Evidence is increasing that some early life exposures affect breast cancer risk. Exposure to secondhand smoke (SHS) during childhood may be one such exposure. As part of the WEB Study (Western New York Exposures and Breast Cancer Study), we conducted a population-based, case-control study with 1166 women aged 35 to 79 diagnosed with histologically confirmed, primary, incident breast cancer. Controls (n = 2105) were randomly selected from the Department of Motor Vehicles driver's license list (< or =age 65) and the Center for Medicare & Medicaid Services rolls (> age 65). Participants were queried regarding household and workplace SHS exposure. Person-years of lifetime cumulative SHS exposure were computed as well as cumulative exposure up to 21 years of age. Unconditional logistic regression adjusting for potential confounders was used to calculate odds ratios (OR) and 95% confidence intervals (95% CI). Lifetime cumulative exposure to household SHS was not associated with an increase in breast cancer risk for premenopausal (OR = 1.17, 95% CI = 0.54-2.56) or postmenopausal (OR = 1.29; 95% CI = 0.82-2.01) women. Neither was risk increased among women exposed to SHS before the age of 21 or at the time of birth, menarche, or a women's first birth. In this study, exposure to SHS either in adult or early life does not appear to be associated with the risk of breast cancer.
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http://dx.doi.org/10.1007/s10552-005-1906-x | DOI Listing |
IUBMB Life
January 2025
Precision Medicine Laboratory, School of Medical Technology and Engineering, Henan University of Science and Technology, Luoyang, China.
Triple-negative breast cancer (TNBC) remains a significant global health challenge, emphasizing the need for precise identification of patients with specific therapeutic targets and those at high risk of metastasis. This study aimed to identify novel therapeutic targets for personalized treatment of TNBC patients by elucidating their roles in cell cycle regulation. Using weighted gene co-expression network analysis (WGCNA), we identified 83 hub genes by integrating gene expression profiles with clinical pathological grades.
View Article and Find Full Text PDFCancer
February 2025
General Medicine Service, VA Puget Sound Health Care System, Seattle, Washington, USA.
Background: Breast cancer screening (BCS) inequities are evident at national and local levels, and many health systems want to address these inequities, but may lack data about contributing factors. The objective of this study was to inform health system interventions through an exploratory analysis of potential multilevel contributors to BCS inequities using health system data.
Methods: The authors conducted a cross-sectional analysis within a large academic health system including 19,774 individuals who identified as Black (n = 1445) or White (n = 18,329) race and were eligible for BCS.
J Adv Nurs
January 2025
Anesthesiology Department, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, Hebei, China.
Cancer
February 2025
Departmental Unit of Molecular and Genomic Diagnostics, Genomics Core Facility, G-STeP, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.
Background: To date, 11 DNA polymerase epsilon (POLE) pathogenic variants have been declared "hotspot" mutations. Patients with endometrial cancer (EC) characterized by POLE hotspot mutations (POLEmut) have exceptional survival outcomes. Whereas international guidelines encourage deescalation of adjuvant treatment in early-stage POLEmut EC, data regarding safety in POLEmut patients with unfavorable characteristics are still under investigation.
View Article and Find Full Text PDFStat Med
February 2025
Department of Mathematical Sciences, University of Texas at Dallas, Richardson, Texas, USA.
Multi-gene panel testing allows efficient detection of pathogenic variants in cancer susceptibility genes including moderate-risk genes such as ATM and PALB2. A growing number of studies examine the risk of breast cancer (BC) conferred by pathogenic variants of these genes. A meta-analysis combining the reported risk estimates can provide an overall estimate of age-specific risk of developing BC, that is, penetrance for a gene.
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