Cancer Epidemiology Biomarkers & Prevention最新文献

{"title":"Excess Mortality in Persons with Concurrent HIV and Cancer Diagnoses: A Retrospective Cohort Study","authors":"Kamaria L. Lee, Varada Sarovar, Jennifer O. Lam, Wendy A. Leyden, Stacey E. Alexeeff, Alexandra N. Lea, Rulin C. Hechter, Haihong Hu, Julia L. Marcus, Qing Yuan, Jennifer R. Kramer, Lilie L. Lin, Elizabeth Y. Chiao, William J. Towner, Michael A. Horberg, Michael J. Silverberg","doi":"10.1158/1055-9965.epi-24-0478","DOIUrl":"https://doi.org/10.1158/1055-9965.epi-24-0478","url":null,"abstract":"Background: With extended lifespans for people with human immunodeficiency virus (PWH), there is a corresponding increased burden of chronic illnesses, including cancer. Our objective was to estimate the excess mortality for PWH with cancer compared with people without HIV (PWoH), accounting for the higher background mortality in the general PWH population. Methods: We identified 39,000 PWH and 387,767 demographically-matched PWoH in three integrated healthcare systems from 2000-2016. We estimated excess mortality for PWH with cancer, computed as the cancer mortality rate difference-in-difference comparing PWH and PWoH. We evaluated five cancer groups: any cancer; virus-, human papillomavirus-, and Epstein-Barr virus (EBV)-related cancers; virus-unrelated cancers, and common individual cancers. We fitted a multivariable additive Poisson model to estimate excess mortality for PWH with cancer. Results: PWH with any cancer had excess mortality compared with PWoH (41.3/1000 person-years [py], 95% Confidence Interval [CI] 34.0, 48.7). The highest excess mortality was observed for EBV-related cancers (63.2/1000 py, 95% CI 47.8, 78.7), lung cancer (147.7/1000 py, 95% CI 41.1, 254.3) and non-Hodgkin lymphoma (70.5/1000 py, 95% CI 51.4, 89.6). Excess mortality for PWH was attenuated 2009-2016, and PWH with cancer had no excess mortality 5 years after diagnosis. Conclusions: PWH in care may have excess mortality from certain cancer types, although disparities may have attenuated over time and do not persist beyond 5 years after diagnosis. Impact: Findings may guide improved clinical practice, and suggest further research is needed to investigate whether cancer treatment or other factors contribute to mortality disparities for PWH with cancer.","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":"5 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142266065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neighborhood Disadvantage and Prostate Tumor Aggressiveness among African American and European American Men","authors":"Joseph Boyle, Jessica Yau, Jimmie L. Slade, Derrick A. Butts, Jessica Wimbush, Jong Y. Park, Arif Hussain, Eberechukwu Onukwugha, Cheryl L. Knott, David C. Wheeler, Kathryn Hughes Barry","doi":"10.1158/1055-9965.epi-24-0450","DOIUrl":"https://doi.org/10.1158/1055-9965.epi-24-0450","url":null,"abstract":"Background: Studies have identified associations between neighborhood disadvantage (ND), which is more likely to affect African American (AA) individuals, and aggressive prostate cancer. Thus, ND may contribute to prostate cancer disparities. However, it is unknown what ND components drive aggressive disease and whether associations vary by race. Methods: We evaluated associations between aggressive prostate cancer and four ND metrics—Area Deprivation Index (ADI), validated Bayesian Neighborhood Deprivation Index (NDI), racial isolation (RI) index, and historical redlining, and whether these factors interacted with race, among men with prostate cancer treated at the University of Maryland Greenebaum Comprehensive Cancer Center (2004–2021). Results: We included 1,458 men (698 European American and 760 AA). AA men were more likely to experience ND. In adjusted models, the ADI, RI, and redlining were significantly associated with aggressive versus nonaggressive prostate cancer overall [ADI, OR for one SD increase = 1.14, 95% confidence interval (CI), 1.00–1.30; RI, OR = 1.27, CI, 1.07–1.51; redlining, OR = 1.77; CI, 1.23–2.56] and among AA men. The NDI was associated with aggressive prostate cancer among AA men (OR = 1.32, 95% credible interval: 1.13–1.57); percent in poverty received the largest importance weight. The ADI (P heterogeneity = 0.002) and NDI (exceedance probability heterogeneity = 98.1%) significantly interacted with race, such that associations were significantly stronger for AA men. Conclusions: We identified novel significant positive associations for racial segregation and historical redlining with aggressive prostate cancer and significant interactions between ND indices and race. Impact: Findings inform specific ND components that are associated with aggressive prostate cancer and suggest the ND effect is stronger for AA men, which has implications for interventions