Scientific Highlights

ALL-CAUSE MORTALITY

Adiposity and Physical Activity

The authors evaluated whether physical activity protects against the adverse effects of high adiposity (assessed by body mass index [BMI] and waist circumference) on all-cause mortality using data on 185,412 men and women in the NIH-AARP Diet and Health Study. During follow-up between 1996 and 2006, overweight (BMI 25 to < 30), obesity (BMI ≥ 30), a large waist circumference (men: ≥ 102 cm; women: ≥ 88 cm), and low physical activity were each independent predictors of mortality. Compared with persons of normal weight (BMI 18.5 to < 25) who were physically active (more than seven hours per week of moderate physical activity), mortality risk ratios were 1.62 for inactive normal-weight persons, 1.79 for active morbidly obese (BMI ≥ 35) persons, and 3.45 for inactive morbidly obese persons. Similar results were found for the combined relation of BMI and vigorous physical activity. Inactive persons with a large waist circumference had two times greater mortality risk than active persons with a normal waist circumference. High physical activity attenuated but did not eliminate the increased mortality risk associated with obesity. (Koster A, Harris TB, Moore SC, Schatzkin A, Hollenbeck AR, van Eijk JT, Leitzmann MF. Joint associations of adiposity and physical activity with mortality: The National Institutes of Health-AARP Diet and Health Study. Am J Epidemiol 2009;169:1344–1351)

 

BRAIN CANCER

Lead Exposure and Oxidative Stress Genes

In a hospital-based case-control study, the authors examined modification of the association between occupational lead exposure and brain tumors by single-nucleotide polymorphisms (SNPs) in genes related to oxidative stress. The study included 362 patients with glioma (of which 176 were glioblastoma multiforme [GBM]), 134 patients with meningioma, and 494 controls. When the analyses were restricted to cases with GBM, RAC2 rs2239774 and two highly correlated GPX1 polymorphisms (rs1050450 and rs18006688) were found to significantly modify the association with lead exposure after adjusting for multiple comparisons. The same GPX1 polymorphisms and XDH rs7574920 were found to significantly modify the association between cumulative lead exposure and meningioma. Results suggest that lead may cause GBM and meningioma through mechanisms related to oxidative damage. (Bhatti P, Stewart PA, Hutchinson A, Rothman N, Linet MS, Inskip PD, Rajaraman P. Lead exposure, polymorphisms in genes related to oxidative stress, and risk of adult brain tumors. Cancer Epidemiol Biomarkers Prev 2009;18:1841–1848)

 

BREAST CANCER

Adding SNPs to a Risk Model

Adding genotypes from seven SNPs that had previously been associated with breast cancer to NCI's Breast Cancer Risk Assessment Tool (BCRAT) increases the area under the receiver operating characteristic curve, a measure of discriminatory accuracy, from 0.607 to 0.632. Criteria based on four clinical or public health applications were used to compare BCRAT with BCRATplus7, a version of the BCRAT tool that includes the seven genotypes. Criteria included number of expected life-threatening events for the decision to take tamoxifen, expected decision losses (in units of the loss from giving a mammogram to a woman without detectable breast cancer) for the decision to have a mammogram, number of lives saved by risk-based allocation of screening mammography, and rates of risk reclassification. Improvements in expected numbers of life-threatening events were 0.07% and 0.81% for deciding whether to take tamoxifen to prevent breast cancer for women aged 50–59 and 40–49 years, respectively. For deciding whether to recommend screening mammograms to women aged 50–54 years, the reduction in expected losses was 0.86% if the ideal breast cancer prevalence threshold for recommending mammography was that of women aged 50–54 years. Improvements from BCRATplus7 were also small for risk-based allocation of mammograms under cost constraints. Cross-classification of risks indicated that some women classified by BCRAT would have different classifications with BCRATplus7, which might be useful if BCRATplus7 was well calibrated. However, models with SNPs, such as BCRATplus7, have not been validated for calibration in independent cohort data. The gains from BCRATplus7 were small in the applications examined. (Gail MH. Value of adding single-nucleotide polymorphism genotypes to a breast cancer risk model. J Natl Cancer Inst 2009;101:959–963)

