Relative Risk Of Pancreatic Cancer Research Articles

Surveillance for Pancreatic Cancer in Chronic Pancreatitis

Pancreatic cancer can arise in the background of chronic pancreatitis (CP). The relative risks for pancreatic cancer in CP vary considerably according to other contributing factors such as disease duration, excess alcohol consumption, tobacco consumption, eating habits, physical activity, and late-onset diabetes. The incidence of pancreatic cancer is estimated to be about 10 per 105 per year, and the incidence and prevalence of CP are estimated to be 5-12 per 105 and 50 per 105 per year, respectively. The pooled relative risk estimates for pancreatic cancer in CP patients range from 2.7 to 13.3. Subsets of CP subjects with a family history of pancreatic cancer or those with newly developed diabetes over the age of 50 have a higher risk for pancreatic cancer. However, the prevalence of pancreatic cancer is not high enough to justify general screening of the adult CP population. Thus, it is necessary to select subsets of CP cohorts with a significantly high risk of pancreatic cancer. We need a better overall disease model that can define the interaction of multiple risk factors and their cumulative or potential effects on pancreatic cancer.

Risk of Pancreatic Cancer Among Individuals With Pathogenic Variants in the ATM Gene

Pathogenic germline variants in the ATM gene have been associated with pancreatic cancer risk. Although genetic testing identifies these variants in approximately 1% to 3% of unselected patients with pancreatic cancer, the lifetime risk of pancreatic cancer among individuals with pathogenic ATM variants has not been well estimated. To estimate age-specific penetrance of pancreatic cancer in individuals with a pathogenic variant in the ATM gene. This was a multicenter cohort study of pancreatic cancer family registries in the US and Canada using pedigree data from 130 pancreatic cancer kindreds with a pathogenic germline ATM variant. Data analyses were performed from January 2020 to February 2021. Observational age-specific risk of pancreatic cancer. Penetrance was estimated using modified segregation analysis. The study population of 130 families (123 [95%] White families) comprised 2227 family members (mean age [SD], 58 [22] years; 1096 [49%] women) with complete records (ie, including familial relationships, pancreatic cancer diagnosis, ATM status, proband status, and age), of which 155 individuals had positive results for an ATM pathogenic variant, 16 had a negative result, and the remainder did not have a test result. In these 130 families, 217 individuals had pancreatic cancer: 78 families had 1 such member; 34 families had 2 such members; and 18 families had 3 or more members with pancreatic cancer. The average (range) age at diagnosis was 64 (31-98) years. The cumulative risk of pancreatic cancer among individuals with a germline pathogenic ATM variant was estimated to be 1.1% (95% CI, 0.8%-1.3%) by age 50 years; 6.3% (95% CI, 3.9%-8.7%) by age 70 years; and 9.5% (95% CI, 5.0%-14.0%) by age 80 years. Overall, the relative risk of pancreatic cancer was 6.5 (95% CI, 4.5-9.5) in ATM variant carriers compared with noncarriers. This multicenter cohort study found that individuals with a germline pathogenic ATM variant were at an increased lifetime risk of pancreatic cancer. These risk estimates can help guide decision-making when evaluating the risks and benefits of enhanced early detection surveillance.

Pancreatic carcinoma underlying a complex presentation in late pregnancy: a case report

