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Philipp Y. Maximov
Researcher at University of Texas MD Anderson Cancer Center
Publications - 39
Citations - 917
Philipp Y. Maximov is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Tamoxifen & Breast cancer. The author has an hindex of 14, co-authored 38 publications receiving 737 citations. Previous affiliations of Philipp Y. Maximov include Fox Chase Cancer Center & Georgetown University.
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The discovery and development of selective estrogen receptor modulators (SERMs) for clinical practice.
TL;DR: The discovery and development of the group of medicines called SERMs are described and these drugs have been shown to be comparably effective to conventional hormone replacement therapy in animal models, with potential indications for an improved safety profile.
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Molecular mechanism of action of bisphenol and bisphenol A mediated by oestrogen receptor alpha in growth and apoptosis of breast cancer cells
TL;DR: The molecular mechanism of oestrogen‐agonistic/antagonistic action of structurally similar ligands, bisphenol (BP) and bispenol A (BPA) on cell proliferation and apoptosis of ERα + ve breast cancer cells is determined.
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Models and Mechanisms of Acquired Antihormone Resistance in Breast Cancer: Significant Clinical Progress Despite Limitations.
TL;DR: This review focuses on the critical role of the few ER-positive cell lines (MCF-7, T47D, BT474, ZR-75-1) that continue to advance the understanding of the estrogen-regulated biology of breast cancer.
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Structure Function Relationships of Estrogenic Triphenylethylenes Related to Endoxifen and 4-Hydroxytamoxifen
TL;DR: 1,1,2-Triphenylethylene (TPE) derivatives were synthesized and evaluated against 17beta-estradiol (E2) for their estrogenic activity in MCF-7 human breast cancer cells and confirmed E2 as a class I estrogen and the TPEs as class II estrogens.
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Estrogen Receptor Mutations Found in Breast Cancer Metastases Integrated With the Molecular Pharmacology of Selective ER Modulators
TL;DR: The consistent reports of mutations at Asp538 and Tyr537 in helix 12 of the ligand-binding domain (LBD) of estrogen receptors (ERs) from antihormone-resistant breast cancer metastases constitute an important advance, thereby confirming an additional mechanism of acquired resistance to antiHormone therapy through cell population selection pressure and enrichment during treatment.