Alcohol and Breast Cancer Risk

The authors studied 184,418 postmenopausal women aged 50–71 years in the NIH-AARP Diet and Health Study to investigate the association between alcohol and breast cancer by different tumor characteristics. Alcohol use, diet, and potential risk factors for cancer were assessed with a mailed questionnaire at baseline. Breast cancer cases and estrogen and progesterone receptor status were identified through links to state cancer registries. During an average of seven years of follow-up, 5,461 breast cancer cases were identified. Alcohol was positively associated with total breast cancer: even a moderate amount of alcohol (> 10 g/day) increased breast cancer risk. In a comparison of > 35 g vs. 0 g/day, the multivariate relative risks (RRs) were 1.35 for total breast cancer, 1.46 for ductal tumors, and 1.52 (95% confidence interval [CI] = 0.95–2.44) for lobular tumors. Compared to 0 g/day, the multivariate RRs for estrogen receptor–positive/progesterone receptor–positive, estrogen receptor–positive/progesterone receptor–negative, and estrogen receptor–negative/progesterone receptor–negative tumors were 1.46 for > 35 g, 1.13 (CI = 0.73–1.77) for > 20 g, and 1.21 (CI = 0.79–1.84) for > 20 g, respectively. Moderate consumption of alcohol was associated with breast cancer, specifically hormone receptor-positive tumors. (Lew JQ, Freedman ND, Leitzmann MF, Brinton LA, Hoover RN, Hollenbeck AR, Schatzkin A, and Park Y. Alcohol and risk of breast cancer by histologic type and hormone receptor status in postmenopausal women. Am J Epidemiol 2009;170:308–317)

Racial Disparity in Breast Cancer Mortality

Breast cancer mortality rates among black women became higher than those among white women during the late 1980s, and the gap has continued to widen. To further explore the underlying causes of this racial disparity, black-to-white rate ratios (RR_BW) for mortality, incidence, hazard of breast cancer death, and incidence-based mortality (IBM) were investigated using data from NCI's Surveillance, Epidemiology, and End Results (SEER) program on 244,786 women diagnosed with breast cancer between 1990 and 2003 and followed through 2004. A counter-factual approach was used to examine the expected IBM RR_BW, assuming equal distributions for estrogen receptor (ER) expression, and/or equal hazard rates of breast cancer death among black and white women. From 1990 to 2004, the mortality RR_BW was greater than 1.0 and increased over time. In contrast, the incidence RR_BW was generally less than 1.0. Absolute hazard rates of breast cancer death declined substantially for ER-positive tumors and modestly for ER-negative tumors but were persistently higher for blacks than for whites. Equalizing the distributions of ER expression in blacks and whites decreased the IBM RR_BW slightly. However, when hazard rates of breast cancer death were matched within each ER category, the BW disparity in IBM RR_BW was essentially eliminated. Identifying and addressing the reasons for the excess hazards of breast cancer death among black women, especially during the first few years following diagnosis, may help reduce the existing racial disparity in breast cancer mortality rates. (Menashe I, Anderson WF, Jatoi I, Rosenberg PS. Underlying causes of the black-white racial disparity in breast cancer mortality: A population-based analysis. J Natl Cancer Inst 2009;101:993–1000)

 

CERVICAL CANCER

Implications of Human Papillomavirus Genotype Distributions

To study how human papillomavirus (HPV) vaccination and HPV-based screening may influence cervical cancer prevention, the authors used the New Mexico SEER registry to ascertain cases of in situ (n = 1,213) and invasive (n = 808) cervical cancer diagnosed during 1985–1999 and 1980–1999, respectively. HPV genotyping was performed on tissues from in situ and invasive cancers and on cervical Papanicolaou test specimens from control subjects (n = 4,007). The most common HPV genotypes detected in invasive cancers were HPV-16 (53.2%), HPV-18 (13.1%), and HPV-45 (6.1%) and in in situ cancers were HPV-16 (56.3%), HPV-31 (12.6%), and HPV-33 (8.0%). Invasive cancer case subjects who were positive for HPV-16 or -18 were diagnosed at younger ages than those who were positive for other carcinogenic HPV genotypes (mean age at diagnosis: 48.1, 45.9, and 52.3 years, respectively). The percentage of subjects with HPV-16–positive in situ and invasive cancers, but not of subjects with HPV-18–positive cancers, declined with more recent calendar year of diagnosis, whereas the percentage that were positive for HPV genotypes other than HPV-16 and HPV-18 increased. The subjects' ages at diagnosis of HPV-16– and HPV-18–related invasive cancers were younger than that of subjects with invasive cancers caused by other carcinogenic HPV genotypes, suggesting that the age at initiation of cervical screening could be delayed in HPV-vaccinated populations. (Wheeler CM, Hunt WC, Joste NE, Key CR, Quint WGV, and Castle PE. Human papillomavirus genotype distributions: Implications for vaccination and cancer screening in the United States. J Natl Cancer Inst 2009;101:475–487)

