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Titlebook: Hormonal Carcinogenesis IV; Jonathan J. Li (Profesor of Pharmacology, Toxicolo Book 2005 Springer-Verlag US 2005 biology.cancer.carcinogen

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書(shū)目名稱(chēng)Hormonal Carcinogenesis IV
編輯Jonathan J. Li (Profesor of Pharmacology, Toxicolo
視頻videohttp://file.papertrans.cn/429/428279/428279.mp4
概述Covers a group of hormonally-associated cancers that present interesting challenges to clinicians and biomedical researchers.Addresses vital questions that impact our understanding of the causation, d
圖書(shū)封面Titlebook: Hormonal Carcinogenesis IV;  Jonathan J. Li (Profesor of Pharmacology, Toxicolo Book 2005 Springer-Verlag US 2005 biology.cancer.carcinogen
描述It has been over a decade since the First International Symposium on Hormonal Carcinogenesis convened in 199 1. Since then, the field has rapidly expanded with considerable progress in both breast and prostate cancers; while ovarian and endometrial cancer have been hampered, in part, due to the absence of suitable hormone-mediated animal models. While knock-out, transgenic, and cell-culture systems have been extremely useful in identifying specific genelprotein alterations and the ensuing pathways affected, the precise molecular mechanisms whereby sex hormones elicit their oncogenic effects still remain elusive. Moreover, despite the considerable progress made in breast cancer research, the exact role of progestins in the presence or absence of estrogen in breast growth, differentiation, and malignant transformation is lacking. Elucidating the incipient molecular alterations in earlylpre-invasive lesions elicited by these hormones is a growing important focus of this field. The main purpose of these Symposia has been to address vital questions that impact our understanding of the causation, dependency, progression, resistance, and prevention of hormonally-associated cancers. We are
出版日期Book 2005
關(guān)鍵詞biology; cancer; carcinogenesis; cell; endometrium; hormones; liver; metabolism; molecular biology; ovarian c
版次1
doihttps://doi.org/10.1007/b102371
isbn_ebook978-0-387-23761-9
copyrightSpringer-Verlag US 2005
The information of publication is updating

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Aromatase Overexpression: Effect of Tissue Estrogen on Phenotypic and Biochemical Changes in Aromatac activity are susceptible to carcinogens. The ARO overexpression-induced MG changes were inhibited with very low letrazole doses, an ARO inhibitor without any effect on normal physiology. The potential clinical importance of this intracrine growth support may provide future clinical and laboratory investigations.
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Deregulation of Cyclin E and Genomic Instabilityrelative to the cell cycle, which can occur if the normal pathway of cyclin E turnover is inactivated. The resulting expression of cyclin E at inappropriate times of the cell cycle can then interfere with efficient progression through both S phase and M phase. Although not yet proven, we propose tha
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Prostate Epithelial Carcinogenesis: Putative and Controversial Precursor Lesionsying genotype of PCA. This should set the stage for the development of new prognostic and therapeutic strategies. The understanding of genetic events which occur during the progression of PIN and other preneoplastic lesions to PCA would be useful for prevention, early detection, and treatment of thi
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Estrogen Can Prevent Breast Cancer by Mimicking the Protective Effect of Pregnancy to MC. All are: susceptible to initiation and development of latent cancers; have a drastically reduced incidence of overt mammary cancers; have a decreased promotional environment with persistently reduced circulatory levels of GH and PRL, as well as a decreased expression of ERα and PRs in the ME
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