BackgroundGestational diabetes mellitus is strongly related to the risk of pancreatic cancer in pregnant women, but gestational diabetes can precede a diagnosis of pancreatic cancer by many years. Women with a history of gestational diabetes showed a relative risk of pancreatic cancer of 7.1. Pancreatic adenocarcinoma is one of the most common malignancies associated with thromboembolic events. A clinical study showed that thromboembolic events were detected in 36% of patients diagnosed as having pancreatic cancer. Studies showed that gestational diabetes mellitus could be one of the important risk factors for pancreatic cancer.Case presentationGestational diabetes mellitus is associated with increased risk of breast and pancreatic cancer. This case report describes a 29-year-old Chinese woman who presented with: gestational diabetes mellitus; International Society on Thrombosis and Haemostasis criteria suggested disseminated intravascular coagulation with a score of 5; hemolysis, elevated liver enzymes, low platelet count syndrome; and pulmonary hypertension. After an intravenous injection of fibrinogen, she gave birth to a normal baby and following delivery, her blood pressure reached 180/110 mmHg. Laboratory analysis results showed elevated lactic dehydrogenase, decreased platelets and fibrinogen, and urine protein was positive. She was transfused with fresh frozen plasma, blood coagulation factor, and fibrinogen. Subsequently, she was transferred to a maternity intensive care unit, where magnesium sulfate seizure prophylaxis was continued for 24 hours to keep her magnesium level at a low therapeutic range. However, continuous oxygen therapy was needed to maintain her oxygenation. Further laboratory investigations revealed elevated carcinoembryonic antigen, carbohydrate antigen 19-9, and carbohydrate antigen 72-4. Positron emission tomography-computed tomography showed malignant carcinoma in the head of her pancreas with lymph node involvement along with bone, peritoneal, and left adrenal metastasis, as well as double lung lymphangitic carcinomatosis.ConclusionA differential diagnosis of digestive system neoplasm should be considered when a pregnant patient presents with gestational diabetes mellitus and disseminated intravascular coagulation, where the disseminated intravascular coagulation has no specific cause and cannot be readily resolved.

Abstract 1780: Differences in pancreatic cancer incidence across five racial/ethnic populations in the Multiethnic Cohort

Abstract Background: The pancreatic cancer incidence is steadily increasing and the death-to-incidence ratio approaches one. While disparity in pancreatic cancer incidence between US blacks and whites has been observed, no study has been conducted to examine disparity in other populations. We examined racial/ethnic differences in pancreatic cancer incidence and assessed the extent to which known risk factors for pancreatic cancer account for differences in risk among African Americans, Native Hawaiians, Japanese Americans, Latinos and whites in the Multiethnic Cohort Study. Methods: During a 16.2 year follow up period, 1,415 incident pancreatic cancer cases were identified among 183,269 at risk participants. Data on risk factors were obtained from the baseline questionnaire (1993-1996). Cox regression was used to calculate the age- and sex-adjusted relative risks (RRs) and 95% confidence intervals (CIs) for pancreatic cancer associated with risk factors and race/ethnicity. Results: Current smoking status (RR<20 pack-years = 1.40; 95% CI: 1.15, 1.71; RR≥20 pack-years = 1.72; 95% CI: 1.42, 2.09, P trend<0.0001), obesity (BMI ≥30 kg/m2) (RR = 1.26; 95% CI: 1.08, 1.47), history of diabetes (RR = 1.38; 95% CI: 1.18, 1.60), family history of pancreatic cancer (RR = 1.91; 95% CI: 1.44, 2.54), and intake of red meat (RR highest vs. lowest quartile = 1.26; 95% CI: 1.08, 1.48, P trend = 0.025) were associated with increased risk of pancreatic cancer. The RRs for pancreatic cancer (vs. whites) were 1.76 (95% CI: 1.42, 2.18) for Native Hawaiians, 1.34 (95% CI: 1.13, 1.58) for African Americans, 1.28 (95% CI: 1.11, 1.48) for Japanese Americans, and 0.93 (95% CI: 0.79, 1.11) for Latinos. After further adjustment for the risk factors above, the RRs were 1.56 (95% CI: 1.26, 1.95) for Native Hawaiians, 1.20 (95% CI: 1.01, 1.43) for African Americans, 1.29 (95% CI: 1.10, 1.50) for Japanese Americans, and 0.87 (95% CI: 0.73, 1.04) for Latinos. Conclusions: In the MEC, Native Hawaiians were at the highest risk of developing pancreatic cancer, followed by African Americans, Japanese Americans, whites, and Latinos. Interethnic differences in pancreatic cancer risk do not appear to be explained by differences in the distribution of known risk factors. The greater risks in Native Hawaiians and Japanese Americans compared to whites are new important findings and elucidating the causes of these high rates may improve our understanding of the disease. Citation Format: Veronica Wendy Setiawan, Christopher A. Haiman, Daniel O. Stram, Stephen J. Pandol, Lynne R. Wilkens, Loic Le Marchand, Kristine R. Monroe. Differences in pancreatic cancer incidence across five racial/ethnic populations in the Multiethnic Cohort. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1780.