Loop Electrosurgical Excision Procedure and Subsequent HPV

To examine the impact of treatment for cervical precancerous lesions, the authors compared the acquisition of new HPV infections among HPV-positive women who underwent colposcopy and who were treated by loop electrosurgical excision procedure (LEEP) (n = 195) with those who were untreated (n = 1,625) at entry into a two-year study. Cumulative incidence rate ratios (IRRs) for treated vs. untreated women at 6 and 24 months of follow-up were calculated for infection by individual HPV genotypes, any HPV genotypes, any carcinogenic HPV genotypes, any noncarcinogenic HPV genotypes, and phylogenetic groups of HPV genotypes. Treated women were 29% less likely than untreated women to have carcinogenic HPV genotypes detected at 6-month follow-up (IRR = 0.71) and were 18% less likely to have these genotypes detected at 24-month follow-up (IRR = 0.82), although neither association was statistically significant. Treated women were 56% less likely to have HPV genotypes of the α9 phylogenetic species, which includes HPV-16, detected at 6-month follow-up (IRR = 0.44) and were 40% less likely to have these genotypes detected at 24-month follow-up (IRR = 0.60). LEEP may reduce the acquisition of certain carcinogenic HPV genotypes related to HPV-16. (Castle PE, Kreimer AR, Wacholder S, Wheeler CM, Koutsky LA, Rydzak G, Buckman DW, Graubard B, Schiffman M. Influence of loop electrosurgical excision procedure on subsequent acquisition of new human papillomavirus infections. J Infect Dis 2009;199:1612–1620)

 

GENETICS

Dyskeratosis Congenita

To investigate the spectrum of cancer susceptibility in dyskeratosis congenita (DC), the authors examined more than 500 cases of DC reported in the literature between 1910 and 2008 and conducted a quantitative analysis of cancer risks in 50 patients with DC from NCI’s Inherited Bone Marrow Failure Syndrome cohort who had enrolled between 2002 and 2007. Sixty cancers were reported among 52 literature cases, while seven occurred among patients in the NCI DC cohort. The two cohorts were comparable in their median overall survival (age 42 years) and cumulative incidence of cancer (40–50% by age 50 years). The most frequent solid tumors were head and neck squamous cell carcinomas, followed by skin and anorectal cancer. The ratio of observed to expected (O/E) cancers in the NCI cohort was 11-fold compared with the general population. Significantly elevated O/E ratios were 1,154 for tongue cancer and 195 for acute myeloid leukemia. Survival after bone marrow transplantation for aplastic anemia or leukemia was poor in both cohorts. (Alter BP, Giri N, Savage SA, and Rosenberg PS. Cancer in dyskeratosis congenita. Blood 2009;113:6549–6557)

 

LYMPHOHEMA TOPOIETIC NEOPLASIA

Caspase Genetic Variation and Non-Hodgkin Lymphoma Risk

Caspase genes play a critical role in regulating apoptosis, cell differentiation, inflammation, and innate immunity, and several are mutated or have altered expression in non-Hodgkin lymphoma (NHL). To study the impact of genetic variation in caspases on NHL risk, the authors analyzed tag SNPs in 12 caspase and related genes in three population-based case-control studies (1,946 cases and 1,808 controls). Gene-based analysis, adjusting for the number of tag SNPs genotyped in each gene, showed significant associations for CASP8, CASP9, and CASP1. SNP-based analysis showed that CASP8 rs6736233 (odds ratio [OR]_CG = 1.21, OR_CC = 2.13); CASP9 rs4661636 (OR_CT = 0.89, OR_TT = 0.77); and CASP1 rs1785882 (OR_AT = 1.12, OR_AA = 1.30) were significantly associated with NHL risk and associations were consistent across studies. Genetic variants of CASP8 were associated with risks of all major NHL subtypes. Findings suggest that genetic variation in caspases may play an important role in lymphomagenesis. (Lan Q, Morton LM, Armstrong B, Hartge P, Menashe I, Zheng T, Purdue MP, Cerhan JR, Zhang Y, Grulich A, Cozen W, Yeager M, Holford TR, Vajdic CM, Davis S, Leaderer B, Kricker A, Schenk M, Zahm SH, Chatterjee N, Chanock SJ, Rothman N, and Wang SS. Genetic variation in caspase genes and risk of non-Hodgkin lymphoma: A pooled analysis of three population-based case-control studies. Blood 2009;114:264–267)

