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Genetic variation at 8q24, family history of cancer, and upper gastrointestinal cancers in a Chinese population.

ABSTRACT: Genetic variation at 8q24 is associated with prostate, bladder, breast, colorectal, thyroid, lung, ovarian, UADT, liver and stomach cancers. However, a role for variation at 8q24 in familial clustering of upper gastrointestinal cancers has not been studied. In order to explore potential inherited susceptibility, we analyzed epidemiologic data from a population-based case-control study of upper gastrointestinal cancers from Taixing, China. The study population includes 204 liver, 206 stomach, and 218 esophageal cancer cases and 415 controls. Associations between 8q24 rs1447295, rs16901979, rs6983267 and these cancers were stratified by family history of cancer. Odds ratios and 95% confidence intervals were adjusted for potential confounders: age, sex, education, tobacco smoking, alcohol consumption, and BMI at interview. We also adjusted for hepatitis B and aflatoxin (liver cancer) and Helicobacter pylori (stomach cancer). In a dominant model, among those with a family history of cancer, rs1447295 was positively associated with liver cancer (OR(adj) 2.80; 95% CI 1.15-6.80). Heterogeneity was observed (P(heterogeneity) = 0.029) with rs6983267 and liver cancer, with positive association in the dominant model among those with a family history of cancer and positive association in the recessive model among those without a family history of cancer. When considered in a genetic risk score model, each additional 8q24 risk genotype increased the odds of liver cancer by two-fold among those with a family history of cancer (OR(adj) 2.00; 95% CI 1.15-3.47). These findings suggest that inherited susceptibility to liver cancer may exist in the Taixing population and that variation at 8q24 might be a genetic component of that inherited susceptibility.

SUBMITTER: Tarleton HP

PROVIDER: S-EPMC3944602 | biostudies-literature | 2014 Mar

REPOSITORIES: biostudies-literature

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Genetic variation at 8q24, family history of cancer, and upper gastrointestinal cancers in a Chinese population.

Tarleton Heather P HP Chang Shen-Chih SC Park Sungshim Lani SL Cai Lin L Ding Baoguo B He Na N Hussain Shehnaz K SK Jiang Qingwu Q Mu Li-Na LN Rao Jianyu J Wang Hua H You Nai-Chieh Y NC Yu Shun-Zhang SZ Zhao Jin-Kou JK Zhang Zuo-Feng ZF

Familial cancer 20140301 1

Genetic variation at 8q24 is associated with prostate, bladder, breast, colorectal, thyroid, lung, ovarian, UADT, liver and stomach cancers. However, a role for variation at 8q24 in familial clustering of upper gastrointestinal cancers has not been studied. In order to explore potential inherited susceptibility, we analyzed epidemiologic data from a population-based case-control study of upper gastrointestinal cancers from Taixing, China. The study population includes 204 liver, 206 stomach, and ...[more]

PMID: 24030569

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Project description:ObjectiveThe objective of this study was to investigate family history (FH) of upper gastrointestinal (UGI) cancer and risk of esophageal squamous cell carcinoma (ESCC), gastric cardia carcinoma (GCC), and gastric non-cardia carcinoma (GNCC) in the Linxian General Population Nutrition Intervention Trial (NIT) cohort. Methods: This prospective analysis was conducted using the Linxian NIT cohort data. Subjects with FH of UGI cancer was treated as an exposed group while the remainders were considered as a comparison group. Hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between FH of UGI cancer and risk of UGI cancer incidence and mortality were estimated using Cox proportional hazards models.ResultsThere were 5,680 newly diagnosed UGI cancer cases during the follow-up period, with a total of 4,573 UGI cancer deaths occurred, including 2,603 ESCC, 1,410 GCC, and 560 GNCC deaths. A positive FH of UGI cancer was associated with a significantly increased risk of ESCC and GCC (Incidence: HRESCC = 1.45, 95%CI: 1.35-1.56; HRGCC = 1.27, 95%CI: 1.15-1.40; Mortality: HRESCC = 1.40, 95%CI: 1.30-1.52; HRGCC = 1.27, 95%CI: 1.14-1.42) after adjusting for age at baseline, gender, smoking status, alcohol drinking, education level, and frequency of fresh fruit and vegetable consumption. Subjects with FH in both parents had the highest risk of ESCC and GCC incidence (HRESCC = 1.65, 95%CI: 1.40-1.95; HRGCC = 1.42, 95%CI: 1.12-1.81) and deaths (HRESCC = 1.65, 95%CI: 1.38-1.97; HRGCC = 1.42, 95%CI: 1.09-1.85). Spouse diagnosed with UGI cancer did not increase the risk of any UGI cancers of the subjects. In subgroup analysis, FH of UGI cancer was shown to significantly increase the risk of GCC in non-drinkers (Incidence: HR = 1.31, 95%CI: 1.17-1.47; Mortality: HR = 1.33, 95%CI: 1.17-1.50). No associations were observed for risk of GNCC. Sensitivity analysis by excluding subjects who were followed up less than three years did not materially alter our results.ConclusionOur data point to the role of the FH of UGI cancer to the risk of ESCC and GCC incidence and mortality. The influence of family history on the risk of UGI cancer varies from different types of family members.

