Factors associated with physical inactivity in adult breast cancer survivors-A population-based study.

BACKGROUND: Physical activity has been shown to reduce the risk of breast cancer-specific mortality. Although factors associated with physical inactivity in breast cancer survivors have been studied, a detailed examination at the population level is still lacking. METHODS: We addressed this gap in 1236 women with a diagnosis of breast cancer from the 2016 Behavioral Risk Factor Surveillance System Cancer Survivorship module. Physical inactivity was defined as self-reported absence of leisure time physical activity. Factors examined in the multivariable logistic regression model included sociodemographic, behavioral factors, access to health care, health history, current cancer treatment, and pain from cancer or treatment. RESULTS: Overall, older age (≥65 years: OR = 2.63, 95% CI: 1.25-5.55) and being underweight (BMI <18.5: OR = 6.11, 95% CI: 1.35-27.66), were identified as significant factors associated with physical inactivity. In models adjusting for sociodemographics (Model 1), and the prior plus behavioral factors (Model 2), pain from cancer or treatment was significantly associated with physical inactivity (Model 2: OR = 2.23, 95% CI: 1.16-4.28); however, after fully adjusting for all variables (Model 3), there was no longer evidence of a significant association between pain from cancer and physical activity in female survivors with breast cancer. CONCLUSIONS: We identified demographic (older age) and physical (low BMI and pain) factors to be significantly associated with physical inactivity among breast cancer survivors. Future interventions to promote physical activity in breast cancer survivors could benefit by taking into account these factors to develop tailored recommendations for increasing activity.

Acrolein-exposed normal human lung fibroblasts in vitro: cellular senescence, enhanced telomere erosion, and degradation of Werner's syndrome protein.

BACKGROUND: Acrolein is a ubiquitous environmental hazard to human health. Acrolein has been reported to activate the DNA damage response and induce apoptosis. However, little is known about the effects of acrolein on cellular senescence. OBJECTIVES: We examined whether acrolein induces cellular senescence in cultured normal human lung fibroblasts (NHLF). METHODS: We cultured NHLF in the presence or absence of acrolein and determined the effects of acrolein on cell proliferative capacity, senescence-associated ß-galactosidase activity, the known senescence-inducing pathways (e.g., p53, p21), and telomere length. RESULTS: We found that acrolein induced cellular senescence by increasing both p53 and p21. The knockdown of p53 mediated by small interfering RNA (siRNA) attenuated acrolein-induced cellular senescence. Acrolein decreased Werner's syndrome protein (WRN), a member of the RecQ helicase family involved in DNA repair and telomere maintenance. Acrolein-induced down-regulation of WRN protein was rescued by p53 knockdown or proteasome inhibition. Finally, we found that acrolein accelerated p53-mediated telomere shortening. CONCLUSIONS: These results suggest that acrolein induces p53-mediated cellular senescence accompanied by enhanced telomere attrition and WRN protein down-regulation.