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  • 1
    Abstract: BACKGROUND: Subjects with non-O ABO blood group alleles have increased risk of pancreatic cancer. Glycosyltransferase activity is greater for the A1 versus A2 variant, while O01 and O02 variants are nonfunctioning. We hypothesized: (1) A1 allele would confer greater risk than A2 allele, (2) protective effect of the O allele would be equivalent for O01 and O02 variants, (3) secretor phenotype would modify the association with risk. METHODS: We determined ABO variants and secretor phenotype from single nucleotide polymorphisms in ABO and FUT2 genes in 1533 cases and 1582 controls from 12 prospective cohort studies. Adjusted odds ratios (ORs) for pancreatic cancer were calculated using logistic regression. RESULTS: An increased risk was observed in participants with A1, but not A2 alleles. Compared to subjects with genotype O/O, genotypes A2/O, A2/A1, A1/O, and A1/A1 had ORs of 0.96 (95% confidence interval [CI], 0.72-1.26), 1.46 (95%CI, 0.98-2.17), 1.48 (95%CI, 1.23-1.78), and 1.71 (95%CI, 1.18-2.47). Risk was similar for O01 and O02 variant O alleles. Compared to O01/O01, the ORs for each additional allele of O02, A1, and A2 were 1.00 (95%CI, 0.87-1.14), 1.38 (95%CI, 1.20-1.58), and 0.96 (95%CI, 0.77-1.20); P-value, O01 versus O02=0.94, A1 versus A2=0.004. Secretor phenotype was not an effect modifier (P-interaction=0.63). CONCLUSIONS: Among participants in a large prospective cohort consortium, ABO allele subtypes corresponding to increased glycosyltransferase activity were associated with increased pancreatic cancer risk.Impact: These data support the hypothesis that ABO glycosyltransferase activity influences pancreatic cancer risk, rather than actions of other nearby genes on chromosome 9q34.
    Type of Publication: Journal article published
    PubMed ID: 20971884
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  • 2
    Keywords: TOBACCO SMOKING ; METAANALYSIS
    Abstract: BACKGROUND: Past investigations of cigarette smoking and multiple myeloma have been underpowered to detect moderate associations, particularly within subgroups. To clarify this association, we conducted a pooled analysis of nine case-control studies in the International Multiple Myeloma Consortium, with individual-level questionnaire data on cigarette smoking history and other covariates. METHODS: Using a pooled population of 2,670 cases and 11,913 controls, we computed odds ratios (OR) and 95% confidence intervals (CI) relating smoking to multiple myeloma risk using unconditional logistic regression adjusting for gender, age group, race, education, body mass index, alcohol consumption, and study center. RESULTS: Neither ever smokers (OR, 0.95; 95% CI, 0.87-1.05), current smokers (OR, 0.82; 95% CI, 0.73-0.93), nor former smokers (OR, 1.03; 95% CI, 0.92-1.14) had increased risks of multiple myeloma compared with never smokers. Analyses of smoking frequency, pack-years, and duration did not reveal significant or consistent patterns, and there was no significant effect modification by subgroups. CONCLUSION: Findings from this large pooled analysis do not support the hypothesis of cigarette smoking as a causal factor for multiple myeloma. IMPACT: Cigarette smoking is one of the most important risk factors for cancer, but the association with multiple myeloma was inconclusive. This study had excellent power to detect modest associations, and had individual-level data to evaluate confounding and effect modification by potentially important factors that were not evaluated in previous studies. Our findings confirm that smoking is not a risk factor for multiple myeloma. Cancer Epidemiol Biomarkers Prev; 24(3); 631-4. (c)2014 AACR.
