Association between family cancer history and risk of pancreatic cancer.

PURPOSE: Family history of pancreatic adenocarcinoma is an established risk factor for the disease. However, associations of pancreatic cancer with other familial cancers are less clear. We analyzed data from the Queensland Pancreatic Cancer Study (QPCS), an Australian population-based case-control study, to investigate associations between family history of various cancer types and risk of pancreatic cancer. MATERIALS AND METHODS: Our study included 591 pancreatic cancer patients and 646 controls, all of whom self-reported the histories of cancer in their first-degree relatives. We used logistic regression to estimate adjusted odds ratios (ORs) and their 95% confidence intervals (CIs). Based on our results, we conducted a systematic literature review using the Medline (OVID) database to identify articles pertaining to the association between family history of melanoma and risk of pancreatic cancer. A meta-analysis including associations in five published studies, unpublished results from a study co-author and the QPCS results was then performed using the DerSimonian and Laird random-effects model. RESULTS: Cases were more likely than controls to report a family history of pancreatic cancer (OR 2.20, 95% CI 1.16-4.19) and melanoma (OR 1.74, 95% CI 1.03-2.95), but not of breast, ovarian, respiratory, other gastrointestinal or prostate cancer. Meta-analysis of melanoma family history and pancreatic cancer risk yielded an OR of 1.22 (95% CI 1.00-1.51). CONCLUSIONS: Our results yield further evidence of increased risk of pancreatic cancer in those with family histories of the disease. We also provide suggestive evidence of an association between family history of melanoma and risk of pancreatic cancer.

Association between Helicobacter pylori and pancreatic cancer risk: a meta-analysis.

PURPOSE: Gastric colonization with Helicobacter pylori (H. pylori) has been implicated in the pathogenesis of pancreatic cancer, but results of epidemiological studies have been inconclusive. We analyzed data from the Queensland Pancreatic Cancer Study, an Australian population-based case-control study, and incorporated our findings into an updated meta-analysis. METHODS: Blood samples were obtained from 580 patients and 626 controls, and enzyme-linked immunosorbent assay kits were used to determine seropositivity to H. pylori and its virulence protein, cytotoxin-associated gene A (CagA). Odds ratios (ORs) and 95 % confidence intervals (CIs) were calculated using logistic regression. Results were incorporated into a meta-analysis along with results of studies identified through systematic literature review. Adjusted ORs and 95 % CIs were calculated using the DerSimonian and Laird random-effects model. RESULTS: No overall association was observed between H. pylori seropositivity and risk of pancreatic cancer (OR 1.00; 95 % CI 0.74-1.35). Nonsignificantly decreased pancreatic cancer risk was observed with CagA seropositivity (OR 0.74; 95 % CI 0.48-1.15) and increased risk with CagA-negative H. pylori seropositivity (OR 1.23; 95 % CI 0.83-1.82). Ten studies were included in the meta-analysis. There was no significant overall association between H. pylori seropositivity and pancreatic cancer risk (OR 1.13; 95 % CI 0.86-1.50), but evidence of CagA strain-specific associations (OR 0.78; 95 % CI 0.67-0.91 and OR 1.30; 95 % CI 1.02-1.65 for CagA-positive and CagA-negative strains, respectively). CONCLUSIONS: Our results provide further evidence for the existence of strain-specific associations between H. pylori and pancreatic cancer.

Occupational exposure to N-nitrosamines and pesticides and risk of pancreatic cancer.

OBJECTIVES: Animal evidence shows that N-nitrosamines and similar xenobiotic compounds are pancreatic carcinogens. We aimed to determine whether occupational exposure to N-nitrosamines or to pesticides increases risk of pancreatic cancer development. METHODS: Participants (504 cases, 643 controls) in a population-based case-control study (The Queensland Pancreatic Cancer Study) provided data on demographic, medical and lifestyle factors and lifetime job histories. Specific questions were asked regarding work in rubber and leather industries, metalworking jobs and occupational or direct use of pesticides on animals or crops. An occupational hygienist reviewed this information (blind to case status) to assess likelihood of exposure to N-nitrosamines and pesticides, and estimated level and frequency of such exposures. RESULTS: No associations were found for risk of pancreatic cancer and occupational exposure to N-nitrosamines (OR=0.85, 95% CI 0.51 to 1.42) and no associations were seen with level or frequency of exposure. No associations were observed for ever exposure to pesticides in general (OR=0.90, 95% CI 0.61 to 1.33) or to any of the pesticide subgroups. Stratification by history of cigarette smoking did not change these results. CONCLUSIONS: This comprehensive analysis of a large case-control study does not support an association between occupational exposure to N-nitrosamines or pesticide use and risk of pancreatic cancer.

Cigarette smoking and pancreatic cancer risk: more to the story than just pack-years.

PURPOSE: Cigarette smoking is an established risk factor for pancreatic adenocarcinoma. However, few studies have thoroughly investigated the effects of independent smoking dimensions (duration, intensity, cumulative dose and time since quitting) on risk estimates. We analysed data from the Queensland Pancreatic Cancer Study (QPCS), an Australian population-based case-control study, with the aim of determining which smoking component is primarily important to pancreatic cancer risk. METHODS: Our study included 705 pancreatic cancer patients and 711 controls. Logistic regression and generalised additive logistic regression (for non-linear dose effects) were used to determine odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: Compared to never-smokers, current smokers had an increased risk of pancreatic cancer (OR=3.4; 95% CI 2.4-5.0) after adjustment for age, sex, education, alcohol intake and birth country. Of the various smoking dimensions, smoking duration and time since quitting had a greater effect on OR estimates (OR 1.3; 95% CI 1.1-1.4 and OR 0.8; 95% CI 0.7-0.8) than smoking intensity (OR 1.1; 95% CI 0.9-1.2), once ever-smoking was accounted for. CONCLUSIONS: This study confirms the association between cigarette smoking and pancreatic adenocarcinoma, and provides evidence to suggest that smoking pattern, in addition to dose effect, may affect disease risk.

Association between ultraviolet radiation, skin sun sensitivity and risk of pancreatic cancer.

BACKGROUND: Ecological studies showing an inverse association between pancreatic cancer incidence and mortality and levels of ultraviolet radiation (UVR), suggest that higher levels of sun exposure may reduce risks of pancreatic cancer but there has been only one individual-level study that examined this issue. We aimed to examine the association between pancreatic cancer and markers of exposure to solar UVR, namely skin type, treatment of skin lesions, ambient UVR and time outdoors on work days. METHODS: We used data from an Australian case-control study. Location at birth, residential location during adulthood, outdoors work, history of skin lesion treatment and sensitivity of the skin to the sun were obtained by questionnaire. We limited the analyses to Caucasians who answered the questionnaire about UVR (controls=589/711 recruited; cases=496/705 recruited). We used NASA's Total Ozone Mapping Spectrometer to estimate ambient UVR. RESULTS: Being born in or living in areas of higher ambient UVR (compared to lower ambient UVR) was associated with about 30-40% lower risk of pancreatic cancer. People with fair skin colour had 47% lower risk of pancreatic cancer than those with dark skin colour (95% CI 0.37-0.75). There was some suggestion of increased risk with increased average number of hours spent outside at work. CONCLUSIONS: This study suggests that people with light skin colour or those born or living in areas of high ambient UVR have lower risk of pancreatic cancer. Our analysis supports an association between UVR and pancreatic cancer, possibly mediated through production of vitamin D.