comparing the highest versus lowest parity was 0.86 (95% CI: 0.73–1.02; Q = 50.49, P<0.001, I2 = 58.4%). Significant inverse associations were also observed in the studies that adjusted for cigarette smoking (RR = 0.81; 95% CI: 0.68–0.98), Type 2 diabetes mellitus (RR = 0.83; 95% CI: 0.75–0.93), and those that included all confounders or important risk factors (RR = 0.85; 95% CI: 0.76–0.96). Additionally, in the dose-response analysis, the summary RR for per one live birth was 0.97 (95% CI: 0.94–1.01; Q = 62.83, P<0.001, I2 = 69.8%), which also indicated a borderline statistically significant inverse effect of parity on PC risk. No evidence of publication bias and significant heterogeneity between subgroups were detected by meta-regression analyses. Conclusion In summary, these findings suggest that higher parity is associated with a decreased risk of PC. Future large consortia or pooled studies are warranted to fully adjust for potential confounders to confirm this association.
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Affiliation(s)
- Hong-Bo Guan
- Department of Obstetrics and Gynecology, Shengjing Hospital, China Medical University, Shenyang, China
- * E-mail:
| | - Lang Wu
- Center for Clinical and Translational Science, Mayo Clinic, Rochester, Minnesota, United States of America
| | - Qi-Jun Wu
- Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
- State Key Laboratory of Oncogene and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
| | - Jingjing Zhu
- Department of Educational Psychology, University of Minnesota, Minneapolis, Minnesota, United States of America
| | - Tingting Gong
- Department of Obstetrics and Gynecology, Shengjing Hospital, China Medical University, Shenyang, China
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10
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Preziosi G, Oben JA, Fusai G. Obesity and pancreatic cancer. Surg Oncol 2014; 23:61-71. [PMID: 24746917 DOI: 10.1016/j.suronc.2014.02.003] [Citation(s) in RCA: 37] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/07/2013] [Accepted: 02/21/2014] [Indexed: 12/18/2022]
Abstract
BACKGROUND Pancreatic cancer is an invariably fatal malignancy. Cigarette smoking and diabetes are established risk factors, but over the last two decades studies have shown that excess adiposity is an additional independent risk factor with 30-50% of cases thought to be attributed to nutritional factors. The aim of this narrative review is to analyze all the epidemiological evidence on the topic and possible pathophysiology. METHODS We searched PubMed, Embase, Cochrane Library and Medline, and all available evidence was included. We firstly analyze meta- and pooled analysis. Then we discuss individual studies to identify sources of discrepancies between studies and attempt to delineate pathophysiology. RESULTS It is estimated that obese individuals have a relative risk (RR) ranging between 1.19 and 1.47, when compared with those of normal weight, regardless of diabetes or smoking status. No significant differences were found between gender. CONCLUSION There is a measurable increased risk of developing pancreatic cancer in obese individuals, and excess adiposity is related to the condition with a "dose-response" curve. Hyperinsulinemia and possibly hyperestrogenism secondary to a metabolic syndrome, and independently from diabetes status, appear to be the key elements of the pathogenesis in pancreatic cancer secondary to excess body fat. Increased efforts should therefore be made in tackling the epidemic levels of obesity in the Western world countries.
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Affiliation(s)
- Giuseppe Preziosi
- Hepato-Pancreatico-Biliary Surgery and Liver Transplant Unit, Royal Free Hospital, London, United Kingdom.
| | - Jude A Oben
- Centre for Liver and Digestive Health, University College London, Royal Free Hospital, London, United Kingdom
| | - Giuseppe Fusai
- Hepato-Pancreatico-Biliary Surgery and Liver Transplant Unit, Royal Free Hospital, London, United Kingdom
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Lee E, Horn-Ross PL, Rull RP, Neuhausen SL, Anton-Culver H, Ursin G, Henderson KD, Bernstein L. Reproductive factors, exogenous hormones, and pancreatic cancer risk in the CTS. Am J Epidemiol 2013; 178:1403-13. [PMID: 24008905 DOI: 10.1093/aje/kwt154] [Citation(s) in RCA: 43] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022] Open
Abstract
Female steroid hormones are hypothesized to play a protective role in pancreatic cancer risk. However, results from epidemiologic studies that examined hormone-related exposures have been inconsistent. The California Teachers Study is a cohort study of female public school professionals that was established in 1995-1996. Of the 118,164 eligible study participants, 323 women were diagnosed with incident invasive pancreatic cancer through December 31, 2009. Multivariable Cox proportional hazards regression methods were used to estimate hazard ratios and 95% confidence intervals for the association of pancreatic cancer risk with reproductive factors and exogenous hormone use. Current users of estrogen-only therapy at baseline (1995-1996) had a lower risk of pancreatic cancer than did participants who had never used hormone therapy (hazard ratio = 0.59, 95% confidence interval: 0.42, 0.84). Use of estrogen-plus-progestin therapy was not associated with the risk of pancreatic cancer. A longer duration of oral contraceptive use (≥10 years of use compared with never use) was associated with an increased risk of cancer (hazard ratio = 1.72, 95% confidence interval: 1.19, 2.49). Reproductive factors, including age at menarche, parity, breastfeeding, and age at menopause, were not associated with pancreatic cancer risk. Our results suggest that increased estrogen exposure through estrogen-only therapy may reduce pancreatic cancer risk in women.
