PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Permanent URI for this collectionhttps://hdl.handle.net/11147/7645
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Article Citation - WoS: 103Citation - Scopus: 112Perinatal Exposure To Bisphenol a Increases Adult Mammary Gland Progesterone Response and Cell Number(The Endocrine Society, 2011) Ayyanan, Ayyakkannu; Laribi, Ouahiba; Schuepbach-Mallepell, Sonia; Schrick, Christina; Gutierrez, Maria; Tanos, Tamara; Lefebvre, Gregory; Rougemont, Jacques; Yalçın Özuysal, Özden; Brisken, CathrinBisphenol A [BPA, 2,2,-bis (hydroxyphenyl) propane] is one of the highest-volume chemicals produced worldwide. It is detected in body fluids of more than 90% of the human population. Originally synthesized as an estrogenic compound, it is currently utilized to manufacture food and beverage containers resulting in uptake with food and drinks. There is concern that exposure to low doses of BPA, defined as less than or equal to 5 mg/kg body weight /d, may have developmental effects on various hormone-responsive organs including the mammary gland. Here, we asked whether perinatal exposure to a range of low doses of BPA is sufficient to alter mammary gland hormone response later on in life, with a possible impact on breast cancer risk. To mimic human exposure, we added BPA to the drinking water of C57/Bl6 breeding pairs. Analysis of the mammary glands of their daughters at puberty showed that estrogen-dependent transcriptional events were perturbed and the number of terminal end buds, estrogen-induced proliferative structures, was altered in a dose-dependent fashion. Importantly, adult females showed an increase in mammary epithelial cell numbers comparable to that seen in females exposed to diethylbestrol, a compound exposure to which was previously linked to increased breast cancer risk. Molecularly, the mRNAs encoding Wnt-4 and receptor activator of nuclear factor kB ligand, two key mediators of hormone function implicated in control of mammary stem cell proliferation and carcinogenesis, showed increased induction by progesterone in the mammary tissue of exposed mice. Thus, perinatal exposure to environmentally relevant doses of BPA alters long-term hormone response that may increase the propensity to develop breast cancer. © 2011 by The Endocrine Society.Article Citation - WoS: 72Citation - Scopus: 75The Effects of Estrogen, Progesterone, and C-Erbb Receptor States on 18f-Fdg Uptake of Primary Breast Cancer Lesions(Society of Nuclear Medicine and Molecular Imaging, 2007) Mavi, Ayşe; Çermik, Tevfik F.; Urhan, Muammer; Püskülcü, Halis; Basu, Sandip; Yu, Jian Q.; Zhuang, Hongming; Czerniecki, Brian; Alavi, AbassThe purpose of this prospective study was to investigate whether correlations exist between 18F-FDG uptake of primary breast cancer lesions and predictive and prognostic factors such as estrogen receptor (ER), progesterone receptor (PR), and C-erbB-2 receptor (C-erbB-2R) states. Methods: Before undergoing partial or total mastectomy, 213 patients with newly diagnosed breast cancer underwent 18F-FDG PET (5.2 MBq/kg of body weight). The maximum standardized uptake value (SUV) of the primary lesion was measured in each patient. Standard immunohistochemistry was performed on a surgical specimen of the cancer lesion to characterize the receptor state of the tumor cells. Pearson χ2 tests were performed on the cross-tables of different receptor states to test any association that may exist among ER, PR, and C-erbB-2R. Maximum SUV measurements for different receptor states were compared using factorial ANOVA in a completely random design. Results: After exclusion of certain lesions, 118 lesions were analyzed for this study. The mean maximum SUVs of ER-positive and ER-negative lesions were 3.03 ± 0.26 and 5.64 ± 0.75, whereas those of PR were 3.24 ± 0.29 and 4.89 ± 0.67, respectively, and those of C-erbB-2R were 4.64 ± 0.70 and 3.70 ± 0.35, respectively, χ2 tests for ER and PR showed that if one is positive then the other tends to be positive as well (χ2 = 71.054, P < 0.01). For ER and C-erbB-2R states, if ER is positive, C-erbB-2R will more likely be negative (χ2 = 13.026, P < 0.01). No relationship was detected between PR and C-erbB-2R states (χ2 = 3.695, P > 0.05). ANOVAs showed that PR state alone (F = 0.095, P > 0.05) and C-erbB-2R state alone (F = 0.097, P > 0.05) had no effect on 18F-FDG uptake but ER state alone had an effect (F = 9.126, P < 0.01). ER and PR being together had no additional effect on 18F-FDG uptake. Our study also demonstrated that interactions exist between ER and C-erbB-2R state and between PR and C-erbB-2R state. Conclusion: SUV measurements may provide valuable information about the state of ER, PR, and C-erbB-2R and the associated glucose metabolism as measured by 18F-FDG uptake of the primary breast cancer lesions. Such an association may be of importance to treatment planning and outcome in these patients.