IntroductionCancer pathogenesis and resulting treatment may lead to bone loss and poor skeletal health in survivorship. The purpose of this investigation was to evaluate the influence of 26 weeks of combined aerobic and resistance-training (CART) exercise on bone mineral density (BMD) in a multi-racial sample of female cancer survivors.MethodsTwenty-six female cancer survivors volunteered to undergo CART for 1 h/day, 3 days/week, for 26 weeks. The Improving Physical Activity After Cancer Treatment (IMPAACT) Program involves supervised group exercise sessions including 20 min of cardiorespiratory training, 25 min of circuit-style resistance-training, and 15 min of abdominal exercises and stretching. BMD at the spine, hip, and whole body was assessed using dual-energy X-ray absorptiometry (DXA) before and after the intervention. Serum markers of bone metabolism (procollagen-type I N-terminal propeptide, P1NP, and C-terminal telopeptides, CTX) were measured at baseline, 13 weeks, and at study completion.ResultsEighteen participants, with the average age of 63.0 ± 10.3 years, completed the program. Mean duration since completion of cancer treatment was 6.2 ± 10.6 years. Paired t-tests revealed significant improvements in BMD of the spine (0.971 ± 0.218 g/cm2 vs. 0.995 ± 0.218 g/cm2, p = 0.012), hip (0.860 ± 0.184 g/cm2 vs. 0.875 ± 0.191 g/cm2, p = 0.048), and whole body (1.002 ± 0.153 g/cm2 vs. 1.022 ± 0.159 g/cm2, p = 0.002). P1NP declined 22% at 13 weeks and 28% at 26 weeks in comparison to baseline (p < 0.01) while CTX showed a non-significant decrease of 8% and 18% respectively.ConclusionsWe report significant improvements in BMD at the spine, hip, and whole body for female cancer survivors who completed 26 weeks of CART. This investigation demonstrates the possible effectiveness of CART at improving bone health and reducing risk of osteoporosis for women who have completed cancer treatment. The IMPAACT Program appears to be a safe and feasible way for women to improve health after cancer treatment.

Objective Green tea has been found to possess anti-inflammatory, anti-oxidative and anti-carcinogenic properties. The present study examines the association between green tea drinking and hepatocellular carcinoma (HCC) and its interactions with other risk or protective factors and single nucleotide polymorphisms (SNP) of inflammation and oxidative stress related genes. Methods A population-based case-control study with 204 primary HCC cases and 415 healthy controls was conducted in Taixing, China. Epidemiological data were collected using a standard questionnaire. SNPs of genes of the inflammation and metabolic pathways were genotyped at the UCLA Molecular Epidemiology Laboratory. Logistic regression was performed to estimate adjusted odds ratios and 95% confidence intervals. Results Longer duration and larger quantities of green tea consumption were inversely associated with primary HCC. Individuals who drank green tea longer than 30 years were at lowest risk (adjusted OR = 0.44, 95% CI: 0.19-0.96) compared with non-drinkers. A strong interaction was observed between green tea drinking and alcohol consumption (adjusted OR for interaction = 3.40, 95% CI: 1.26-9.16). Green tea drinking was also observed to have a potential effect modification on HBV/HCV infection, smoking and polymorphisms of inflammation related cytokines, especially for IL-10. Conclusion Green tea consumption may protect against development of primary HCC. Potential effect modifications of green tea on associations between primary HCC and alcohol drinking, HBV/HCV infection, and inflammation-related SNPs were suggested.

Body mass index (BMI) and waist circumference (WC) are two common anthropometric measures of obesity in clinical and public health practice. Consensus, however, remains elusive regarding their utility for predicting cardiovascular disease risk in multiethnic populations. We address this gap in the literature by analyzing cross-sectional data from the first round of the Los Angeles County Health and Nutrition Examination Survey, 2011. We characterized the relationships between BMI, WC, waist-to-hip ratios, waist-to-height ratios, and chronic disease extent, as confirmed by the presence of hypertension, diabetes, and/or two or more other chronic conditions as defined by a composite indicator ‘comorbidity’. To account for race/ethnicity, age, gender, and cigarette smoking frequency, adjusted odds ratios (aOR) were generated and reported for each of the regression analyses. Whereas being overweight was associated with hypertension alone (aOR 2.10; 95% CI 1.12–3.94), obesity was associated with hypertension (aOR 5.04; 95% CI 2.80–9.06) as well as diabetes (aOR 5.28; 95% CI 2.25–12.3) and comorbidity (aOR 3.69; 95% CI 2.02–6.77). In whites and African-Americans, BMI and WC were positively related to diabetes, hypertension and comorbidity. In Hispanics, BMI and WC were also positively related to diabetes and comorbidity, but only the former measure was associated with hypertension (p<0.050). In Asians, BMI was not a significant predictor of diabetes, hypertension and/or comorbidity. Collectively, the findings suggest that BMI is not universally informative and waist circumference and its derivatives may represent a viable, more racially/ethnically appropriate alternative for use with selected minority groups.

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 (ORadj 2.80; 95% CI 1.15–6.80). Heterogeneity was observed (Pheterogeneity=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 (ORadj 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.

Body-mass-index (BMI) has been inversely associated with lung and upper aerodigestive tract (UADT) cancers. However, only a few studies have assessed BMI change in adulthood in relation to cancer. To understand the relationship between BMI change and these cancers in both men and women, we analyzed data from a population-based case-control study conducted in Los Angeles County. Adulthood BMI change was measured as the proportional change in BMI between age 21 and one year prior to interview or diagnosis. Five categories of BMI change were included and individuals with no more than a 5% loss or gain were defined as having a stable BMI (reference group). Adjusted odds ratios (ORs) and their 95% confidence intervals (CIs) were estimated using logistic regression models. Potential confounders included age, gender, ethnicity, education, tobacco smoking, and energy intake. For UADT cancers, we also adjusted for alcohol drinking status and frequency. A BMI gain of 25% or higher in adulthood was inversely associated with lung cancer (OR 0.53, 95% CI 0.33-0.84) and UADT cancers (OR 0.44, 95% CI 0.27-0.71). In subgroup analyses, a BMI gain of ≥25% was inversely associated with lung and UADT cancers among current and former smokers, as well as among current and former alcohol drinkers. The inverse association persisted among moderate and heavy smokers (≥20 pack-years). The observed inverse associations between adulthood BMI gain and lung and UADT cancers indicate a potential role for body weight-related biological pathways in the development of lung and UADT cancers.