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Duell EJ, Travier N, Lujan-Barroso L, Dossus L, Boutron-Ruault MC, Clavel-Chapelon F, Tumino R, Masala G, Krogh V, Panico S, Ricceri F, Redondo ML, Dorronsoro M, Molina-Montes E, Huerta JM, Barricarte A, Khaw KT, Wareham NJ, Allen NE, Travis R, Siersema PD, Peeters PHM, Trichopoulou A, Fragogeorgi E, Oikonomou E, Boeing H, Schuetze M, Canzian F, Lukanova A, Tjønneland A, Roswall N, Overvad K, Weiderpass E, Gram IT, Lund E, Lindkvist B, Johansen D, Ye W, Sund M, Fedirko V, Jenab M, Michaud DS, Riboli E, Bueno-de-Mesquita HB. Menstrual and reproductive factors in women, genetic variation in CYP17A1, and pancreatic cancer risk in the European prospective investigation into cancer and nutrition (EPIC) cohort. Int J Cancer 2012; 132:2164-75. [PMID: 23015357 DOI: 10.1002/ijc.27875] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/22/2011] [Accepted: 07/18/2012] [Indexed: 12/14/2022]
Abstract
Menstrual and reproductive factors and exogenous hormone use have been investigated as pancreatic cancer risk factors in case-control and cohort studies, but results have been inconsistent. We conducted a prospective examination of menstrual and reproductive factors, exogenous hormone use and pancreatic cancer risk (based on 304 cases) in 328,610 women from the EPIC cohort. Then, in a case-control study nested within the EPIC cohort, we examined 12 single nucleotide polymorphisms (SNPs) in CYP17A1 (an essential gene in sex steroid metabolism) for association with pancreatic cancer in women and men (324 cases and 353 controls). Of all factors analyzed, only younger age at menarche (<12 vs. 13 years) was moderately associated with an increased risk of pancreatic cancer in the full cohort; however, this result was marginally significant (HR = 1.44; 95% CI = 0.99-2.10). CYP17A1 rs619824 was associated with HRT use (p value = 0.037) in control women; however, none of the SNPs alone, in combination, or as haplotypes were associated with pancreatic cancer risk. In conclusion, with the possible exception of an early age of menarche, none of the menstrual and reproductive factors, and none of the 12 common genetic variants we evaluated at the CYP17A1 locus makes a substantial contribution to pancreatic cancer susceptibility in the EPIC cohort.
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Affiliation(s)
- Eric J Duell
- Unit of Nutrition, Environment and Cancer, Catalan Institute of Oncology, Bellvitge Biomedical Research Institute (IDIBELL), Barcelona, Spain.
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Abstract
OBJECTIVES To investigate the role of menstrual, reproductive, and hormonal factors, as well as benign female conditions, on pancreatic cancer risk. METHODS We analyzed the combined data from 2 Italian case-control studies including 285 female case patients of pancreatic cancer and 713 female controls. All subjects were interviewed by trained interviewers during their hospital stay using similar structured questionnaires. Odds ratios (ORs) and their corresponding 95% confidence intervals (CIs) were estimated using multiple logistic regression models adjusted for selected covariates. RESULTS Compared to nulliparae, the OR was 0.76 (95% CI, 0.51-1.12) for parous women and 0.46 (95% CI, 0.26-0.85) for women with 4 or more births, in the absence, however, of a significant trend with increasing number of births. Pancreatic cancer risk was also nonsignificantly reduced among women with age at first birth lower than 25 years (OR, 0.65; 95% CI, 0.42-1.01). Other factors, including age at menarche and menopause, menopausal status, type of menopause, history of spontaneous and induced abortions, use of oral contraceptives and hormone replacement therapy, and history of most female benign conditions were not related to pancreatic cancer risk. CONCLUSIONS This study provides little support for the hypothesis that menstrual, reproductive, or hormonal factors are related to the development of pancreatic cancer.
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Abstract
OBJECTIVES This study was undertaken to examine whether there is an association between parity and age at first birth and risk of pancreatic cancer. METHODS The study cohort consisted of all women with a record of a first and singleton childbirth in the Birth Registration System between 1978 and 1987. We tracked each woman from the time of their first childbirth and linked their vital status with mortality database. Cox proportional hazard regression models were used to estimate the relative risks (RRs) of death from pancreatic cancer associated with parity and age at first birth. RESULTS A trend of increasing risk of pancreatic cancer was seen with increasing age at first birth. The adjusted RR was 0.69 (95% confidence interval, 0.49-0.98) for women who born 2 children and 0.64 (95% confidence interval, 0.44-0.93) for women with 3 or more births, respectively, when compared with women who had given birth to only 1 child. There was a significant decreasing trend in the RR of pancreatic cancer with increasing parity. CONCLUSIONS This study provides evidence that reproductive factors (parity and early age at first birth) may confer a protective effect on the risk of pancreatic cancer.
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Duell EJ, Holly EA, Kelsey KT, Bracci PM. Genetic variation in CYP17A1 and pancreatic cancer in a population-based case-control study in the San Francisco Bay Area, California. Int J Cancer 2010; 126:790-5. [PMID: 19642097 DOI: 10.1002/ijc.24792] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]
Abstract
Pancreatic cancer is the fourth leading cause of cancer-related death in men and women in the United States. Reproductive factors and steroid hormones have been suspected risk factors for many years, but the results from epidemiologic studies to date have been inconclusive. CYP17A1 encodes cytochrome P450c17alpha, an enzyme with 17alpha-hydroxylase and 17,20-lyase activities in estradiol biosynthesis. A polymorphism in the 5'UTR promoter region of CYP17A1-34T/C(A1/A2) has been associated with circulating estrogens in premenopausal women and with susceptibility to breast, prostate, and endometrial cancer. Questionnaire data and germline DNA collected in a San Francisco Bay Area population-based case-control study of pancreatic cancer (cases = 532, controls = 1701) were used to conduct analyses of pancreatic cancer susceptibility related to the CYP17A1 polymorphism and whether effects associated with smoking and reproductive risk factors were modified by this polymorphism. Mass spectrometry- and TaqMan-based methods were used to determine CYP17A1 genotypes in DNA samples from 308 cases and 964 controls. Results showed that carriers of the A2 allele (vs. A1/A1) were significantly less likely to have been diagnosed with pancreatic cancer (A1/A2, adjusted odds ratio (OR) = 0.77, 95% confidence interval (CI) = 0.58-1.0; A2/A2, OR = 0.63, 95%CI = 0.42-0.93; p-trend = 0.01). ORs for CYP17A1 genotypes did not differ by sex, but the observed inverse association was stronger in postmenopausal women. ORs for smoking and pancreatic cancer were not modified by CYP17A1 genotype. Our results suggest that the CYP17A1 A2 allele may be associated with a lower risk of pancreatic cancer in both men and women.