    Type of Publication: Journal article published
    PubMed ID: 25538226
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  • 3
    Keywords: CANCER ; BLOOD ; MODEL ; SYSTEM ; COHORT ; DISEASE ; incidence ; POPULATION ; RISK ; GENE ; ASSOCIATION ; VARIANTS ; PROSPECTIVE COHORT ; smoking ; GENOTYPES ; SMOKERS ; pancreatic cancer ; ONCOLOGY ; REGRESSION ; ASSOCIATIONS ; PANCREATIC-CANCER ; ALLELES ; GENOTYPE ; LOCUS ; prospective ; CANCER-RISK ; GENETIC-BASIS ; GENOME-WIDE ASSOCIATION ; BOSTON ; Type ; COHORTS ; STRATIFICATION ; GROUP ANTIGENS
    Abstract: A recent genome-wide association study (PanScan) identified significant associations at the ABO gene locus with risk of pancreatic cancer, but the influence of specific ABO genotypes remains unknown. We determined ABO genotypes (OO, AO, AA, AB, BO, and BB) in 1,534 cases and 1,583 controls from 12 prospective cohorts in PanScan, grouping participants by genotype-derived serologic blood type (O, A, AB, and B). Adjusted odds ratios (ORs) for pancreatic cancer by ABO alleles were calculated using logistic regression. Compared with blood type O, the ORs for pancreatic cancer in subjects with types A, AB, and B were 1.38 [95% confidence interval (95% CI), 1.18-1.62], 1.47 (95% CI, 1.07-2.02), and 1.53 (95% CI, 1.21-1.92), respectively. The incidence rates for blood types O, A, AB, and B were 28.9, 39.9, 41.8, and 44.5 cases per 100,000 subjects per year. An increase in risk was noted with the addition of each non-O allele. Compared with OO genotype, subjects with AO and AA genotype had ORs of 1.33 (95% CI, 1.13-1.58) and 1.61 (95% CI, 1.22-2.18), whereas subjects with BO and BB genotypes had ORs of 1.45 (95% CI, 1.14-1.85) and 2.42 (1.28-4.57). The population attributable fraction for non-O blood type was 19.5%. In a joint model with smoking, current smokers with non-O blood type had an adjusted OR of 2.68 (95% CI, 2.03-3.54) compared with nonsmokers of blood type O. We concluded that ABO genotypes were significantly associated with pancreatic cancer risk. Cancer Res; 70(3); 1015-23. (C)2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20103627
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  • 4
    Abstract: A family history of pancreatic cancer has consistently been associated with increased risk of pancreatic cancer. However, uncertainty remains about the strength of this association. Results from previous studies suggest a family history of select cancers (i.e., ovarian, breast and colorectal) could also be associated, although not as strongly, with increased risk of pancreatic cancer. We examined the association between a family history of 5 types of cancer (pancreas, prostate, ovarian, breast and colorectal) and risk of pancreatic cancer using data from a collaborative nested case-control study conducted by the Pancreatic Cancer Cohort Consortium. Cases and controls were from cohort studies from the United States, Europe and China, and a case-control study from the Mayo Clinic. Analyses of family history of pancreatic cancer included 1,183 cases and 1,205 controls. A family history of pancreatic cancer in a parent, sibling or child was associated with increased risk of pancreatic cancer [multivariate-adjusted odds ratios (ORs) = 1.76, 95% confidence interval (Cl) = 1.19-2.61]. A family history of prostate cancer was also associated with increased risk (OR = 1.45, 95% Cl = 1.12-1.89). There were no statistically significant associations with a family history of ovarian cancer (OR = 0.82, 95% Cl = 0.52-1.31), breast cancer (OR = 1.21, 95% Cl = 0.97-1.51) or colorectal cancer (OR = 1.17, 95% Cl = 0.93-1.47). Our results confirm a moderate sized association between a family history of pancreatic cancer and risk of pancreatic cancer and also provide evidence for an association with a family history of prostate cancer worth further study
    Type of Publication: Journal article published
    PubMed ID: 20049842
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  • 5
    Keywords: CANCER ; COHORT ; RISK ; ASSOCIATION ; SUSCEPTIBILITY ; HEALTH ; DESIGN ; WOMEN ; MEN ; cancer risk ; NETHERLANDS ; UNITED-STATES ; TOBACCO ; ALCOHOL ; ALCOHOL-CONSUMPTION ; CONSUMPTION ; pancreatic cancer ; NESTED CASE-CONTROL ; LIFE-STYLE FACTORS ; ONCOLOGY ; case-control study ; REGRESSION ; ASSOCIATIONS ; PANCREATIC-CANCER ; pooled analysis ; CANCER-RISK ; BASE-LINE CHARACTERISTICS ; nested case-control study ; GENOME-WIDE ASSOCIATION ; WOMENS HEALTH ; COFFEE CONSUMPTION ; Type ; nested case control study