Association between autoimmune pancreatitis and malignancy.

Chronic inflammatory diseases are often associated with malignancy, and this phenomenon occurs even in the field of gastroenterology. For example, chronic pancreatitis has been reported to be highly associated with the occurrence of pancreatic cancer. However, the association between autoimmune pancreatitis (AIP) and pancreatic cancer is still an unsolved problem. As AIP is associated with immunoglobulin G4-related disease, which causes a variety of inflammatory and fibrotic lesions, the association between AIP and total malignancies is also a matter of interest. Here, we discuss the association between AIP and malignancy. As for the association between AIP and pancreatic cancer, there is no conclusive evidence, although several reports have suggested that the relative risk of pancreatic cancer is high in AIP. Concerning the association between AIP and total malignancies, there are two reports from Japan. Neither report supported the idea that chronic inflammation in AIP caused the increased risk of total malignancies. However, one report proposed the possibility that AIP might develop as a paraneoplastic syndrome in some patients because many cancers occurred within 1 year of AIP diagnosis, and thereby concluded that patients with AIP were at high risk of having various cancers. The paraneoplastic syndrome hypothesis should be tested in future studies.

Diabetes mellitus and risk of pancreatic cancer: A meta-analysis of cohort studies

BackgroundDiabetes mellitus (DM) is widely considered to be associated with risk of pancreatic cancer (PaC), however, whether DM is a cause or a consequence of PaC is still controversial. We examined this association by conducting a detailed meta-analysis of cohort studies. MethodsStudies were identified by searching Medline and Embase through November 30, 2010. Summary relative risks (RRs) with their corresponding 95% confidence intervals (CIs) were calculated using a random-effects model. ResultsA total of thirty-five cohort studies were included in this meta-analysis. DM was associated with an increased risk of PaC (the summary RRs=1.94; 95% CI, 1.66–2.27), with significant evidence of heterogeneity among these studies (p<0.001, I2=93.6%). Subgroup analyses revealed that the increased risk of PaC was independent of geographic locations, sex, study design, alcohol consumption, body mass index (BMI) and smoking status. In addition, the relative risk of PaC was correlated negatively with the duration of DM, with the highest risk of PaC found among patients diagnosed within less than 1year. There was no significant publication bias (p=0.136 for Egger’s regression asymmetry test). ConclusionsFindings from this meta-analysis strongly support that diabetes is associated with an increased risk of PaC in both males and females and that DM is both an early manifestation and an etiologic factor of pancreatic cancer.

Association between the peroxisome proliferator-activated receptor gamma Pro12Ala variant and haplotype and pancreatic cancer in a high-risk cohort of smokers: a pilot study.

The Pro12Ala variant in the peroxisome proliferator-activated receptor gamma (PPARG) gene has been associated with diabetes and several cancers. This pilot study tested for the association between Pro12Ala and pancreatic cancer risk in a high-risk sample of smokers. A nested case-control study was conducted in 83 incident cases of pancreatic cancer and 166 matched controls originally recruited into a cohort chemoprevention study of lung cancer. Associations between Pro12Ala and pancreatic cancer risk were measured using conditional logistic regression. Carriers of the G allele (Ala) of the Pro12Ala variant had a borderline increased relative risk of pancreatic cancer compared with homozygous carriers of the C allele (Pro), with an odds ratio of 1.79 (95% confidence interval [CI], 0.96-3.33; P=0.06). Among subjects randomized to high-dose vitamin A, the odds ratio was 2.80 (95% CI, 1.16-6.74; P=0.02) versus 1.20 (95% CI, 0.45-3.23; P=0.71) in the placebo group. A haplotype including Pro12Ala was also significantly associated with pancreatic cancer risk in all subjects and in subjects randomized to vitamin A. This analysis presents the first evidence that PPARG may be associated with pancreatic cancer risk, and this candidate gene should be investigated in future, larger studies.