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Affiliation(s)
- Eric J Duell
- Unit of Nutrition, Environment and Cancer, Cancer Epidemiology Research Programme, Catalan Institute of Oncology (ICO), L'Hospitalet de Llobregat, Barcelona, Spain.
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Zhang Y, Coogan PF, Palmer JR, Strom BL, Rosenberg L. A case-control study of reproductive factors, female hormone use, and risk of pancreatic cancer. Cancer Causes Control 2009; 21:473-8. [PMID: 19941157 DOI: 10.1007/s10552-009-9478-9] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/25/2009] [Accepted: 11/11/2009] [Indexed: 01/02/2023]
Abstract
Findings from several previous studies that have assessed the relation of reproductive factors and female hormone use to the risk of pancreatic cancer are inconclusive. The authors examined the association between reproductive factors and the use of oral contraceptives and postmenopausal hormone therapy to the risk of pancreatic cancer among 284 patients with pancreatic cancer and 1,096 controls using data from the hospital-based Case-Control Surveillance Study. Older age at first pregnancy and long-duration oral contraceptive use were associated with an increased risk of pancreatic cancer: the odds ratio was 2.0 (95% CI: 1.1-3.3) for first birth at age 30 or older compared with before age 20 (p for trend = 0.042) and 2.0 (95% CI: 1.0-4.0) for ten or more years of use of oral contraceptive use relative to no-use (p for trend < 0.01). Risk of pancreatic cancer risk was not associated with postmenopausal female hormone use. The findings suggest that increased exposure to estrogen during the reproductive years may play a role in the development of pancreatic cancer in women. Further studies are needed to confirm the findings.
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Affiliation(s)
- Yuqing Zhang
- Boston University School of Medicine, MA 02118, USA.
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Duell EJ, Maisonneuve P, Baghurst PA, Bueno-de-Mesquita HB, Ghadirian P, Miller AB, Zatonski W, Vrieling A, Boffetta P, Boyle P. Menstrual and reproductive factors and pancreatic cancer in the SEARCH program of the IARC. Cancer Causes Control 2009; 20:1757-62. [PMID: 19653108 DOI: 10.1007/s10552-009-9408-x] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/30/2009] [Accepted: 07/15/2009] [Indexed: 01/02/2023]
Abstract
We conducted a population-based case-control study on the relation of menstrual and reproductive factors and hormone use with pancreatic cancer risk among female participants of the SEARCH program study. We evaluated 367 cases of ductal adenocarcinoma and 821 controls for associations between pancreatic cancer and age at menarche, age at menopause, number of pregnancies, exogenous hormone use, and history of gynaecologic surgery. Among directly interviewed and proxy participants, we found a statistically significant association for having age of menarche at 11 years or younger compared with menarche at ages 12-13 years (OR = 1.8, 95% CI = 1.1-3.1). This result was consistent, but not statistically significant, among three of the four studies analyzed, and when the data were analyzed separately by response status (direct vs. proxy interviews). No other menstrual or reproductive factors were associated with pancreatic cancer risk in this study. In conclusion, earlier age at menarche may be weakly associated with pancreatic cancer, but it seems unlikely that menstrual and reproductive factors play more than only a minor role in pancreatic cancer. Additional analyses in large prospective study populations and in pooled studies may help to clarify remaining inconsistencies.
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Affiliation(s)
- Eric J Duell
- Unit of Nutrition, Environment and Cancer, Cancer Epidemiology Research Programme, Institut Català d'Oncologia (ICO), Catalan Institute of Oncology, Avda Gran Via 199-203, 08907 L'Hospitalet de Llobregat, Barcelona, Spain.
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Stevens RJ, Roddam AW, Green J, Pirie K, Bull D, Reeves GK, Beral V. Reproductive history and pancreatic cancer incidence and mortality in a cohort of postmenopausal women. Cancer Epidemiol Biomarkers Prev 2009; 18:1457-60. [PMID: 19423523 DOI: 10.1158/1055-9965.epi-08-1134] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Abstract
There is inconsistent evidence about the effect of reproductive history on women's risk of pancreatic cancer. In the Million Women Study, a prospective cohort of middle-aged women in the United Kingdom, we examined associations between reproductive history and pancreatic cancer incidence and mortality, controlling for age, socioeconomic status, geographic region, body mass index, smoking, and history of diabetes. During 7.1 million person-years of follow-up in 995,192 postmenopausal women, there were 1,182 incident pancreatic cancers. Pancreatic cancer incidence and mortality did not vary significantly with age at menarche, number of children, age at first birth, breast-feeding, type of menopause, age at menopause, or time since menopause. Any effect of reproductive history and pancreatic cancer risk in women is likely to be weak, if it exists at all.