    Abstract: The literature has consistently reported no association between low to moderate alcohol consumption and pancreatic cancer; however, a few studies have shown that high levels of intake may increase risk. Most single studies have limited power to detect associations even in the highest alcohol intake categories or to examine associations by alcohol type. We analyzed these associations using 1,530 pancreatic cancer cases and 1,530 controls from the Pancreatic Cancer Cohort Consortium (PanScan) nested case-control study. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using unconditional logistic regression, adjusting for potential confounders. We observed no significant overall association between total alcohol (ethanol) intake and pancreatic cancer risk (OR = 1.38, 95% CI = 0.86-2.23, for 60 or more g/day vs. 〉 0 to 〈 5 g/day). A statistically significant increase in risk was observed among men consuming 45 or more grams of alcohol from liquor per day (OR = 2.23, 95% CI = 1.02-4.87, compared to 0 g/day of alcohol from liquor, P-trend = 0.12), but not among women (OR = 1.35, 95% CI = 0.63-2.87, for 30 or more g/day of alcohol from liquor, compared to none). No associations were noted for wine or beer intake. Overall, no significant increase in risk was observed, but a small effect among heavy drinkers cannot be ruled out
    Type of Publication: Journal article published
    PubMed ID: 20373013
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  • 6
    Keywords: CANCER ; MODEL ; LUNG-CANCER ; COHORT ; EXPOSURE ; RISK ; RISK-FACTORS ; CARCINOGENESIS ; ASSOCIATION ; TRIAL ; prevention ; PATTERNS ; HEALTH ; CIGARETTE-SMOKING ; MEN ; smoking ; RISK FACTOR ; case-control studies ; pancreatic cancer ; NESTED CASE-CONTROL ; case-control study ; REGRESSION ; pancreas ; PANCREATIC-CANCER ; intensity ; METAANALYSIS ; pooled analysis ; USA ; smoking cessation ; RISK-FACTOR ; pancreatic neoplasms ; LOGISTIC-REGRESSION ; CONSORTIUM ; CONFIDENCE ; MODELING TOTAL EXPOSURE ; SHANGHAI ; tobacco use cessation
    Abstract: Smoking is an established risk factor for pancreatic cancer; however, detailed examination of the association of smoking intensity, smoking duration, and cumulative smoking dose with pancreatic cancer is limited. The authors analyzed pooled data from the international Pancreatic Cancer Cohort Consortium nested case-control study (1,481 cases, 1,539 controls). Odds ratios and 95% confidence intervals were calculated by using unconditional logistic regression. Smoking intensity effects were examined with an excess odds ratio model that was linear in pack-years and exponential in cigarettes smoked per day and its square. When compared with never smokers, current smokers had a significantly elevated risk (odds ratio (OR) = 1.77, 95% confidence interval (CI): 1.38, 2.26). Risk increased significantly with greater intensity (〉= 30 cigarettes/day: OR = 1.75, 95% CI: 1.27, 2.42), duration (〉= 50 years: OR = 2.13, 95% CI: 1.25, 3.62), and cumulative smoking dose (〉= 40 pack-years: OR = 1.78, 95% CI: 1.35, 2.34). Risk more than 15 years after smoking cessation was similar to that for never smokers. Estimates of excess odds ratio per pack-year declined with increasing intensity, suggesting greater risk for total exposure delivered at lower intensity for longer duration than for higher intensity for shorter duration. This finding and the decline in risk after smoking cessation suggest that smoking has a late-stage effect on pancreatic carcinogenesis
    Type of Publication: Journal article published
    PubMed ID: 19561064
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  • 7
    Keywords: RISK ; MICE ; SUSCEPTIBILITY ; chemotherapy ; GEMCITABINE ; DUCTAL ADENOCARCINOMA ; GENE POLYMORPHISMS ; LUNG-CANCER PATIENTS ; MYOTUBULARIN-RELATED PROTEIN-2 ; SBF2
    Abstract: Background and objective Survival of patients with pancreatic adenocarcinoma is limited and few prognostic factors are known. We conducted a two-stage genome-wide association study (GWAS) to identify germline variants associated with survival in patients with pancreatic adenocarcinoma. Methods We analysed overall survival in relation to single nucleotide polymorphisms (SNPs) among 1005 patients from two large GWAS datasets, PanScan I and ChinaPC. Cox proportional hazards regression was used in an additive genetic model with adjustment for age, sex, clinical stage and the top four principal components of population stratification. The first stage included 642 cases of European ancestry (PanScan), from which the top SNPs (p10(-5)) were advanced to a joint analysis with 363 additional patients from China (ChinaPC). Results In the first stage of cases of European descent, the top-ranked loci were at chromosomes 11p15.4, 18p11.21 and 1p36.13, tagged by rs12362504 (p=1.63x10(-7)), rs981621 (p=1.65x10(-7)) and rs16861827 (p=3.75x10(-7)), respectively. 131 SNPs with p10(-5) were advanced to a joint analysis with cases from the ChinaPC study. In the joint analysis, the top-ranked SNP was rs10500715 (minor allele frequency, 0.37; p=1.72x10(-7)) on chromosome 11p15.4, which is intronic to the SET binding factor 2 (SBF2) gene. The HR (95% CI) for death was 0.74 (0.66 to 0.84) in PanScan I, 0.79 (0.65 to 0.97) in ChinaPC and 0.76 (0.68 to 0.84) in the joint analysis. Conclusions Germline genetic variation in the SBF2 locus was associated with overall survival in patients with pancreatic adenocarcinoma of European and Asian ancestry. This association should be investigated in additional large patient cohorts.