to reduce disparities.","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":"12 1","pages":"OF1-OF9"},"PeriodicalIF":3.8,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142200142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a breast cancer risk prediction model integrating monogenic, polygenic, and epidemiologic risk","authors":"Sarah S. Kalia, Nicholas J. Boddicker, Siddhartha Yadav, Hongyan Huang, Jie Na, Chunling Hu, Christine B. Ambrosone, Song Yao, Christopher A. Haiman, Fei Chen, Esther M. John, Allison W. Kurian, Boya Guo, Sara Lindström, Paul Auer, James V. Lacey, Susan L. Neuhausen, Maria Elena. Martinez, Dale P. Sandler, Katie M. O'Brien, Jack A. Taylor, Lauren R. Teras, James M. Hodge, Adriana Lori, Clara Bodelon, Amy Trentham-Dietz, Elizabeth S. Burnside, Celine M. Vachon, Stacey J. Winham, David E. Goldgar, Susan M. Domchek, Katherine L. Nathanson, Jeffrey N. Weitzel, Fergus J. Couch, Peter Kraft","doi":"10.1158/1055-9965.epi-24-0594","DOIUrl":"https://doi.org/10.1158/1055-9965.epi-24-0594","url":null,"abstract":"Background: Breast cancer has been associated with monogenic, polygenic, and epidemiologic (clinical, reproductive and lifestyle) risk factors, but studies evaluating the combined effects of these factors have been limited. Methods: We extended previous work in breast cancer risk modeling, incorporating pathogenic variants (PV) in six breast cancer predisposition genes and a 105-SNP polygenic risk score (PRS), to include an epidemiologic risk score (ERS) in a sample of non-Hispanic White women drawn from prospective cohorts and population-based case-control studies, with 23,518 cases and 22,832 controls, from the Cancer Risk Estimates Related to Susceptibility (CARRIERS) Consortium. Results: The model predicts 4.4-fold higher risk of breast cancer for postmenopausal women with no predisposition PV and median PRS, but with the highest versus lowest ERS. Overall, women with CHEK2 PVs had >20% lifetime risk of breast cancer. However, 15.6% of women with CHEK2 PVs and a family history of breast cancer, and 45.1% of women with CHEK2 PVs but without a family history of breast cancer, had low (<20%) predicted lifetime risk and thus were below the threshold for MRI screening. CHEK2 PV carriers at the 10th percentile of the joint distribution of ERS and PRS, without a family history of breast cancer, had a predicted lifetime risk similar to the general population. Conclusions: These results illustrate that an ERS, alone and combined with the PRS, can contribute to clinically relevant risk stratification. Impact: Integrating monogenic, polygenic, and epidemiologic risk factors in breast cancer risk prediction models may inform personalized screening and prevention efforts.","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":"61 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142225754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recalibrating the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO) Environmental Risk Score for Use in US Veterans","authors":"April R. Williams, Thomas S. Redding, Brian A. Sullivan, Robin N. Baidya, Belinda Ear, Kelly Cho, Kerry L. Ivey, Christina D. Williams, Jason A. Dominitz, David Lieberman, Elizabeth R. Hauser","doi":"10.1158/1055-9965.epi-24-0791","DOIUrl":"https://doi.org/10.1158/1055-9965.epi-24-0791","url":null,"abstract":"Background: Risk for colorectal cancer (CRC) may accumulate through multiple environmental factors. Understanding their effects, along with genetics, age and family history, could allow improvements in clinical decisions for screening protocols. We aimed to extend previous work by recalibrating an environmental risk score (e-Score) for CRC among a sample of US Veteran participants of the Million Veteran Program (MVP). Methods: Demographic, lifestyle, and CRC data from 2011-2022 were abstracted from survey responses and health records of 227,504 male MVP participants. Weighting for each environmental factor’s effect size was recalculated using VA training data to create a recalibrated e-Score. This recalibrated score was compared with the original weighted e-Score in a validation sample of 113,752 (n cases=590). Nested multiple logistic regression models tested associations between quintiles for recalibrated and original e-Scores. Likelihood Ratio Tests were used to compare model performance. Results: Age (p<0.0001), education (p<0.0001), diabetes (p<0.0001), physical activity (p<0.0001), smoking (p<0.0001), NSAID use (p<0.0001), calcium (p=0.015), folate (p=0.020), and fruit consumption (p=0.019) were significantly different between CRC case and control groups. In the validation sample, the recalibrated e-Score model significantly improved the base model performance (p<0.001), but the original e-Score model did not (p=0.07). The recalibrated