A food pattern that is predictive of flavonol intake and risk of pancreatic cancer

Background:In the Multiethnic Cohort (MEC) study, we showed inverse associations between flavonols and pancreatic cancer risk. Objective:We aimed to define a food pattern associated with intakes of quercetin, kaempferol, and myricetin; to examine the association of that pattern with pancreatic cancer risk; and to investigate the associations in an independent study. Design:Reduced rank regression was applied to dietary data for 183 513 participants in the MEC. A food group pattern was extracted and simplified and applied to dietary data of 424 978 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Dietary intake in both studies was assessed by using specially developed questionnaires. Multivariate Cox proportional hazards models were used to estimate relative risks for pancreatic cancer in the MEC (610 cases) and the EPIC (517 cases) studies. Results:The food group pattern consisted mainly of tea, fruit, cabbage, and wine. In the MEC, inverse associations with pancreatic cancer in smokers were observed for the food group pattern [relative risk: 0.59 (95% CI: 0.31, 1.12) when extreme quintiles were compared;P for trend = 0.03]. In the EPIC study, the simplified pattern was not associated with pancreatic cancer risk (P for trend = 0.78). Conclusions:A food pattern associated with the intake of quercetin, kaempferol, and myricetin was associated with lower pancreatic cancer risk in smokers in a US-based population. However, failure to replicate the associations in an independent study weakens the conclusions and raises questions about the utility of food patterns for flavonols across populations.

Survival from cancer of the pancreas in England and Wales up to 2001.

Survival from cancer of the pancreas in England and Wales up to 2001.

Estimating the relative risk of pancreatic cancer associated with exposure agents in job title data in a hierarchical Bayesian meta-analysis

The study demonstrates the application of a hierarchical Bayesian meta-analysis of epidemiologic studies that show an association between pancreatic cancer risk and job titles, using a job-exposure matrix to estimate risks for occupational exposure agents. Altogether 261 studies published from 1969 through 1998 on pancreatic cancer and job titles were identified. When proportional studies are excluded, 77 studies were informative for 9 selected occupational agents. These studies included more than 3799 observed pancreatic cancer cases. Hierarchical Bayesian models were used for job titles (lower-level data) and agents (higher-level data), the latter from a Finnish job-exposure matrix. Non-Bayesian random effects models were applied for job titles to check consistency with the Bayesian results. The results suggest that occupational exposures to chlorinated hydrocarbon compounds may increase the risk of pancreatic cancer; the meta-relative risk (MRR) was 2.21 [95% credible interval (CrI) 1.31-3.68]. A suggestive weak excess was found for exposure to insecticides (MRR 1.95, 95% CrI 0.51-7.41). Hierarchical models are applicable in meta-analyses when studies addressing the agent(s) under study are lacking or are very few, but several studies address job titles with potential exposure to these agents. Hierarchical meta-analytic models involving durations and intensities of exposure to occupational agents from a job-exposure matrix should be developed.

Pancreatic cancer, animal protein and dietary fat in a population-based study, San Francisco Bay Area, California

The associations between animal protein or fat and risk of pancreatic cancer have been reported previously with inconsistent results. A population-based case-control study of pancreatic cancer was conducted in the San Francisco Bay Area to examine these associations. A semi-quantitative food-frequency questionnaire was administered to 532 cases and 1,701 controls between 1995 and 1999. Odds ratios (OR) and 95% confidence intervals (CI) were computed as estimates of the relative risk of pancreatic cancer. When comparing highest versus lowest levels of intake in multivariable adjusted models, positive associations were observed for several beef/lamb and individual animal protein items, including beef/lamb as a main dish (OR = 2.2, 95% CI: 1.0-4.5), regular hamburger (OR = 1.7, 95% CI: 1.2-2.4), whole eggs (OR = 1.6, 95% CI: 1.0-2.4), butter (OR = 2.4, 95% CI: 1.6-3.5), and total dairy not including butter (OR = 2.6, 95% CI: 1.8-3.7). Some high-fat/processed-meat products (i.e., sausage, salami, bacon), but not all (i.e., beef, pork, or poultry hot dogs), also were positively associated with risk. An inverse association was noted for greater chicken/turkey consumption (OR = 0.7, 95% CI: 0.5-1.0). The risk comparing the highest versus lowest quartiles for fats and cholesterol consumption were: total fat (OR = 1.6, 95% CI: 1.2-2.1); animal fat (OR = 1.9, 95% CI: 1.4-2.5); saturated fat (OR = 1.9, 95% CI: 1.4-2.6); monounsaturated fat (OR = 1.3, 95% CI: 1.0-1.8); and dietary cholesterol (OR = 1.5, 95% CI: 1.1-2.0, all p-trends < or = 0.02). These data provide some evidence that beef or lamb, eggs, dairy, fat, or cholesterol may increase the risk of pancreatic cancer.

