G
Gauri Sabnis
Researcher at University of Maryland, Baltimore
Publications - 65
Citations - 2223
Gauri Sabnis is an academic researcher from University of Maryland, Baltimore. The author has contributed to research in topics: Aromatase & Aromatase inhibitor. The author has an hindex of 27, co-authored 65 publications receiving 2044 citations. Previous affiliations of Gauri Sabnis include West Coast University & University of Maryland Marlene and Stewart Greenebaum Cancer Center.
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Aromatase, aromatase inhibitors, and breast cancer.
TL;DR: Three aromatase inhibitors (AIs) are now FDA approved and have been shown to be more effective than the antiestrogen tamoxifen and are well tolerated and are now a standard treatment for postmenopausal patients.
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Role of Androgens on MCF-7 Breast Cancer Cell Growth and on the Inhibitory Effect of Letrozole
TL;DR: It is reported that androgens, such as the aromatizable androstenedione and the non-aromatizable 5alpha-dihydrotestosterone, inhibit MCF-7 cell proliferation and suppression of the estrogen-induced antiapoptotic protein Bcl-2 may be involved in the antiproliferative effects of androgens and letrozole.
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Functional Activation of the Estrogen Receptor-α and Aromatase by the HDAC Inhibitor Entinostat Sensitizes ER-Negative Tumors to Letrozole
TL;DR: The results show that ENT treatment can be used to restore the letrozole responsiveness of ER-negative tumors, and provide a strong rationale for immediate clinical evaluation of combinations of histone deacetylase and aromatase inhibitors to treat ER- negative and endocrine-resistant breast cancers.
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Activation of Mitogen-Activated Protein Kinase in Xenografts and Cells during Prolonged Treatment with Aromatase Inhibitor Letrozole
TL;DR: Combined treatment with ER down-regulator fulvestrant and letrozole prevented increases in erbB-2 and activation of MAPK and was highly effective in inhibiting tumor growth throughout 29 weeks of treatment.
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Trastuzumab reverses letrozole resistance and amplifies the sensitivity of breast cancer cells to estrogen.
TL;DR: It is suggested that LTLT-Ca cells survive estrogen deprivation by activation of Her-2/mitogen-activated protein kinase (MAPK) pathway, and trastuzumab is beneficial in hormone-refractory cells and xenografts by restoring ER, implicating Her- 2 as a negative regulator of ERalpha.