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Wahi MM, Shah N, Schrock CE, Rosemurgy AS, Goldin SB. Reproductive Factors and Risk of Pancreatic Cancer in Women: A Review of the Literature. Ann Epidemiol 2009; 19:103-11. [DOI: 10.1016/j.annepidem.2008.11.003] [Citation(s) in RCA: 32] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/23/2008] [Revised: 11/13/2008] [Accepted: 11/19/2008] [Indexed: 12/13/2022]
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Abstract
The involvement of estrogen and its receptors in the development of cancer has been known for years. However, the exact mechanism responsible is far from clear. The estrogen-mediated carcinogenic process is complicated by recent findings, which reveal that estrogens have multiple functions in cells, which can be either adverse or beneficial, and that the effects of estrogen may be cell-type or organ dependent. The estrogenic effect may be also greatly influenced by the state of two estrogen receptors, ERalpha and ERbeta. This review will discuss the role and function of estrogens and its receptors in cancers of three categories: (1) Breast cancer and gynecologic cancers, (2) Cancers of endocrine organs, (3) Lung cancer and cancers of digestive system. We will also review some novel treatments aiming to interfere with relevant pathways mediated by estrogens and its receptors.
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Affiliation(s)
- George G Chen
- Department of Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, N.T., Hong Kong SAR, China.
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21
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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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22
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Heuch I, Jacobsen BK, Albrektsen G, Kvåle G. Reproductive factors and pancreatic cancer risk: a Norwegian cohort study. Br J Cancer 2007; 98:189-93. [PMID: 18000501 PMCID: PMC2359696 DOI: 10.1038/sj.bjc.6604095] [Citation(s) in RCA: 23] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/29/2022] Open
Abstract
A cohort of 63 090 Norwegian women born 1886–1928 was followed more than 38 years, and relations between reproductive factors and risk of pancreatic cancer were explored; 449 cases were recorded at ages 50–89 years. Age at menopause showed a moderately positive association with risk (rate ratio (RR)=1.08 per 2 years delay in menopause; 95% confidence interval (CI)=1.00–1.17). Neither parity nor duration of breastfeeding showed significant associations with risk after adjusting only for demographic factors. With mutual adjustment, however, parity became positively associated (RR=1.13 per delivery; 95% CI=1.05–1.22) while duration of breastfeeding was inversely associated (RR=0.87 per 12 months; 95% CI=0.78–0.97). These associations lessened in magnitude with increasing age, and were essentially absent above age 80 years. Risk was raised among women reporting at least one abortion, but no trend was seen with number of abortions. Together with previous studies, the findings raise questions about the role of chance, but do not exclude hormonal factors related to breastfeeding and pregnancy from affecting pancreatic cancer risk.
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Affiliation(s)
- I Heuch
- Department of Mathematics, University of Bergen, Johannes Bruns Gate 12, N-5008 Bergen, Norway.
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23
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Lo AC, Soliman AS, El-Ghawalby N, Abdel-Wahab M, Fathy O, Khaled HM, Omar S, Hamilton SR, Greenson JK, Abbruzzese JL. Lifestyle, occupational, and reproductive factors in relation to pancreatic cancer risk. Pancreas 2007; 35:120-9. [PMID: 17632317 DOI: 10.1097/mpa.0b013e318053e7d3] [Citation(s) in RCA: 66] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/21/2022]
Abstract
OBJECTIVES This study examined the epidemiology of pancreatic cancer in Egypt. METHODS We obtained detailed information on smoking, occupational, medical, and reproductive histories from 194 pancreatic cancer cases and 194 controls. RESULTS Compared with not smoking, smoking cigarettes alone or in conjunction with other smoking methods (eg, water pipe, cigar) was associated with an increased risk (odds ratio [OR], 4.5 and 7.8; 95% confidence interval [95% CI], 1.9-10.7 and 3.0-20.6, respectively). Passive smoking was also a significant risk factor (OR, 6.0; 95% CI, 2.4-14.8). The risk of pancreatic cancer was elevated among subjects exposed to pesticides (OR, 2.6; 95% CI, 0.97-7.2). A prior diagnosis of diabetes mellitus for a period of 10 years was associated with higher risk (OR, 5.4; 95% CI, 1.5-19.9). For women, having 7 or more live births and lactating for 144 months or longer were associated with a reduced risk (OR, 0.5 and 0.2; 95% CI, 0.2-1.3 and 0.1-0.9, respectively). No association was found between family history, allergy, or obesity and pancreatic cancer in Egypt. CONCLUSIONS Multiple tobacco consumption methods, passive smoking, pesticide exposures, and diabetes are associated with an increased risk for pancreatic cancer. Prolonged lactation and increased parity are associated with a reduced risk for pancreatic cancer.
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Affiliation(s)
- An-Chi Lo
- Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, MI 48109, USA
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Ansary-Moghaddam A, Huxley R, Barzi F, Lawes C, Ohkubo T, Fang X, Jee SH, Woodward M. The effect of modifiable risk factors on pancreatic cancer mortality in populations of the Asia-Pacific region. Cancer Epidemiol Biomarkers Prev 2007; 15:2435-40. [PMID: 17164367 DOI: 10.1158/1055-9965.epi-06-0368] [Citation(s) in RCA: 77] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/19/2022] Open
Abstract
BACKGROUND Pancreatic cancer accounts for about 220,000 deaths each year. Known risk factors are smoking and type 2 diabetes. It remains to be seen whether these risk factors are equally important in Asia and whether other modifiable risk factors have important associations with pancreatic cancer. METHODS An individual participant data analysis of 30 cohort studies was carried out, involving 420,310 Asian participants (33% female) and 99,333 from Australia/New Zealand (45% female). Cox proportional hazard models, stratified by study and sex and adjusted for age, were used to quantify risk factors for death from pancreatic cancer. RESULTS During 3,558,733 person-years of follow-up, there were 324 deaths from pancreatic cancer (54% Asia and 33% female). Mortality rates (per 100,000 person-years) from pancreatic cancer were 10 for men and 8 for women. The following are age-adjusted hazard ratios (95% confidence interval) for death from pancreatic cancer: for current smoking, 1.61 (1.12-2.32); for diabetes, 1.76 (1.15-2.69); for a 2-cm increase in waist circumference, 1.08 (1.02-1.14). All three relationships remained significant (P < 0.05) after adjustment for other risk factors. There was no evidence of heterogeneity in the strength of these associations between either cohorts from Asia and Australia/New Zealand or between the sexes. In men, the combination of cigarette smoking and diabetes more than doubled the likelihood of pancreatic cancer (2.47; 95% confidence interval, 1.17-5.21) in both regions. CONCLUSIONS Smoking, obesity, and diabetes are important and are potentially modifiable risk factors for pancreatic cancer in populations of the Asia-Pacific region. Activities to prevent them can be expected to lead to a major reduction in the number of deaths from this cancer, particularly in Asia with its enormous population.