Project description:Malnutrition is prevalent in people with upper gastrointestinal (GI) cancers and is associated with shorter survival and poor quality of life. In order to effectively prevent or treat malnutrition, nutrition interventions must ensure appropriate energy provision to meet daily metabolic demands. In practice, the energy needs of people with cancer are frequently estimated from predictive equations which are not cancer-specific and are demonstrated to be inaccurate in this population. The purpose of this scoping review was to synthesize the existing evidence regarding energy expenditure in people with upper GI cancer. Three databases (Ovid MEDLINE, Embase via Ovid, CINAHL plus) were systematically searched to identify studies reporting on resting energy expenditure using indirect calorimetry and total energy expenditure using doubly labeled water (DLW) in adults with any stage of upper GI cancer at any point from diagnosis. A total of 57 original research studies involving 2,125 individuals with cancer of the esophagus, stomach, pancreas, biliary tract, or liver were eligible for inclusion. All studies used indirect calorimetry, and one study used DLW to measure energy expenditure, which was reported unadjusted in 42 studies, adjusted for body weight in 32 studies, and adjusted for fat-free mass in 13 studies. Energy expenditure in upper GI cancer was compared with noncancer controls in 19 studies and measured compared with predicted energy expenditure reported in 31 studies. There was heterogeneity in study design and in reporting of important clinical characteristics between studies. There was also substantial variation in energy expenditure between studies and within and between cancer types. Given this heterogeneity and known inaccuracies of predictive equations in patients with cancer, energy expenditure should be measured in practice wherever feasible. Additional research in cohorts defined by cancer type, stage, and treatment is needed to further characterize energy expenditure in upper GI cancer.

Project description:BackgroundWe sought to investigate how penetrance of familial cancer syndromes varies with family history using a population-based cohort.MethodsWe analysed 454,712 UK Biobank participants with exome sequence and clinical data (data collected between March 2006 and June 2021). We identified participants with a self-reported family history of breast or colorectal cancer and a pathogenic/likely pathogenic variant in the major genes responsible for hereditary breast cancer or Lynch syndrome. We calculated survival to cancer diagnosis (controlled for sex, death, recruitment centre, screening and prophylactic surgery).FindingsWomen with a pathogenic BRCA1 or BRCA2 variant had an increased risk of breast cancer that was higher in those with a first-degree family history (relative hazard 10.3 and 7.8, respectively) than those without (7.2 and 4.7). Penetrance to age 60 was also higher in those with a family history (44.7%, CI 32.2-59.3 and 24.1%, CI 17.5-32.6) versus those without (22.8%, CI 15.9-32.0 and 17.9%, CI 13.8-23.0). A similar pattern was seen in Lynch syndrome: individuals with a pathogenic MLH1, MSH2 or MSH6 variant had an increased risk of colorectal cancer that was significantly higher in those with a family history (relative hazard 35.6, 48.0 and 9.9) than those without (13.0, 15.4 and 7.2). Penetrance to age 60 was also higher for carriers of a pathogenic MLH1 or MSH2 variant in those with a family history (30.9%, CI 18.1-49.3 and 38.3%, CI 21.5-61.8) versus those without (20.5% CI 9.6-40.5 and 8.3% CI 2.1-30.4), but not for MSH6 (6.5% CI 2.7-15.1 with family history versus 8.3%, CI 5.1-13.2). Relative risk increases were also observed both within and across conditions.InterpretationIndividuals with pathogenic cancer syndrome variants may be at a less elevated risk of cancer in the absence of a first-degree family history, so in the context of results return, family history should be considered when counselling patients on the risks and benefits of potential follow-up care.FundingThe current work is supported by the MRC (grant no MR/T00200X/1). The MRC had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

Dataset Information

Genetic variation at 8q24, family history of cancer, and upper gastrointestinal cancers in a Chinese population.

Publications

Genetic variation at 8q24, family history of cancer, and upper gastrointestinal cancers in a Chinese population.

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