Gestational diabetes as a risk factor for pancreatic cancer: a prospective cohort study

BackgroundDiabetes is known to be associated with cancer of the pancreas, though there is some debate as to whether it is a cause or a consequence of the disease. We investigated the incidence of pancreatic cancer in a cohort of 37926 Israeli women followed for 28–40 years for whom information on diabetes had been collected at the time they gave birth, in 1964–1976, in Jerusalem. There were 54 cases of pancreatic cancer ascertained from the Israel Cancer Registry during follow-up.MethodsWe used Cox proportional hazards models to adjust for age at baseline and explore effects of other risk factors, including ethnic groups, preeclampsia, birth order and birth weight of offspring.ResultsWe observed no cases of pancreatic cancer in the women with insulin dependent diabetes; however, there were five cases in the women with gestational diabetes. The interval between the record of diabetes in pregnancy and the diagnosis of pancreatic cancer ranged from 14–35 years. Women with a history of gestational diabetes showed a relative risk of pancreatic cancer of 7.1 (95% confidence interval, 2.8–18.0).ConclusionWe conclude that gestational diabetes is strongly related to the risk of cancer of the pancreas in women in this population, and that gestational diabetes can precede cancer diagnosis by many years.

The risk of pancreatic cancer in patients with gastric or duodenal ulcer disease

Although Helicobacter pylori (H. pylori) seropositivity is linked to an excess risk of pancreatic cancer, the biologic mechanism is unknown. Gastric ulcer is primarily associated with corpus colonization of H. pylori, atrophic gastritis and formation of N-nitrosamines. Duodenal ulcer is a marker of antral colonization, hyperacidity and uninhibited secretin release. We estimated relative risks for pancreatic cancer among patients with gastric or duodenal ulcer, based on a register-based retrospective cohort study with 88,338 patients hospitalized for gastric ulcer and 70,516 patients for duodenal ulcer recorded in the Swedish Inpatient Register between 1965 and 2003. Following operation, the 14,887 patients who underwent gastric resection and 8,205 with vagotomy were analyzed separately. Multiple record-linkages allowed complete follow-up and identification of all incident cases of pancreatic cancer until December 31, 2003. Standardized incidence ratios (SIRs) estimated relative risks. During years 3-38 of follow-up, we observed a 20% excess risk (95% confidence interval [CI] 10-40%) for pancreatic cancer among unoperated gastric ulcer patients. The excess increased to 50% (95% CI 10-110%) 15 years after first hospitalization (p for trend = 0.03). SIR was 2.1 (95% CI 1.4-3.1) 20 years after gastric resection. Unoperated duodenal ulcer was not associated with pancreatic cancer risk, nor was vagotomy. Our results lend indirect support to the nitrosamine hypothesis, but not to the hyperacidity hypothesis in the etiology of pancreatic cancer.