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Lin Y, Kikuchi S, Tamakoshi A, Kawamura T, Inaba Y, Kurosawa M, Motohashi Y, Yagyu K, Obata Y, Ishibashi T. Association of menstrual and reproductive factors with pancreatic cancer risk in women: findings of the Japan Collaborative Cohort Study for Evaluation of Cancer Risk. J Gastroenterol 2006; 41:878-83. [PMID: 17048052 DOI: 10.1007/s00535-006-1869-z] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/18/2006] [Accepted: 06/26/2006] [Indexed: 02/04/2023]
Abstract
BACKGROUND The etiology of pancreatic cancer remains largely unknown. We examined the association of pancreatic cancer deaths with menstrual and reproductive factors in a cohort study involving Japanese women. METHODS A total of 63,273 women were followed up for mortality from 1988 to 1999. Information on menstrual and reproductive factors was obtained by a questionnaire survey at baseline. Cox proportional-hazards models were used to estimate the relative risks (RRs) and 95% confidence intervals (CIs) for death from pancreatic cancer in relation to menstrual and reproductive factors. RESULTS During 631,401 person-years of follow-up, 154 women died from pancreatic cancer. Parity was not significantly associated with the risk of death from pancreatic cancer; the RR was 0.80 (95% CI, 0.31-2.11) for women with six or more births compared with women with zero or one birth. We found no significant overall association with other reproductive factors, including pregnancy, age at first birth, and menopause. The risk appeared to increase with increasing age at menarche; the RR was 1.49 (95% CI, 0.95-2.34) for women who had menarche after 16 years of age compared to those who had menarche before they were 15 years old. CONCLUSIONS Our prospective data indicate that menstrual and reproductive factors are not associated with the risk of death from pancreatic cancer among Japanese women.
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Affiliation(s)
- Yingsong Lin
- Department of Public Health, Aichi Medical University School of Medicine, 21 Karimata, Yazako, Nagakute, Aichi-gun, Aichi 480-1195, Japan
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Berrington de González A, Spencer EA, Bueno-de-Mesquita HB, Roddam A, Stolzenberg-Solomon R, Halkjaer J, Tjønneland A, Overvad K, Clavel-Chapelon F, Boutron-Ruault MC, Boeing H, Pischon T, Linseisen J, Rohrmann S, Trichopoulou A, Benetou V, Papadimitriou A, Pala V, Palli D, Panico S, Tumino R, Vineis P, Boshuizen HC, Ocke MC, Peeters PH, Lund E, Gonzalez CA, Larrañaga N, Martinez-Garcia C, Mendez M, Navarro C, Quirós JR, Tormo MJ, Hallmans G, Ye W, Bingham SA, Khaw KT, Allen N, Key TJ, Jenab M, Norat T, Ferrari P, Riboli E. Anthropometry, physical activity, and the risk of pancreatic cancer in the European prospective investigation into cancer and nutrition. Cancer Epidemiol Biomarkers Prev 2006; 15:879-85. [PMID: 16702364 DOI: 10.1158/1055-9965.epi-05-0800] [Citation(s) in RCA: 93] [Impact Index Per Article: 4.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Abstract
Tobacco smoking is the only established risk factor for pancreatic cancer. Results from several epidemiologic studies have suggested that increased body mass index and/or lack of physical activity may be associated with an increased risk of this disease. We examined the relationship between anthropometry and physical activity recorded at baseline and the risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition (n = 438,405 males and females age 19-84 years and followed for a total of 2,826,070 person-years). Relative risks (RR) were calculated using Cox proportional hazards models stratified by age, sex, and country and adjusted for smoking and self-reported diabetes and, where appropriate, height. In total, there were 324 incident cases of pancreatic cancer diagnosed in the cohort over an average of 6 years of follow-up. There was evidence that the RR of pancreatic cancer was associated with increased height [RR, 1.74; 95% confidence interval (95% CI), 1.20-2.52] for highest quartile compared with lowest quartile (P(trend) = 0.001). However, this trend was primarily due to a low risk in the lowest quartile, as when this group was excluded, the trend was no longer statistically significant (P = 0.27). A larger waist-to-hip ratio and waist circumference were both associated with an increased risk of developing the disease (RR per 0.1, 1.24; 95% CI, 1.04-1.48; P(trend) = 0.02 and RR per 10 cm, 1.13; 95% CI, 1.01-1.26; P(trend) = 0.03, respectively). There was a nonsignificant increased risk of pancreatic cancer with increasing body mass index (RR, 1.09; 95% CI, 0.95-1.24 per 5 kg/m(2)), and a nonsignificant decreased risk with total physical activity (RR, 0.82; 95% CI, 0.50-1.35 for most active versus inactive). Future studies should consider including measurements of waist and hip circumference, to further investigate the relationship between central adiposity and the risk of pancreatic cancer.
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Affiliation(s)
- Amy Berrington de González
- Cancer Epidemiology Unit, University of Oxford, Richard Doll Building, Roosevelt Drive, Oxford OX3 7LF, United Kingdom.