Cell Cycle, Apoptosis, and Lymphocyte Development Regulatory Genes

Because many NHL-associated translocations involve cell cycle, apoptosis, and lymphocyte development regulatory genes, the authors studied NHL risk associated with common genetic variation in 20 candidate genes in these pathways. Genotyping of 203 tag SNPs was conducted in 1,946 NHL cases and 1,808 controls pooled from three independent population-based case-control studies. The most striking associations were observed for tag SNPs in the proapoptotic gene BCL2L11 (BIM) and BCL7A, which is involved in a rare NHL-associated translocation. Variants in BCL2L11 were strongly related to follicular lymphoma only, particularly rs3789068 (OR_AG = 1.41; OR_GG = 1.65). Variants in BCL7A were strongly related to diffuse large B cell lymphoma only, particularly rs1880030 (OR_AG = 1.34; OR_AA = 1.60). The associations for both variants were similar in all three studies and supported by haplotype analyses. Associations for variants in BCL6, CCND1, and MYC were also observed. Results support the role of common genetic variation in cell cycle, apoptosis, and lymphocyte development regulatory genes in lymphomagenesis and suggest that effects may vary by NHL subtype. (Morton LM, Purdue MP, Zheng T, Wang SS, Armstrong B, Zhang Y, Menashe I, Chatterjee N, Davis S, Lan Q, Vajdic CM, Severson RK, Holford TR, Kricker A, Cerhan JR, Leaderer B, Grulich A, Yeager M, Cozen W, Zahm SH, Chanock SJ, Rothman N, Hartge P. Risk of non-Hodgkin lymphoma associated with germline variation in genes that regulate the cell cycle, apoptosis, and lymphocyte development. Cancer Epidemiol Biomarkers Prev 2009;18:1259–1270)

Mortality among Formaldehyde Workers

The authors examined associations between quantitative formaldehyde (FA) exposure and death from lymphohematopoietic malignancies for 25,619 workers employed in FA-using or FA-producing plants before 1966 and followed through 2004. They found increased risks for the highest vs. lowest peak FA exposure category (≥ 4 parts per million [ppm] vs. > 0 to < 2.0 ppm) and all lymphohematopoietic malignancies (RR = 1.37). Excess risk was seen for Hodgkin lymphoma (RR = 3.96) and possibly several other subgroups of these malignancies, notably myeloid leukemia, with a 1.78-fold higher risk (CI = 0.87–3.64, p for trend = 0.13). Myeloid leukemia is the type most often associated with chemical exposures. For peak exposure, the highest FA-related risks for myeloid leukemia occurred before 1980, but trend tests did not attain statistical significance until 1990; after the mid-1990s, the FA-related risk of myeloid leukemia declined. Evaluation of risks over time suggests a possible link between FA exposure and lymphohematopoietic malignancies, particularly myeloid leukemia, but also perhaps Hodgkin lymphoma and multiple myeloma. (Beane Freeman LE, Blair A, Lubin JH, Stewart PA, Hayes RB, Hoover RN, Hauptmann M. Mortality from lymphohematopoietic malignancies among workers in formaldehyde industries: The National Cancer Institute Cohort. J Natl Cancer Inst 2009;101:751–761)