    Type of Publication: Journal article published
    PubMed ID: 23180869
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  • 8
    Keywords: CELLS ; neoplasms ; COHORT ; CIGARETTE-SMOKING ; DIET ; TOBACCO ; DRINKING ; NON-HODGKIN-LYMPHOMA ; CONNECTICUT WOMEN ; BEVERAGES
    Abstract: BACKGROUND: Recent findings suggest that alcohol consumption may reduce risk of multiple myeloma. METHODS: To better understand this relationship, we conducted an analysis of six case-control studies participating in the International Multiple Myeloma Consortium (1,567 cases, 7,296 controls). Summary ORs and 95% confidence intervals (CI) relating different measures of alcohol consumption and multiple myeloma risk were computed by unconditional logistic regression with adjustment for age, race, and study center. RESULTS: Cases were significantly less likely than controls to report ever drinking alcohol (men: OR = 0.72; 95% CI, 0.59-0.89; women: OR = 0.81; 95% CI, 0.68-0.95). The inverse association with multiple myeloma was stronger when comparing current to never drinkers (men: OR = 0.57; 95% CI, 0.45-0.72; women: OR = 0.55; 95% CI, 0.45-0.68), but null among former drinkers. We did not observe an exposure-response relationship with increasing alcohol frequency, duration, or cumulative lifetime consumption. Additional adjustment for body mass index, education, or smoking did not affect our results; and the patterns of association were similar for each type of alcohol beverage examined. CONCLUSIONS: Our study is, to our knowledge, the largest of its kind to date, and our findings suggest that alcohol consumption may be associated with reduced risk of multiple myeloma. IMPACT: Prospective studies, especially those conducted as pooled analyses with large sample sizes, are needed to confirm our findings and further explore whether alcohol consumption provides true biologic protection against this rare, highly fatal malignancy. Cancer Epidemiol Biomarkers Prev; 22(9); 1620-7. (c)2013 AACR.
    Type of Publication: Journal article published
    PubMed ID: 23964064
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  • 9
    Keywords: SUSCEPTIBILITY ; MUTATIONS ; GENETIC EPIDEMIOLOGY ; METAANALYSIS ; FAMILY-HISTORY ; HEREDITARY PANCREATITIS ; GENOME-WIDE ASSOCIATION ; POOLED-ANALYSIS ; COHORT-CONSORTIUM PANSCAN ; ABO BLOOD-GROUP
    Abstract: PURPOSE: We developed an absolute risk model to identify individuals in the general population at elevated risk of pancreatic cancer. PATIENTS AND METHODS: Using data on 3,349 cases and 3,654 controls from the PanScan Consortium, we developed a relative risk model for men and women of European ancestry based on non-genetic and genetic risk factors for pancreatic cancer. We estimated absolute risks based on these relative risks and population incidence rates. RESULTS: Our risk model included current smoking (multivariable adjusted odds ratio (OR) and 95% confidence interval: 2.20 [1.84-2.62]), heavy alcohol use (〉3 drinks/day) (OR: 1.45 [1.19-1.76]), obesity (body mass index 〉30 kg/m(2)) (OR: 1.26 [1.09-1.45]), diabetes 〉3 years (nested case-control OR: 1.57 [1.13-2.18], case-control OR: 1.80 [1.40-2.32]), family history of pancreatic cancer (OR: 1.60 [1.20-2.12]), non-O ABO genotype (AO vs. OO genotype) (OR: 1.23 [1.10-1.37]) to (BB vs. OO genotype) (OR 1.58 [0.97-2.59]), rs3790844(chr1q32.1) (OR: 1.29 [1.19-1.40]), rs401681(5p15.33) (OR: 1.18 [1.10-1.26]) and rs9543325(13q22.1) (OR: 1.27 [1.18-1.36]). The areas under the ROC curve for risk models including only non-genetic factors, only genetic factors, and both non-genetic and genetic factors were 58%, 57% and 61%, respectively. We estimate that fewer than 3/1,000 U.S. non-Hispanic whites have more than a 5% predicted lifetime absolute risk. CONCLUSION: Although absolute risk modeling using established risk factors may help to identify a group of individuals at higher than average risk of pancreatic cancer, the immediate clinical utility of our model is limited. However, a risk model can increase awareness of the various risk factors for pancreatic cancer, including modifiable behaviors.
    Type of Publication: Journal article published
    PubMed ID: 24058443
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