Vitamin D Intake and the Risk for Pancreatic Cancer in Two Cohort Studies

Vitamin D and its analogues exhibit potent antitumor effects in many tissues, including the pancreas. Normal and malignant pancreatic tissues were recently shown to express high levels of vitamin D 1-alpha-hydroxylase, which converts circulating 25-hydroxyvitamin D to active 1,25-dihydroxyvitamin D. We examined associations between dietary intake of vitamin D, calcium, and retinol and subsequent risk for pancreatic cancer. We conducted prospective studies in cohorts of 46,771 men ages 40 to 75 years as of 1986 (the Health Professionals Follow-up Study), and 75,427 women ages 38 to 65 years as of 1984 (the Nurses' Health Study), documenting incident pancreatic cancer through the year 2000. Diet was ascertained by semiquantitative food-frequency questionnaire. We identified 365 incident cases of pancreatic cancer over 16 years of follow-up. Compared with participants in the lowest category of total vitamin D intake (<150 IU/d), pooled multivariate relative risks for pancreatic cancer were 0.78 [95% confidence interval (95% CI), 0.59-1.01] for 150 to 299 IU/d, 0.57 (95% CI, 0.40-0.83) for 300 to 449 IU/d, 0.56 (95% CI, 0.36-0.87) for 450 to 599 IU/d, and 0.59 (95% CI, 0.40-0.88) for >/=600 IU/d (P(trend) = 0.01). These associations may be stronger in men than women. After adjusting for vitamin D intake, calcium and retinol intakes were not associated with pancreatic cancer risk. In two U.S. cohorts, higher intakes of vitamin D were associated with lower risks for pancreatic cancer. Our results point to a potential role for vitamin D in the pathogenesis and prevention of pancreatic cancer.

Re: “Smokeless tobacco use and risk of cancer of the pancreas and other organs” by Boffettaet al.

The study presented recently in the Journal of Cancer by Boffetta et al.1 suffers from several weaknesses that make the conclusions highly questionable. Their conclusion that “…smokeless tobacco products may be carcinogenic on the pancreas” is, somewhat surprisingly, based on the finding that users of smokeless tobacco had an increase of the relative risk of pancreatic cancer that “…was restricted to current tobacco smokers.” This calls for a careful assessment of the possible confounding of tobacco smoking, something that requires a good set of exposure data both at baseline and follow-up. Baseline data are weak by neglecting to identify the different kinds of smokeless tobaccos (skrå, Norwegian snuff, Swedish snuff) with different characteristics that were in use in Norway at that time. Even more seriously, follow-up data are totally absent. Commenting on this, Boffetta et al.1 speak about “…the decrease in the prevalence and use of snus among Norwegian men during the study period.” This is highly misleading, because the full picture shows a downward trend till 1983 only, and after that year, a substantial increase. According to the official Norwegian statistics the per capita consumption of snuff at the end of the study period, 2001, was 41% higher than that in 1983. During the study period there have also been quite substantial changes of the smoking habits of Norwegian men. The annual smoking surveys by Statistics Norway, commissioned by the Directorate for Health and Social Affairs, report that the prevalence of daily smoking among Norwegian men has decreased from above 50% in 1973 to 30% in 2001. The picture is further complicated by the probability that, in addition to the changes during the study period in smoking and snus use per se, there has been an interaction between smoking and snuff use. Many of those who have quit smoking may have done so using snus as a cessation aid, so as has been the case in Sweden. Another development during the study period is the switch from Norwegian snuff to Swedish snuff, the only one of these products that has been recognized as a low-Nitrosamine product. At the beginning of the study period the market share of Swedish snuff was small, but has thereafter been rapidly increasing to reach a dominating position.2 The total absence of analysis of all these developments during follow-up is a very serious weakness of the study. Beside their core subject area Boffetta et al.1 also discuss whether the use of products like low-Nitrosamine snuff should be encouraged as an alternative to tobacco smoking. Although their own findings confirm that snuff entails no risk for a number of cancers and less risk than smoking for pancreatic cancer, they try to deny that tobacco-attributed mortality would be lower if people were using snuff instead of smoking. The absurdity of this “conclusion” of theirs is well illustrated by the recent study by Levi et al.3 They report an international expert consensus that snuff users' excess mortality above the level of non-tobacco-users is <10% of smokers' excess mortality. This is well consistent with assessments by prestigious and authoritative bodies like the Royal College of Physicians of London, that in its Response to Commissioner Byrne's Reflection Process for a New EU Health Strategy, makes the following statement (under the headline “Encourage the use of safer sources of nicotine”): “Medicinal nicotine products are safe and should be strongly encouraged as an alternative regular source of nicotine. Some smokeless tobacco products (such as snus, which is widely used in Sweden) can also provide nicotine in a formulation that is a proven acceptable alternative to cigarettes for many smokers, and although more harmful than medicinal nicotine is much less harmful than cigarettes.” The divergent position expressed by Boffetta et al.1 further illustrates the weakness of their article. Yours sincerely, Lars RamstrÖm.