Obesity, Lifestyle Risk Factors, and Myelodysplastic Syndromes

The authors examined the relations of obesity and lifestyle factors to myelodysplastic syndromes (MDS) in a cohort of 471,799 persons aged 50–71 years who were recruited into the NIH-AARP Diet and Health Study during 1995–1996. Incident MDS was diagnosed in 193 persons during 2001–2003. A significant positive association was observed between BMI at baseline and MDS. Compared with persons with a BMI < 25, hazard ratios (HRs) for persons with BMIs of 25 to < 30 and ≥ 30 were 1.15 (CI = 0.81–1.64) and 2.18, respectively. The association was not affected by physical activity, cigarette smoking, or alcohol intake. The risk of MDS was elevated among former smokers (HR = 1.68) and current smokers (HR = 3.17) but not never smokers. Physical activity, alcohol consumption, meat intake, and fruit and vegetable intake did not appear to significantly influence the risk of MDS in this analysis. This prospective investigation of MDS implicates both obesity and smoking as modifiable risk factors. (Ma X, Lim U, Park Y, Mayne ST, Wang R, Hartge P, Hollenbeck AR, and Schatzkin A. Obesity, lifestyle factors, and risk of myelodysplastic syndromes in a large U.S. cohort. Am J Epidemiol 2009;169:1492–1499)

Occupational Pesticide Exposure and Risk of Monoclonal Gammopathy of Undetermined Significance

The authors assessed the risk of monoclonal gammopathy of undetermined significance (MGUS) among 678 men (aged 30–94 years) from a prospective cohort of pesticide applicators. Age-adjusted prevalence estimates of MGUS were compared with prevalence among 9,469 men from Minnesota. Among 555 study participants older than 50 years of age, 38 (6.8%) were found to have MGUS. Compared with men from Minnesota, the age-adjusted prevalence of MGUS was 1.9-fold higher among male pesticide applicators. Among applicators, a 5.6-fold, 3.9-fold, and 2.4-fold increased risk of MGUS prevalence was observed among users of the chlorinated insecticide dieldrin, the fumigant mixture carbon-tetrachloride/carbon disulfide, and the fungicide chlorothalonil, respectively. Results support the hypothesis that specific pesticides are causatively linked to myelomagenesis. (Landgren O, Kyle RA, Hoppin JA, Beane-Freeman LE, Cerhan JR, Katzmann JA, Rajkumar SV, Alavanja MC. Pesticide exposure and risk of monoclonal gammopathy of undetermined significance in the Agricultural Health Study. Blood 2009;113:6386–6391)

Polychlorinated Biphenyl and Organochlorine Pesticide Exposures

Carpet dust was used to examine the risk of childhood leukemia in relation to residential exposure to six polychlorinated biphenyl (PCB) congeners and the pesticides α- and γ-chlordane, p,p´-DDT (dichlorodiphenyltrichloroethane), p,p´-DDE (dichlorodiphenyldichloroethylene), methoxychlor, and pentachlorophenol in a California population-based case-control study conducted in 2001–2006 among 184 acute lymphocytic leukemia (ALL) cases aged seven years or younger and 212 matched controls. Detection of any PCB congener in the dust conferred a 2.0-fold increased risk of ALL. Compared with those in the lowest quartile of total PCBs, the highest quartile was associated with a 2.8-fold risk. Significant positive trends in ALL risk were apparent with increasing concentrations of PCB congeners 118, 138, and 153. No positive associations were observed for chlordane, DDT, DDE, methoxychlor, or pentachlorophenol. The associations with PCBs were stronger among non-Hispanic whites than Hispanics despite similar distributions of PCB levels among controls in each racial/ethnic group. Findings suggest that PCBs may represent a previously unrecognized risk factor for childhood leukemia. (Ward MH, Colt JS, Metayer C, Gunier RB, Lubin J, Crouse V, Nishioka MG, Reynolds P, Buffler PA. Residential exposure to polychlorinated biphenyls and organochlorine pesticides and risk of childhood leukemia. Environ Health Perspect 2009;117:1007–1013)

 

PANCREATIC CANCER

Risks Associated with Alcohol Use

The authors examined the relation between alcohol use and pancreatic cancer risk among 470,681 participants aged 50–71 years during 1995 through 1996 in the NIH-AARP Diet and Health Study, including 1,149 eligible exocrine pancreatic cancer cases identified through 2003. With the referent group being light drinkers (< 1 drink per day), the RRs of developing pancreatic cancer were 1.45 for heavy total alcohol use (≥ 3 drinks per day) and 1.62 for heavy liquor use, compared with the respective referent group. The increased risk with heavy total alcohol use was suggested in never smokers (RR = 1.35; CI = 0.79–2.30) and observed in participants who quit smoking 10 or more years before baseline (RR = 1.41). Findings suggest a moderately increased pancreatic cancer risk with heavy alcohol use, particularly liquor; however, possible residual confounding by cigarette smoking cannot be completely excluded. (Jiao L, Silverman DT, Schairer C, Thiébaut AC, Hollenbeck AR, Leitzmann MF, Schatzkin A, Stolzenberg-Solomon RZ. Alcohol use and risk of pancreatic cancer: The NIH-AARP Diet and Health Study. Am J Epidemiol 2009;169:1043–1051)

