Background: Estrogen receptor (ER)- and progesterone receptor (PR)-negative (ER-PR-) breast cancer is associated with higher grade and poorer prognosis compared with other breast cancer subtypes. High parity, coupled with lack of breastfeeding, has been associated with an increased risk of ER-PR- cancer. The mechanism of this etiology is unclear, and may be obfuscated by ER and PR correlation with each other as well as other prognostic tumor characteristics. Methods: Using population-based and clinic-based ascertained cases and controls from the Breast Cancer Family Registry, I examined reproductive risk factors, including parity, breastfeeding, and oral contraceptive (OC) use, in relation to ER and PR status, using polytomous logistic regression (for the population-based data) and the method of generalized estimating equations (GEE) (for the clinic-based data) as well as the pseudo-conditional likelihood approach, which accounts for correlated outcome variables. Results: High parity (≥ 3 live births) combined with lack of breastfeeding, was positively associated with ER-PR- tumors (odds ratio [OR]=1.57, 95% confidence interval [CI] 1.10-2.24, population-based cases vs. controls) relative to nulliparity. There was no association with ER-PR- tumors and parity in women who breastfed (OR=0.93, 95%CI 0.71-1.22) relative to nulliparous women. Associations with ER-PR- cancer were higher across all races/ethnicities among women who did not breastfeed compared with women who did. Population-based and clinic-based data were generally in agreement (OR=2.07, 95% CI 1.09-3.91, clinic-based cases vs. controls, relative to nulliparity). When adjusted for the correlation of PR-status and grade, to ER-status, the association between high parity +lack of breastfeeding and ER- status, was maintained. OC use before year 1975 was associated with an increased risk of ER-PR- tumors (OR=1.32, 95% CI 1.04-1.67, population-based data, cases vs. controls) relative to never use of OCs. For women who began OC use in 1975 or later there was no increased risk. Analysis of OC use in clinic-based data agreed with the findings of the population-based data. Conclusions: My findings support that there are modifiable factors for ER-PR- breast cancer, and that breastfeeding in particular may mitigate the increased risk of ER-PR-cancers seen from multiparity. The mechanism of both risk and risk mitigation may operate primarily through the estrogen, rather than progesterone, pathway.

Indiana University-Purdue University Indianapolis (IUPUI) / Hispanics are more likely to die from breast cancer compared to non - Hispanic whites matched on stage and age at diagnosis. Higher mortality rates among Hispanics are attributed to cancer - related disparities across the cancer continuum including later - stage detection. While research has shown that socioeconomic factors play a significant role in the development and maintenance of cancer - related disparities, differences persist when these factors are controlled. Thus far, research on cultural factors and cognitions surrounding cancer is limited. The current study investigated illness representations of cancer and their determinants among Hispanic men and women (N = 120) using a cross - sectional survey approach. The study sample was comprised of predominantly first generation, employed Hispanic women in their early - thirties from Mexico. Most had not resided in the U.S. for more than 5 - 9 years. Half of the sample reported an annual income of $20,001 - $30,000 and completing at least a middle school education. While the majority indicated that they did not have health insurance, most indicated that they did have a regular source of health care. Additionally, while most had not been diagnosed with cancer, nearly half of the sample knew of someone diagnosed with cancer. Descriptive data regarding illness identity, illness coherence, timeline, causes, consequences, and controllability are provided. Results suggest that demographic factors (i.e. acculturation, education, and income), cultural constructs (i.e. fatalism and familism), intrapersonal factors (state and trait anxiety), and previous experience with cancer were associated with illness representations of breast cancer. The study adds to theliterature by systematically investigate illness representations of breast cancer and their determinants among a diverse sample of Hispanic men and women. This is a significant first step that can be used to guide and develop effective and culturally appropriate interventions that ultimately reduce disparities across the cancer continuum.

This study investigated potential apoptotic and anti-proliferative effects of the phytochemicals, genistein and anthocyanin extract, as single and combined treatments in MCF-7 human breast cancer cells. Cells were exposed to single and combined treatments with the phytochemiclas for 48 and 72 hours. Cell viability was assessed using the MTT bioassay. Apoptosis induction was assessed using acridine orange ethidium bromide and rhodamine 123 ethidium bromide fluorescence assays. Both singe and combination treatments induced dose- and time-dependent apoptotic cell death in MCF-7 cells. The percentage of apoptosis was higher in combination treatments than single treatments with either phytochemical, although the difference was not statistically significant. The combination of genistein and anthocyanin extract peaked in efficacy at 48 hours of treatment, to exhibit significantly greater (P<. O5) dose- and time-dependent cell cytotoxicity than single treatments. This study reveals potential chemopreventive implications for the complementary effects of genistein and anthocyanin extract. / by Corine M. Stinson. / Thesis (M.S.)--Florida Atlantic University, 2011. / Includes bibliography. / Electronic reproduction. Boca Raton, Fla., 2011. Mode of access: World Wide Web.