Smokeless tobacco use and risk of cancer of the pancreas and other organs

Limited data are available on the carcinogenicity of smokeless tobacco products in organs other than the mouth. Snus is a smokeless tobacco product widely used in Norway. We studied 10,136 Norwegian men enrolled since 1966 in a prospective cohort study, 31.7% of whom were exposed to snus. The relative risk of pancreatic cancer for snus use was 1.67 (95% confidence interval [CI] = 1.12, 2.50); that of oral and pharyngeal cancer was 1.10 (95% CI = 0.50, 2.41), that of esophageal cancer was 1.40 (95% CI = 0.61, 3.24), and that of stomach cancer was 1.11 (95% CI = 0.83, 1.48). The relative risks of cancers of the lung (either all histological types or adenocarcinoma), urinary bladder and kidney were not increased among snus users. The increase in the relative risk of pancreatic cancer was similar in former and current snus users and was restricted to current tobacco smokers. Our study suggests that smokeless tobacco products may be carcinogenic on the pancreas. Tobacco-specific N-nitrosamines are plausible candidates for the carcinogenicity of smokeless tobacco products in the pancreas.

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Does an aspirin a day keep pancreas cancer away?

Does an aspirin a day keep pancreas cancer away?

A prospective study of folate intake and the risk of pancreatic cancer in men and women.

Laboratory and human studies suggest that folate intake may influence the risk of some cancers. However, prospective information about the relation between folate intake and the risk of exocrine pancreatic cancer is limited. The authors examined the relation of dietary folate intake to the risk of pancreatic cancer in two large prospective US cohorts. Folate intake was assessed by food frequency questionnaire in 1984 in women and in 1986 in men. Multivariate relative risks were adjusted for age, energy intake, cigarette smoking, body mass index, diabetes, and height. During 14 years' follow-up in each cohort, 326 incident cases of pancreatic cancer were identified. Compared with participants in the lowest category of folate intake, participants in increasing 100- micro g categories of total energy-adjusted folate intake had pooled multivariate relative risks for pancreatic cancer of 1.08, 1.10, and 1.03 (95% confidence interval: 0.74, 1.43; p(trend) = 0.99). For energy-adjusted folate from food, the pooled relative risks for increasing 100- micro g categories of intake were 0.81, 0.89, and 0.66 (95% confidence interval: 0.42, 1.03; p(trend) = 0.12). There was no statistical interaction between folate intake and methionine, alcohol, fat, or caffeine. The results from these two large prospective cohorts do not support a strong association between energy-adjusted folate intake and the risk of pancreatic cancer.

Association between nonsteroidal anti-inflammatory drug use and the incidence of pancreatic cancer.

Laboratory studies indicate that nonsteroidal anti-inflammatory drugs (NSAIDs) may inhibit pancreatic cancer, but epidemiologic data to support this finding are limited. We conducted a prospective study from 1992 through 1999 among 28 283 postmenopausal women who lived in Iowa to examine the association between the self-reported use of aspirin and other NSAIDs and the incidence of pancreatic cancer. Eighty incident cases of pancreatic cancer were identified during 7 years of follow-up. The multivariate-adjusted relative risk of pancreatic cancer associated with any current use of aspirin versus no use was 0.57 (95% confidence interval = 0.36 to 0.90). There was a trend of decreasing risk of pancreatic cancer incidence with increasing frequency of aspirin use per week (P(trend) =.005). Nonaspirin NSAID use was not associated with incident pancreatic cancer. These data indicate that aspirin might be chemopreventive for pancreatic cancer.