e-Score model quintile 5 was associated with significantly higher odds for CRC compared with quintile 1 (Q5 vs Q1: 1.79, 95% CI: 1.38-2.33). Conclusions: Multiple environmental factors, and the recalibrated e-Score quintiles were significantly associated with CRC cases. Impact: A recalibrated, Veteran-specific e-Score could be used to help personalize CRC screening and prevention strategies.","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":"8 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142225730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The University of North Carolina Cancer Survivorship Cohort: A resource for collaborative survivorship research.","authors":"Chelsea Anderson, Jeannette T Bensen, Emma H Allott, Patricia V Basta, Debra E Irwin, Adrian Gerstel, Laura Farnan, Hung-Jui Tan, Erin E Kent, Tzy-Mey Kuo, Christopher D Baggett, Andrew F Olshan, H Shelton Earp, Hazel B Nichols","doi":"10.1158/1055-9965.EPI-24-0794","DOIUrl":"https://doi.org/10.1158/1055-9965.EPI-24-0794","url":null,"abstract":"<p><strong>Background: </strong>Rapid growth in the number of U.S. cancer survivors drives the need for ongoing research efforts to improve outcomes and experiences after cancer. Here we describe the University of North Carolina (UNC) Cancer Survivorship Cohort, a medical center-based cohort of adults with cancer that integrates medical record-abstracted cancer information, patient-reported outcomes, and biologic specimens.</p><p><strong>Methods: </strong>Participants ages 18+ were recruited from UNC oncology clinics between April 2010 and August 2016. After enrollment, participants completed questionnaires on a range of topics including demographics, health history, health care access and utilization, quality of life, and symptoms. Blood samples and tumor tissue specimens were collected and processed by study staff, and cancer characteristics and other clinical data were abstracted from electronic medical records. Participants consented to recontact for future studies and linkage of their data with other data resources.</p><p><strong>Results: </strong>In total, 3,999 participants with a cancer diagnosis were enrolled in the cohort. The most common cancer types among those enrolled included breast (N=866), uterine (N=458), colorectal (N=300), prostate (N=296), and head and neck (N=248). Blood specimens were collected for 3,027 (76%). Additional participants without cancer (N=1,299) were also enrolled, and the majority (62%) provided biospecimen samples.</p><p><strong>Conclusions: </strong>We encourage wide collaboration with investigators across institutions seeking to advance research in cancer survivorship. Procedures are in place to support proposals for use of existing or linked data and for proposals that require participant recontact or analysis of biospecimens.</p><p><strong>Impact: </strong>The UNC Cancer Survivorship Cohort is a unique resource for cancer survivorship research.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142139387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatocellular Carcinoma Etiology Drives Survival Outcomes: A Population-Based Analysis.","authors":"Hannah M Cranford, Patricia D Jones, Robert J Wong, Qinran Liu, Erin N Kobetz, Isildinha M Reis, Tulay Koru-Sengul, Paulo S Pinheiro","doi":"10.1158/1055-9965.EPI-24-0626","DOIUrl":"https://doi.org/10.1158/1055-9965.EPI-24-0626","url":null,"abstract":"<p><strong>Background: </strong>Previous survival studies on hepatocellular carcinoma (HCC) by etiology are limited to hospital-based series, restricted cohorts, and monolithic etiological categories. We studied population-based survival by seven mutually exclusive HCC etiologic groups-standalone hepatitis-C virus (HCV), hepatitis-B virus (HBV), alcohol-related liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), and dual etiology HCV&HBV, HCV&ALD, and HBV&ALD-accounting for clinical and socio-demographic characteristics.</p><p><strong>Methods: </strong>All HCC cases diagnosed during 2005-2018 from the Florida Cancer Registry were linked for etiology using statewide discharge and viral hepatitis data. We performed cause-specific survival analysis including Cox regression for the matched 15,616 cases by HCC etiology.</p><p><strong>Results: </strong>The leading etiology was HCV only (n=4,983; 31.9%); the leading dual etiology was HCV&ALD (n=2,552; 16.3%). Five-year adjusted survival was low, 17.6% overall and <22% across all HCC etiologies; yet ALD-related etiologies [ALD only (14.4%; 95%CI:12.7-16.0), HCV&ALD (10.2%; 95%CI:8.7-11.7), HBV&ALD (8.2%; 95%CI:2.2-14.1)] showed lower survival than non-ALD causes-HCV only, HBV only, and NAFLD only. After adjustment for clinical and socio-demographic covariates, ALD- and HBV&ALD-HCC had 1.20 (95%CI:1.13-1.27) and 1.28 (95%CI:1.06-1.54) times higher risk of death, compared to those with HCV only-HCC.