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Eberle CA, Bracci PM, Holly EA. Anthropometric factors and pancreatic cancer in a population-based case-control study in the San Francisco Bay area. Cancer Causes Control 2006; 16:1235-44. [PMID: 16215874 DOI: 10.1007/s10552-005-0354-y] [Citation(s) in RCA: 49] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/11/2005] [Accepted: 06/24/2005] [Indexed: 11/30/2022]
Abstract
OBJECTIVE To investigate the association between pancreatic cancer, anthropometric factors, physical activity and caloric intake. METHODS Participants in our population-based case-control study of adenocarcinoma of the exocrine pancreas (532 cases, 1701 frequency-matched controls) in the San Francisco Bay Area were accrued between 1995 and 1999 and interviewed in-person. Data were analyzed by sex in age-adjusted unconditional logistic models and main effects were considered significant for two-sided p-values < or = 0.05. RESULTS Odds ratios were elevated for body mass index (BMI) at age 25 years (4th versus 1st quartile: odds ratio (OR) = 2.0, 95% confidence interval (CI): 1.4-3.1), maximum BMI (OR = 1.8, 95% CI: 1.2-2.7) and usual adult BMI (OR = 2.1, 95% CI: 1.4-3.2) among men. Odds ratios were elevated for increased caloric intake among men (4th versus 1st quartile: OR = 2.6, 95% C: 1.7-3.8). Increased physical activity was suggestive of decreased risk in men and women although CIs included unity. Our results suggest that increased BMI and caloric intake are associated with pancreatic cancer among men. CONCLUSIONS These results are consistent with other cancer studies and support further research to determine the mechanism by which increased BMI may influence the development of pancreatic cancer.
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Affiliation(s)
- Carey A Eberle
- Department of Epidemiology and Biostatistics, University of California, 3333 California Street, Suite 280, San Francisco, CA, USA
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Teras LR, Patel AV, Rodriguez C, Thun MJ, Calle EE. Parity, other reproductive factors, and risk of pancreatic cancer mortality in a large cohort of U.S. women (United States). Cancer Causes Control 2006; 16:1035-40. [PMID: 16184468 DOI: 10.1007/s10552-005-0332-4] [Citation(s) in RCA: 43] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/25/2005] [Accepted: 04/28/2005] [Indexed: 12/25/2022]
Abstract
Several studies have found an inverse relationship between parity and risk of pancreatic cancer. However, most of the studies of pancreatic cancer in relation to parity and other reproductive factors have been small and the results inconsistent. Most recently, a well-conducted, prospective cohort study found a linear inverse association between parity and pancreatic cancer. To clarify the relationship between parity and other reproductive factors and risk of pancreatic mortality, we examined these associations among 387,981 postmenopausal U.S. women in the Cancer Prevention Study (CPS)-II cohort. CPS-II participants completed a self-administered questionnaire in 1982 and were followed for mortality through 2000. During follow-up, 1959 pancreatic cancer deaths occurred. Using Cox proportional hazards modeling, we calculated rate ratios (RR) adjusted for age, race, education, personal history of diabetes, body mass index, height, exercise, family history of pancreatic cancer, and cigarette smoking status, frequency, and duration. Overall, we did not observe a significant association between parity and pancreatic cancer mortality (trend p = 0.07). However, women who had five or more births had lower death rates from pancreatic cancer than nulliparous women (RR = 0.80, 95% CI = 0.66-0.96). We observed no association between any other reproductive factors examined (age at first birth, menarche, or menopause; type of menopause; diethylstilbestrol (DES) use; or duration of oral contraceptive or estrogen replacement therapy use) and pancreatic cancer mortality. In summary, our results support the observation that high parity is associated with lower risk of pancreatic cancer but do not show a linear trend with increasing parity. Furthermore, we find no evidence that other reproductive factors are associated with pancreatic cancer mortality.
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Affiliation(s)
- Lauren R Teras
- Department of Epidemiology and Surveillance Research, American Cancer Society, National Home Office, Atlanta, GA 30329-4251, USA.
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Pezzilli R, Morselli-Labate AM, Migliori M, Manca M, Bastagli L, Gullo L. Obesity and the risk of pancreatic cancer: an italian multicenter study. Pancreas 2005; 31:221-4. [PMID: 16163052 DOI: 10.1097/01.mpa.0000175163.42327.91] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/10/2022]
Abstract
OBJECTIVE The purpose of this work was to determine whether obesity is a risk factor for pancreatic cancer. METHODS We studied 400 patients with this tumor and 400 controls matched for sex and age from various Italian cities. We used a standardized questionnaire that was compiled at personal interview, with particular attention to body weight at the time of the interview, and for those with the tumor, their weight before onset of the disease. Body mass index (BMI) was calculated as the patient's weight in kilograms divided by their height in meters squared. RESULTS The risk of pancreatic cancer adjusted for smoking was 5-fold higher (P < 0.001) in patients with a BMI less than 23 kg/m2 after diagnosis compared with patients with a BMI ranging from 23 to 29.9 kg/m2, whereas the risk in patients with BMI of at least 30 kg/m2 was not significant (P = 0.689). Taking into account BMI before diagnosis, smoking was confirmed as a significant risk factor (odds ratio = 1.68; P = 0.001) for pancreatic cancer, whereas no significant relationship was found between BMI classes and the risk of pancreatic cancer (P = 0.984). CONCLUSIONS These findings indicate that obesity is not a risk factor for pancreatic cancer.
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Affiliation(s)
- Raffaele Pezzilli
- Department of Internal Medicine, Sant'Orsola-Malpighi Hospital, Alma Mater Studiorum, Bologna, Italy.
