Pancreatic Cancer: Associations of Inflammatory Potential of Diet, Cigarette Smoking, and Long-Standing Diabetes

Abstract

Purpose: Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used in the general population, and regular NSAID use is associated with improved survival among colorectal cancer (CRC) patients. We examined the association of NSAID use prior to, and after, diagnosis in relation to CRC-specific and overall survival. Methods: Study subjects were incident, invasive CRC cases from the population-based Seattle Colon Cancer Family Registry. Eligible cases were 20-74 years of age, diagnosed from 1997 to 2008, and identified from the Puget Sound Surveillance, Epidemiology and End Results (SEER) Registry. NSAID use two years prior to the interview date ("pre-diagnosis period") was collected by telephone interview at study enrollment an average of eight months after diagnosis. A follow-up questionnaire was administered approximately five years after the cases' CRC diagnosis ("post-diagnosis period"). Regular NSAID use was defined as having taken aspirin or ibuprofen at least twice per week for more than a month. Follow-up for survival and cause of death was completed through linkage to the National Death Index. Cox proportional hazard regression was used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for associations of pre-and post-diagnostic NSAID use, and initiation, continuation and discontinuation of NSAIDs between pre-and post-diagnostic periods with survival after CRC diagnosis. Results: Compared to never users, regular NSAID use after diagnosis was associated with better overall survival (HR ¼ 0.69, 95% CI, 0.54-0.89) and CRC-specific survival (HR ¼ 0.48, 95% CI, 0.29-0.80). Among people who survived five years after diagnosis, both overall and CRC-specific survival were better for patients who initiated NSAID use postdiagnosis compared to never users, with HRs (95% CI) of 0.70 (0.51-0.95) and 0.43 (0.23-0.82), respectively. HR estimates were stronger for CRC-specific survival among those with non-advanced (local and regional) CRC (HR ¼ 0.38, 95% CI, 0.18-0.77). Conclusion: Our results suggest that among longterm CRC survivors, regular use of NSAID after CRC diagnosis, including when initiated after diagnosis, is significantly associated with longer CRC-specific survival. This association is more pronounced for patients with non-advanced CRC. Studies of dietary patterns and cancer outcomes also suggest that diet might influence an individual's risk of PanC through modulation of inflammation. We, therefore, examined independent and joint associations between inflammatory potential of diet, cigarette smoking and long-standing type II diabetes (greater than 5 years) in relation to risk of PanC. Methods: Data were from a clinic-based, case-control study of rapidly ascertained patients with incident adenocarcinoma of the exocrine pancreas (n ¼ 819) evaluated at Mayo Clinic and non-cancer control patients (n ¼ 1,769) recruited from Mayo Clinic primary care facilities. Controls were frequency-matched to cases on age, race, and sex. Inflammatory potential of diet was measured using the dietary inflamm...

Risk of pancreatic cancer in Minia district, Egypt

“…[7][8][9][10][11] Our results are broadly consistent with the published literature, although our estimate for current smoking of 3.4 versus non-smoker is similar to that of a recent study, it is somewhat higher than those previously reported, which range from approximately 1.7 to 2.2. 7,9,10 It is possible that control selection bias contributed to this apparently higher risk.…”

“…Consistent with previous studies, we found that long-term diabetes (≥5 years) was associated with increased risk of pancreatic cancer compared to nondiabetics. 8,12 While short-term diabetes (1-4 years) was associated with nonsignificant higher risk. Unlike other studies that found that patients with short-term (1-4 years) diabetes had a higher pancreatic cancer risk than non-diabetics.…”

Pancreatic cancer risk is modulated by inflammatory potential of diet and ABO genotype: a consortia-based evaluation and replication study

“…Together, the findings suggest that a pro-inflammatory dietary pattern and genotype-derived non-O blood type are each individually associated with increased PC risk, and that the two exposures do not interact to influence PC risk. Two previous case-control studies conducted at Mayo Clinic (14) and in Italy (15) by our collaborators found that a higher E-DII score was associated with a 2.5-fold increased odds of PC risk. In this study, we replicated those findings in a large, multicenter retrospective case-control sample that included the two prior studies, followed by replication with prospectively collected dietary data from PanScan.…”

“…Diet was assessed in each study with validated food frequency questionnaires (FFQ) (14,16,(24)(25)(26)(27)32,(34)(35)(36) or diet history questionnaires (DHQ) (33). All of the dietary instruments used in the participating studies were designed to measure usual dietary habits; however, the periods of diet assessment differed among studies, particularly among the PanC4 studies (Supplementary Tables 5 and 6, available at Carcinogenesis Online).…”

“…The inflammatory potential of a person's diet is determined by summing inflammatory index scores across the dietary components. Based on the DII, two previous studies reported increased PC risk for individuals with greater dietary inflammatory potential (14,15); however, questions remain as to the validity and consistency of the association, and applicability of the findings to populations from different geographic regions and population subgroups with varying environmental and genetic risks for PC.…”