</p><p><strong>Conclusions: </strong>ALD only and dual etiologies involving ALD show worse prognosis for HCC, compared to viral etiology alone. To increase survival, improved screening and treatment are needed for patients with multiple HCC risk factors.</p><p><strong>Impact: </strong>Understanding US disparities in HCC survival by etiology can help guide the identification of etiologically specific biomarkers and potential therapeutic targets and inform public health measures.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142139386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Update from the Editor-in-Chief.","authors":"Elizabeth A Platz","doi":"10.1158/1055-9965.EPI-24-1031","DOIUrl":"https://doi.org/10.1158/1055-9965.EPI-24-1031","url":null,"abstract":"","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":"33 9","pages":"1143-1146"},"PeriodicalIF":3.7,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Geographic Access to Fertility Counseling among Adolescent and Young Adult Women with Cancer in North Carolina.","authors":"Nidia Rodriguez-Ormaza, Chelsea Anderson, Christopher D Baggett, Paul L Delamater, Melissa A Troester, Stephanie B Wheeler, Alexis C Wardell, Allison M Deal, Andrew Smitherman, Jennifer Mersereau, Valerie L Baker, Hazel B Nichols","doi":"10.1158/1055-9965.EPI-24-0482","DOIUrl":"10.1158/1055-9965.EPI-24-0482","url":null,"abstract":"<p><strong>Background: </strong>Fertility counseling is recommended for adolescent and young adult women facing gonadotoxic cancer therapy. However, fertility care is subspecialized medical care offered at a limited number of institutions, making geographic access a potential barrier to guideline-concordant care. We assessed the relationship between geographic access and receipt of fertility counseling among adolescent and young adult women with cancer.</p><p><strong>Methods: </strong>Using data from the North Carolina Central Cancer Registry, we identified women diagnosed with lymphoma, gynecologic cancer, or breast cancer at ages 15 to 39 years during 2004 to 2015. Eligible women were invited to complete an online survey on various topics, including fertility counseling. Geographic access was measured, using geocoded addresses, as vehicular travel time from residence to the nearest fertility clinic available at diagnosis. Multivariable regression models were used to examine the association between travel time and receipt of fertility counseling by provider type: health care provider versus fertility specialist.</p><p><strong>Results: </strong>Analyses included 380 women. The median travel time to a fertility clinic was 31 (IQR: 17-71) minutes. Overall, 75% received fertility counseling from a health care provider and 16% by a fertility specialist. Women who lived ≥30 minutes from a clinic were 13% less likely to receive fertility counseling by a health care provider (prevalence ratio: 0.87; 95% confidence interval, 0.75-1.00) and 49% less likely to receive counseling by a fertility specialist (prevalence ratio: 0.51; 95% confidence interval, 0.28-0.93).</p><p><strong>Conclusions: </strong>Women who lived further away from fertility clinics were less likely to receive fertility counseling.</p><p><strong>Impact: </strong>Interventions to improve access to fertility counseling should include strategies to alleviate the burden of geographic access.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"1194-1202"},"PeriodicalIF":3.7,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11371502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141562644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of the Immune Response within the Tumor Microenvironment in African American and Non-Hispanic White Patients with Non-Small Cell Lung Cancer.","authors":"Matthew R Trendowski, Donovan Watza, Christine M Lusk, Fulvio Lonardo, Valerie Ratliff, Angela S Wenzlaff, Hirva Mamdani, Christine Neslund-Dudas, Julie L Boerner, Ann G Schwartz, Heather M Gibson","doi":"10.1158/1055-9965.EPI-24-0333","DOIUrl":"10.1158/1055-9965.EPI-24-0333","url":null,"abstract":"<p><strong>Background: </strong>African Americans have higher incidence and mortality from lung cancer than non-Hispanic Whites, but investigations into differences in immune response have been minimal. Therefore, we compared components of the tumor microenvironment among African Americans and non-Hispanic Whites diagnosed with non-small cell lung cancer based on PDL1 or tertiary lymphoid structure (TLS) status to identify differences of translational relevance.</p><p><strong>Methods: </strong>Using a cohort of 280 patients with non-small cell lung cancer from the Inflammation, Health, Ancestry, and Lung Epidemiology study (non-Hispanic White: n = 155; African American: n = 125), we evaluated PDL1 tumor proportion score (<1% vs. ≥1%) and TLS status (presence/absence), comparing differences within the tumor microenvironment based on immune cell distribution and differential expression of genes.