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Navarro Silvera SA, Miller AB, Rohan TE. Hormonal and reproductive factors and pancreatic cancer risk: a prospective cohort study. Pancreas 2005; 30:369-74. [PMID: 15841050 DOI: 10.1097/01.mpa.0000160301.59319.ba] [Citation(s) in RCA: 42] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
Abstract
OBJECTIVES We examined pancreatic cancer risk in association with hormonal and reproductive factors in a prospective cohort study of 89,835 Canadian women, aged 40-59 at recruitment, who were enrolled in the National Breast Screening Study (NBSS). METHODS Linkages to national cancer and mortality databases yielded data on cancer incidence and deaths of all causes, respectively, with follow-up ending between 1998 and 2000. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association between hormonal and reproductive factors and risk of pancreatic cancer. RESULTS During a mean of 16.4 years of follow-up, we observed 187 incident pancreatic cancer cases. Compared with women who were premenopausal at baseline, postmenopausal women were at significantly increased risk of pancreatic cancer (odds ratio = 2.44, 95% confidence interval [CI] = 1.45-4.09). Age at first livebirth, parity, age at menarche, use of oral contraceptive, and use of hormone replacement therapy (HRT) were not associated with altered pancreatic cancer risk in our study population. However, among parous women, risk increased with increasing parity. CONCLUSION Other than the increased risk among postmenopausal women, the present study provides little support for associations with hormonal factors. Additional prospective data are needed.
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Abstract
PURPOSE The aim of the study was to evaluate hormonal risk factors for carcinoma of the exocrine pancreas among postmenopausal women. METHODS Mailed questionnaire data from 52 cases and 233 population-based controls in Ontario were used to assess parity, age at first birth, and other hormonal factors on pancreatic cancer risk. RESULTS Reduced risk was seen with three or more pregnancies [adjusted odds ratio (OR) = 0.22, 95% confidence interval (CI) = 0.07-0.65] and use of oral contraceptives (adjusted OR = 0.36, 95% CI = 0.13-0.96), whereas no significant associations were found for age at menarche or menopause, or estrogen replacement therapy. Among parous women, later age at first full-term pregnancy significantly increased the risk of this cancer (adjusted OR = 4.05, 95% CI = 1.50-10.92 for ages 25-29 years, adjusted OR = 3.78, 95% CI = 1.02-14.06 for ages 30+ years). CONCLUSIONS Our data support the hypothesis that pancreatic cancer is, at least in part, an estrogen-dependent disease; there is growing epidemiological evidence that aspects of reproductive history and hormonal exposure are associated with risk of this disease.
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Affiliation(s)
- N Kreiger
- Division of Preventive Oncology, Research Unit, Cancer Care Ontario, Toronto, Ontario, Canada
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Hanley AJ, Johnson KC, Villeneuve PJ, Mao Y. Physical activity, anthropometric factors and risk of pancreatic cancer: results from the Canadian enhanced cancer surveillance system. Int J Cancer 2001; 94:140-7. [PMID: 11668489 DOI: 10.1002/ijc.1446] [Citation(s) in RCA: 81] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/12/2022]
Abstract
To explore the hypothesis that insulin resistance may be an etiologic factor in pancreatic cancer, we assessed the pancreatic cancer risk associated with anthropometric factors and physical activity, both of which are important determinants of insulin sensitivity in humans. Three hundred and twelve patients with histologically confirmed pancreatic cancer were compared to 2,919 controls in a population-based, case-control study in 7 of the 10 Canadian provinces. Participants were asked to report their exposure status for the period 2 years before interview. Men in the highest quartile of body mass index (BMI, > or =28.3 kg/m(2)) were at increased risk of pancreatic cancer [adjusted odds ratio (OR) = 1.90, 95% confidence interval (CI) 1.08-3.35]. In addition, men who reported a decrease in weight of at least 2.9% from their lifetime maximum were at reduced risk compared to those reporting a < or =2.9% loss (> or =10.2% loss, OR = 0.51, 95% CI 0.30-0.86). BMI 2 years before interview was not associated with pancreatic cancer risk among women, though those reporting a > or =12.5% decrease in weight from their lifetime maximum had substantially lower risk compared to those in the baseline quartile (OR = 0.53, 95% CI 0.29-0.99). After adjustment for age, province of residence, dietary intake and anthropometric factors, men in the highest quartile of the composite moderate and strenuous physical activity index were at reduced risk of pancreatic cancer (OR = 0.53, 95% CI 0.31-0.90). Physical activity did not appear to be associated with pancreatic cancer among women, though a tendency for reduced risk with increasing levels of strenuous activity was suggested (p for trend = 0.06). Our findings support the hypothesis that insulin resistance is an etiologic factor in the development of pancreatic neoplasms among men and possibly women.
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Affiliation(s)
- A J Hanley
- Division of Epidemiology and Biostatistics, Samuel Lunenfeld Research Institute, Mt. Sinai Hospital, 850-600 University Ave., Toronto, Ontario, M5G 1X5, Canada.
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Abstract
Smoking is the only generally accepted risk factor for pancreatic cancer. Reproductive history has in recent studies been associated with pancreatic cancer, but with contradictory results. In order to evaluate a possible association between age at first birth and the number of births and pancreatic cancer, we conducted a nested case-control study by linking 2 Swedish nationwide registries: the Cancer Registry and The Fertility Registry. Among women born between 1925 and 1970, 1,015 patients with pancreatic cancer were compared with 5,073 age-matched controls. No association between pancreatic cancer and number of births was found. Age at first birth was inversely related with the risk of pancreatic cancer (OR per 5 years = 0.90; 95% CI 0.83-0.97; p = 0.01), an association mainly confined to women with a diagnosis of pancreatic cancer before 50 years of age (OR per 5 years = 0.85; 95% CI 0.73-1.00; p = 0.04). This trend remained after adjustment for parity, but was less prominent. Young age at first birth and high parity in Sweden are, however, associated with an increased frequency of smoking, thus at least some of the increased risk for pancreatic cancer in women with young age at first birth is likely to be explained by smoking acting as a confounder.
