Breast Cancer And The Environment: A Life Cours... ((BETTER))
Along those lines, Hiatt adds, the National Institute of Environmental Health Sciences and the National Cancer Institute are collaborating on the Breast Cancer and the Environment Research Program, which recruits subjects starting at the age of 6 years. The two institutes also collaborate on the Interagency Breast Cancer and Environmental Research Coordinating Committee, a congressionally mandated body currently preparing a comprehensive report on federal research on the environmental and genomic factors related to breast cancer. This report is expected in mid-2012.
Breast Cancer and the Environment: A Life Cours...
Breast cancer remains the most common invasive cancer among women. The primary patients of breast cancer are adult women who are approaching or have reached menopause; 90 percent of new cases in U.S. women in 2009 were diagnosed at age 45 or older. Growing knowledge of the complexity of breast cancer stimulated a transition in breast cancer research toward elucidating how external factors may influence the etiology of breast cancer.
Breast Cancer and the Environment reviews the current evidence on a selection of environmental risk factors for breast cancer, considers gene-environment interactions in breast cancer, and explores evidence-based actions that might reduce the risk of breast cancer. The book also recommends further integrative research into the elements of the biology of breast development and carcinogenesis, including the influence of exposure to a variety of environmental factors during potential windows of susceptibility during the full life course, potential interventions to reduce risk, and better tools for assessing the carcinogenicity of environmental factors. For a limited set of risk factors, evidence suggests that action can be taken in ways that may reduce risk for breast cancer for many women: avoiding unnecessary medical radiation throughout life, avoiding the use of some forms of postmenopausal hormone therapy, avoiding smoking, limiting alcohol consumption, increasing physical activity, and minimizing weight gain.
Objectives: We examine (a) how breast cancer onset and survival are affected by various dimensions of early-life socioeconomic status (SES) and (b) the extent to which women's characteristics in adulthood mediate the associations between early-life conditions and breast cancer.
Results: Higher levels of mothers' education and early-life family income were associated with a greater risk of breast cancer incidence. The effect of mothers' education was mediated by women's adult SES and reproductive behaviors. Fathers' education was related negatively to breast cancer mortality, yet this effect was fully mediated by women's own education.
Discussion: This study identifies mechanisms linking early-life social environment to breast cancer onset and mortality. The findings emphasize the role of social factors in breast cancer incidence and survival.
Abstract:Advances in breast cancer science, early detection, and treatment have resulted in improvements in breast cancer survival but not in breast cancer incidence. After skin cancer, breast cancer is the most common cancer diagnosis in the United States. Each year, nearly a quarter million U.S. women receive a breast cancer diagnosis, and the number continues to rise each year with the growth in the population of older women. Although much remains to be understood about breast cancer origins and prevention, action can be taken on the existing scientific knowledge to address the systemic factors that drive breast cancer risk at the population level. The California Breast Cancer Research Program funded a team at Breast Cancer Prevention Partners (BCPP) to convene leaders in advocacy, policy, and research related to breast cancer prevention from across the state of California. The objective was the development of a strategic plan to direct collective efforts toward specific and measurable objectives to reduce the incidence of breast cancer. The structured, innovative approach used by BCPP to integrate scientific evidence with community perspectives provides a model for other states to consider, to potentially change the future trajectory of breast cancer incidence in the United States.Keywords: breast cancer; California; cancer plan; comprehensive cancer control; environmental exposure; incidence; intervention; policy; primary prevention; risk factor
Figure 1. The First D: Exposures occurring during a specific window like in utero may have an impact on risk for chronic disease/breast cancer but the same exposure at a different life stage will not have the same impact.
An integrative model of breast cancer research is needed to determine the impact and mechanisms of action of endocrine disruptors at different WOS. By focusing on environmental chemical exposure during specific WOS, scientists and their community partners may identify when prevention efforts are likely to be most effective.
Despite the considerable personal and societal burden from breast cancer, primary prevention efforts encounter challenges. Unlike other cancers that are linked to a predominant risk factor (e.g., smoking and lung cancer [1], human papillomavirus, and cervical cancer [2]), most established breast cancer risk factors have modest associations; moreover, many risk factors are not conducive to population-level intervention. The American Cancer Society guidelines for breast cancer prevention include limiting alcohol intake, avoiding post-menopausal hormone use, increasing physical activity, and maintaining a healthy body weight [3]. Yet even considering these factors, estimates indicate that a substantial proportion of breast cancer risk remains unexplained [4, 5].
BCERP framework. A model of transdisciplinary community-engaged research by epidemiologists, basic scientists, communication researchers, and advocates to examine environmental causes of breast cancer, as conducted by the Breast Cancer and the Environment Research Program (BCERP)
Breast cancer etiology appears to be driven in part by perturbations to breast tissue as well as alterations of the mammary gland micro-environment during critical windows. Here we briefly summarize breast tissue changes occurring during each WOS, review evidence that addresses environmental carcinogenesis during each WOS, and outline the motivation for ongoing research on the chemicals and metals targeted in BCERP.
The prenatal period is a particularly vulnerable WOS because breast tissue begins to develop in the embryonic stage when epidermal cells in concert with embryonic mesenchyme become breast buds [15,16,17,18]. Faster fetal growth and greater birth-weight increase breast cancer risk later in life [19,20,21]. Proposed mechanisms by which chemicals can alter normal mammary development trajectories [15, 18, 19, 22, 23] include changes in maternal hormone levels regulating development and sex differentiation, high levels of growth factors, potential DNA damage and mutations in germ cells, and other genetic or epigenetic processes [24].
Like DDT and other organochlorines, PAH are lipophilic and stored in fat tissue including breast tissue [36]. Most PAH compounds are weakly estrogenic and may induce cell proliferation via activation of the estrogen receptor (ER) [37]. Exposure to PAH was linked to mammary cancer in rodents [38]. PAH exposure has been measured directly in both blood [39] and breast tissue [40], and higher levels of PAH-DNA adducts have been found in breast cancer cases compared with women without breast cancer [41]. Similarly, breast cancer cases reported higher levels of PAH exposures than controls based on questionnaire assessments of indirect exposure [42,43,44,45,46]. For all these epidemiologic studies, specific WOS were not investigated. Because experimental and epidemiologic associations implicate prenatal PAH exposure in multiple adverse health effects including obesity [47,48,49], one focus of BCERP is the impact of PAH exposure during the prenatal WOS. BCERP research specifically addresses how exposure to PAH during the prenatal and pregnancy WOS may increase the development of mammary tumors in mice. Concurrent human studies within BCERP evaluate how prenatal PAH exposure alters breast tissue development and tissue composition in adolescent girls. 041b061a72