</p><p><strong>Results: </strong>Tumors from African Americans had a higher proportion of plasma cell signatures within the tumor microenvironment than non-Hispanic Whites. In addition, gene expression patterns in African American PDL1-positive samples suggest that these tumors contained greater numbers of γδ T cells and resting dendritic cells, along with fewer CD8+ T cells after adjusting for age, sex, pack-years, stage, and histology. Investigation of differential expression of B cell/plasma cell-related genes between the two patient populations revealed that two immunoglobulin genes (IGKV2-29 and IGLL5) were associated with decreased mortality risk in African Americans.</p><p><strong>Conclusions: </strong>In the first known race-stratified analysis of tumor microenvironment components in lung cancer based on PDL1 expression or TLS status, differences within the immune cell composition and transcriptomic signature were identified that may have therapeutic implications.</p><p><strong>Impact: </strong>Future investigation of racial variation within the tumor microenvironment may help direct the use of immunotherapy.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"1220-1228"},"PeriodicalIF":3.7,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11371519/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141490965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genome-Wide Analysis to Assess if Heavy Alcohol Consumption Modifies the Association between SNPs and Pancreatic Cancer Risk.","authors":"Zhanmo Ni, Prosenjit Kundu, David F McKean, William Wheeler, Demetrius Albanes, Gabriella Andreotti, Samuel O Antwi, Alan A Arslan, William R Bamlet, Laura E Beane-Freeman, Sonja I Berndt, Paige M Bracci, Paul Brennan, Julie E Buring, Stephen J Chanock, Steven Gallinger, J M Gaziano, Graham G Giles, Edward L Giovannucci, Michael G Goggins, Phyllis J Goodman, Christopher A Haiman, Manal M Hassan, Elizabeth A Holly, Rayjean J Hung, Verena Katzke, Charles Kooperberg, Peter Kraft, Loic LeMarchand, Donghui Li, Marjorie L McCullough, Roger L Milne, Steven C Moore, Rachel E Neale, Ann L Oberg, Alpa V Patel, Ulrike Peters, Kari G Rabe, Harvey A Risch, Xiao-Ou Shu, Karl Smith-Byrne, Kala Visvanathan, Jean Wactawski-Wende, Emily White, Brian M Wolpin, Herbert Yu, Anne Zeleniuch-Jacquotte, Wei Zheng, Jun Zhong, Laufey T Amundadottir, Rachael Z Stolzenberg-Solomon, Alison P Klein","doi":"10.1158/1055-9965.EPI-24-0096","DOIUrl":"10.1158/1055-9965.EPI-24-0096","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic cancer is a leading cause of cancer-related death globally. Risk factors for pancreatic cancer include common genetic variants and potentially heavy alcohol consumption. We assessed if genetic variants modify the association between heavy alcohol consumption and pancreatic cancer risk.</p><p><strong>Methods: </strong>We conducted a genome-wide interaction analysis of single-nucleotide polymorphisms (SNP) by heavy alcohol consumption (more than three drinks per day) for pancreatic cancer in European ancestry populations from genome-wide association studies. Our analysis included 3,707 cases and 4,167 controls from case-control studies and 1,098 cases and 1,162 controls from cohort studies. Fixed-effect meta-analyses were conducted.</p><p><strong>Results: </strong>A potential novel region of association on 10p11.22, lead SNP rs7898449 (interaction P value (Pinteraction) = 5.1 × 10-8 in the meta-analysis; Pinteraction = 2.1 × 10-9 in the case-control studies; Pinteraction = 0.91 in the cohort studies), was identified. An SNP correlated with this lead SNP is an expression quantitative trait locus for the neuropilin 1 gene. Of the 17 genomic regions with genome-wide significant evidence of association with pancreatic cancer in prior studies, we observed suggestive evidence that heavy alcohol consumption modified the association for one SNP near LINC00673, rs11655237 on 17q25.1 (Pinteraction = 0.004).</p><p><strong>Conclusions: </strong>We identified a novel genomic region that may be associated with pancreatic cancer risk in conjunction with heavy alcohol consumption located near an expression quantitative trait locus for neuropilin 1, a protein that plays an important role in the development and progression of pancreatic cancer.</p><p><strong>Impact: </strong>This work can provide insights into the etiology of pancreatic cancer, particularly in heavy drinkers.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"1229-1239"},"PeriodicalIF":4.3,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141310127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}