Risks Associated with Dietary Fats

The authors analyzed the association between intakes of fat, fat subtypes, and fat food sources and exocrine pancreatic cancer among 308,736 men and 216,737 women who, as participants in the NIH-AARP Diet and Health Study, had completed a 124-item food frequency questionnaire during 1995–1996. Over an average follow-up of 6.3 years, 865 men and 472 women were diagnosed with exocrine pancreatic cancer. After conducting multivariable adjustment and combining data for men and women, the authors found that pancreatic cancer risk was directly related to the intakes of total fat (highest vs. lowest quintile; 46.8 vs. 33.2 cases per 100,000 person-years [p-y]; HR = 1.23), saturated fat (51.5 vs. 33.1 cases per 100,000 p-y; HR = 1.36), and monounsaturated fat (46.2 vs. 32.9 cases per 100,000 p-y; HR = 1.22) but not polyunsaturated fat. The associations were strongest for saturated fat from animal food sources (52.0 vs. 32.2 cases per 100,000 p-y; HR = 1.43); specifically, intakes from red meat and dairy products were both significantly associated with increased pancreatic cancer risk (HR = 1.27 and 1.19, respectively) (see Figure 1). In this large prospective cohort with a wide range of intakes, dietary fat of animal origin was associated with increased pancreatic cancer risk. (Thiébaut AC, Jiao L, Silverman DT, Cross AJ, Thompson FE, Subar AF, Hollenbeck AR, Schatzkin A, Stolzenberg-Solomon RZ. Dietary fatty acids and pancreatic cancer in the NIH-AARP Diet and Health Study. J Natl Cancer Inst 2009;101:1001–1011)

Variants in ABO Locus Related to Risk

The investigators conducted a two-stage genome-wide association study of pancreatic cancer, a cancer with one of the lowest survival rates worldwide. They genotyped 558,542 SNPs in 1,896 individuals with pancreatic cancer and 1,939 controls drawn from 12 prospective cohorts and one hospital-based case-control study. They then performed a combined analysis of these groups, plus an additional 2,457 affected individuals and 2,654 controls from eight case-control studies, adjusting for study, sex, ancestry, and five principal components. The investigators identified an association between a locus on 9q34 and pancreatic cancer marked by the SNP rs505922 (combined p = 5.37 x 10^–8; multiplicative per-allele OR = 1.20). This SNP maps to the first intron of the ABO blood group gene. Results are consistent with earlier epidemiologic evidence suggesting that people with blood group O may have a lower risk of pancreatic cancer than those with blood group A or B (see Figure 2). (Amundadottir L, Kraft P, Stolzenberg-Solomon RZ, Fuchs CS, Petersen GM, Arslan AA, Bueno-de-Mesquita HB, Gross M, Helzlsouer K, Jacobs EJ, Lacroix A, Zheng W, Albanes D, Bamlet W, Berg CD, Berrino F, Bingham S, Buring JE, Bracci PM, Canzian F, Clavel-Chapelon F, Clipp S, Cotterchio M, de Andrade M, Duell EJ, Fox Jr JW, Gallinger S, Gaziano JM, Giovannucci EL, Goggins M, González CA, Hallmans G, Hankinson SE, Hassan M, Holly EA, Hunter DJ, Hutchinson A, Jackson R, Jacobs KB, Jenab M, Kaaks R, Klein AP, Kooperberg C, Kurtz RC, Li D, Lynch SM, Mandelson M, McWilliams RR, Mendelsohn JB, Michaud DS, Olson SH, Overvad K, Patel AV, Peeters PH, Rajkovic A, Riboli E, Risch HA, Shu XO, Thomas G, Tobias GS, Trichopoulos D, Van Den Eeden SK, Virtamo J, Wactawski-Wende J, Wolpin BM, Yu H, Yu K, Zeleniuch-Jacquotte A, Chanock SJ, Hartge P, Hoover RN. Genome-wide association study identifies variants in the ABO locus associated with susceptibility to pancreatic cancer. Nat Genet 2009;41:986–990)

 

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