Secular trends in breast cancer incidence in younger women suggest environmental factors, like exposure to environmental chemicals, may play a role in rising incidence. One of the strongest risk factors for developing breast cancer, next to family history, is high mammographic breast density, which is defined as the proportion of fibroglandular breast tissue relative to fat as seen on a mammogram. Phthalates, a ubiquitous endocrine disrupting chemical, have the potential to interfere with endogenous hormones like estrogen and androgens. There is growing evidence from animal and epidemiologic studies indicating distinct periods of heightened susceptibility to endocrine disrupting chemicals throughout the life course, particularly during critical windows of breast development. Exposure to hormonally active environmental chemicals like phthalates may be a modifiable risk factor for breast cancer, therefore reducing or eliminating exposure could have substantial public health benefits. The overarching goal of this dissertation was to assess the relationship between exposure to phthalates during two critical windows of susceptibility, the prenatal and pregnancy periods, and its effect on breast tissue composition in adolescence and adulthood. First, a comprehensive review of epidemiologic studies summarized the body of evidence for the association between phthalate exposure and intermediate markers known to be in the causal pathway of breast cancer risk (age at breast development, menarche, and breast tissue composition). This systematic review of the literature aimed to identify potential patterns of evidence by outcome and timing of exposure. Evidence from this review suggested that phthalate exposure during the prenatal and childhood periods may play a role in altering menarche. Findings for phthalate exposure and age at breast development were inconclusive. There was a considerable lack of epidemiologic data on phthalate exposure and breast tissue composition throughout the life course. Based on one study, there is a potential association between phthalate exposure during pre-puberty and altered breast tissue density in adolescent girls. No study assessed the relationship between phthalate exposure during the prenatal or pregnancy period and subsequent breast tissue composition. Second, an examination for the association between prenatal phthalate exposure and breast tissue composition measured in adolescence (Chapter 3) and the association between phthalate exposure during pregnancy and breast tissue composition measured during or after the postpartum transient period (Chapter 4) aimed to address this major gap identified from the comprehensive review. The empirical chapters of this dissertation used data from an ongoing longitudinal birth cohort study of mothers and their children conducted by the New York City Columbia Center for Children's Environmental Health and the Breast Cancer and the Environment Research Project (CCCEH-BCERP). The CCCEH-BCERP study cohort has prospective data on nine phthalate metabolite concentrations measured during the third trimester of pregnancy and breast tissue composition measured in a subsample of mother-daughter dyads. Notably, we used novel non-invasive methods (optical breast spectroscopy) in this younger cohort of mothers and daughters to objectively measure specific components of the bulk breast composition before mammography screening age. There was significant evidence of altered breast tissue composition in both mothers and daughters. For daughters (n=127, mean age 15.2 ± 1.9 years), prenatal exposures to select low molecular weight (LMW) and high molecular weight (HMW) phthalate metabolites altered overall breast density in opposing directions, which appears to be driven by significant altered percent breast water. There was a significant association between higher prenatal levels of a LMW phthalate metabolite (monobutyl phthalate) and lower levels of overall breast density (adjusted β = -0.32; 95% CI: -0.51, -0.13) and significant association between sum of di(2-ethylhexyl) phthalate (∑DEHP), a HMW phthalate metabolite, and higher levels of overall breast density in girls (adjusted β = 0.20; 95% CI: 0.05, 0.34). For mothers (n=133, mean age 41 ± 5.3 years at follow-up), there was a significant association between two LMW phthalate metabolites and lower levels of percent breast collagen. Additionally, there was a significant inverse relationship between levels of mono-(3-carboxypropyl), a HMW phthalate metabolite, and percent total hemoglobin of the breast (adjusted β =-0.03; 95% CI: -0.06, 0.00, p=0.05). Overall, this dissertation increased our understanding of the impact that exposure to phthalates during critical windows of susceptibility may have on specific components of the breast. Reducing exposure to both HMW and LMW phthalates may have an impact in reducing breast cancer risk, particularly for girls prenatally exposed, as there was stronger evidence of higher overall breast density and percent water from exposure to select HMW phthalates. Future prospective studies should confirm these results as findings might provide an opportunity for modifying potential breast cancer risk.

Breast cancer is the most common cancer and the second most common cause of cancer death in women. In 2008 there were 182,460 women diagnosed with breast cancer, and 40,480 women died of this disease. Breast cancer can be prevented by medical (tamoxifen or raloxifene) or surgical approaches (bilateral mastectomy or oophorectomy). Prevention is only recommended for women at high risk for developing breast cancer; therefore, proper risk calculation is essential in identifying women that may benefit from prevention measures. There is an easy-to-use and easily accessible risk calculation tool for determining a woman's risk of developing breast cancer and need for referral for counseling, gene testing, and possibly preventive therapy. This article reviews the components of risk assessment, the most frequently used risk calculation tool, and approaches to breast cancer risk reduction including medical and surgical therapies. The use of these therapies results in a risk reduction of 50-90%.

Breast cancer poses a serious public health concern. This case-control study describes the relationship of night-shift working on the development of breast cancer in 57 women diagnosed with breast cancer compared to 49 women with other types of cancer in the Vaal Triangle area (selected through non-probability purposive sampling from CANSA). The study revealed that women who work night-shift developed breast cancer 1.24 times more often than women who do not work nightshift (OR=1.24 [95% CI 0.52 to 2.89]). The odds ratio was further increased in women who worked rotating-shift (OR=1.44 [95% CI 0.58 to 3.59]). Night-shift work exposure was not statistically related to the development of breast cancer. It is recommended that the relationship between night-shift exposure and breast cancer risk be further explored through cross-sectional and cohort studies, and other breast cancer pathways. / Health Studies / M.A. (Public Health)

Breast cancer poses a serious public health concern. This case-control study describes the relationship of night-shift working on the development of breast cancer in 57 women diagnosed with breast cancer compared to 49 women with other types of cancer in the Vaal Triangle area (selected through non-probability purposive sampling from CANSA). The study revealed that women who work night-shift developed breast cancer 1.24 times more often than women who do not work nightshift (OR=1.24 [95% CI 0.52 to 2.89]). The odds ratio was further increased in women who worked rotating-shift (OR=1.44 [95% CI 0.58 to 3.59]). Night-shift work exposure was not statistically related to the development of breast cancer. It is recommended that the relationship between night-shift exposure and breast cancer risk be further explored through cross-sectional and cohort studies, and other breast cancer pathways. / Health Studies / M. A. (Public Health)