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Affiliation(s)
- B M Karlson
- Department of Surgery, University Hospital, Uppsala, Sweden.
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Ji BT, Hatch MC, Chow WH, McLaughlin JK, Dai Q, Howe GR, Gao YT, Fraumeni JF. Anthropometric and reproductive factors and the risk of pancreatic cancer: a case-control study in Shanghai, China. Int J Cancer 1996; 66:432-7. [PMID: 8635856 DOI: 10.1002/(sici)1097-0215(19960516)66:4<432::aid-ijc4>3.0.co;2-x] [Citation(s) in RCA: 73] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/01/2023]
Abstract
To examine the possible role of body size and reproductive factors in pancreatic cancer, data were analyzed from a population-based case-control study conducted in Shanghai, China. Cases (n = 451) were permanent residents of Shanghai, 30-74 years of age, newly diagnosed with pancreatic cancer between October 1, 1990, and June 30, 1993. Deceased cases (19%) were excluded from the study. Controls (n = 1,552) were randomly selected from permanent Shanghai residents and frequency-matched to cases by gender and age. Information on body size and reproductive and other possible risk factors was collected through personal interviews. After adjustment for age, income, smoking and other confounders, a positive dose-response relation between body mass index and risk of pancreatic cancer was observed in both sexes. Among women, the risk of pancreatic cancer was significantly associated with number of pregnancies and live births. Compared with 0-2 pregnancies or live births, the odds ratio (OR) for 8 or more pregnancies was 1.90, while that for 5 or more births was 1.88. A modest elevation in risk, independent of parity, was associated with early age at first birth. Risk increased over 40% among women with a first birth at or before age 19 years relative to those at age 26 years or older. Ever use of oral contraceptives was associated with excess risk, though based on small numbers of users. Our findings suggest that, in Shanghai, obesity, gravidity, parity and perhaps use of oral contraceptives are associated with moderate increases in risk of pancreatic cancer, indicating that hormonal determinants deserve further investigation.
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Affiliation(s)
- B T Ji
- Division of Epidemiology, Columbia University, School of Public Health, New York, NY, USA
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Fernandez E, La Vecchia C, D'Avanzo B, Negri E. Menstrual and reproductive factors and pancreatic cancer risk in women. Int J Cancer 1995; 62:11-4. [PMID: 7601558 DOI: 10.1002/ijc.2910620104] [Citation(s) in RCA: 42] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/26/2023]
Abstract
To investigate possible correlates of the systematically higher pancreatic cancer rates in males than in females, the role of menstrual, reproductive and hormonal factors in females have been assessed using data from a case-control study conducted in Northern Italy. Cases were 133 women with histologically confirmed incident cancer of the pancreas, and controls were 377 women in hospital for acute, non-neoplastic, non-digestive-tract disorders. After allowance for age, education, area of residence and smoking habit, an increased risk of pancreatic cancer was observed in women with early menarche (< or = 13 years) (OR = 1.9; 95% CI: 1.0-3.6), but no significant association was observed with age at menopause or length of fertile life. Parous women were at reduced risk as compared to nulliparous women (OR = 0.7), although the trend in risk with number of births was not significant. No association with spontaneous or induced abortions was observed. Pancreatic cancer risk was inversely related to early age at first birth (first birth < 25 versus nulliparae: OR = 0.5; 95% CI: 0.3-0.9; p-value for trend < 0.01) and to age at last birth (last birth < 25 versus nulliparae: OR = 0.3; 95% CI: 0.1-0.8; p-value for trend < 0.05). Ever-users of estrogen replacement therapy showed a non-significantly increased risk (OR = 2.2). Although no clear pattern of association is evident, the present results are in agreement with previous epidemiological observations and experimental research indicating that hormonal (menstrual and reproductive) factors could explain part of the male-to-female differential in incidence and mortality from pancreatic cancer.
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Affiliation(s)
- E Fernandez
- Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy
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Kalapothaki V, Tzonou A, Hsieh CC, Toupadaki N, Karakatsani A, Trichopoulos D. Tobacco, ethanol, coffee, pancreatitis, diabetes mellitus, and cholelithiasis as risk factors for pancreatic carcinoma. Cancer Causes Control 1993; 4:375-82. [PMID: 8347787 DOI: 10.1007/bf00051341] [Citation(s) in RCA: 121] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/30/2023]
Abstract
A hospital-based case-control study of pancreatic cancer was conducted in Athens in 1991-92. One hundred and eighty-one patients operated on for cancer of the exocrine pancreas in eight teaching hospitals formed the case series, whereas hospital patient controls and hospital visitor controls formed two independent comparison series. Cases and controls were matched by hospital, gender, and age in a 1:1:1 ratio, and every matched triplet was interviewed in person by the same researcher. Results indicate that tobacco smoking increased the risk of pancreatic cancer, whereas neither coffee drinking nor consumption of alcoholic beverages were associated with the disease. Diabetes mellitus, cholelithiasis, and pancreatitis were associated positively with risk of pancreatic cancer, whereas allergic asthma was inversely (but not significantly) related to the disease. There was a suggestion that earlier age at menarche was associated with increased risk of pancreatic cancer and that parous women were at lower risk. No consistent associations were noted with respect to gastrectomy, other medical conditions or operations, birth order, height, weight, broad occupational groups, or other reproductive variables. The two comparison series were remarkably similar with respect to the whole spectrum of the study variables.
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Affiliation(s)
- V Kalapothaki
- Department of Hygiene and Epidemiology, University of Athens Medical School, Greece
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