about
Upregulation of AIB1, aromatase and ERα provides long-term estrogen-deprived human breast cancer cells with a mechanistic growth advantage for survivalNovel retinoic acid metabolism blocking agents have potent inhibitory activities on human breast cancer cells and tumour growth.Intrauterine growth retardation associated with precocious puberty and sertoli cell hyperplasia.Sensitivity to the aromatase inhibitor letrozole is prolonged after a "break" in treatment.GP88 (PC-Cell Derived Growth Factor, progranulin) stimulates proliferation and confers letrozole resistance to aromatase overexpressing breast cancer cellsProlonging hormone sensitivity in prostate cancer xenografts through dual inhibition of AR and mTOR.The prodrug DHED selectively delivers 17β-estradiol to the brain for treating estrogen-responsive disorders.Treatment with an orally bioavailable prodrug of 17β-estradiol alleviates hot flushes without hormonal effects in the periphery.Aromatase resistance mechanisms in model systems in vivo.Functional activation of the estrogen receptor-α and aromatase by the HDAC inhibitor entinostat sensitizes ER-negative tumors to letrozoleToremifene-atamestane; alone or in combination: predictions from the preclinical intratumoral aromatase modelThe Coffey Lecture: steroidogenic enzyme inhibitors and hormone dependent cancerAromatase inhibitors and xenograft studies.Adaptive changes result in activation of alternate signaling pathways and acquisition of resistance to aromatase inhibitorsTherapeutic observations in MCF-7 aromatase xenografts.Stopping treatment can reverse acquired resistance to letrozole.Trastuzumab reverses letrozole resistance and amplifies the sensitivity of breast cancer cells to estrogen.HDAC inhibitor entinostat restores responsiveness of letrozole-resistant MCF-7Ca xenografts to aromatase inhibitors through modulation of Her-2Nonhypoxic regulation and role of hypoxia-inducible factor 1 in aromatase inhibitor resistant breast cancer.Adaptive changes results in activation of alternate signaling pathways and resistance to aromatase inhibitor resistance.Advances in mechanisms of resistance to aromatase inhibitors.mTOR inhibitors: changing landscape of endocrine-resistant breast cancer.Combined cancer therapy: strategies to overcome acquired aromatase inhibitor resistance.Histone deacetylase inhibitor entinostat in combination with a retinoid downregulates HER2 and reduces the tumor initiating cell population in aromatase inhibitor-resistant breast cancer.A nude mouse model of obesity to study the mechanisms of resistance to aromatase inhibitors.Histone Deacetylase Inhibitor Entinostat Inhibits Tumor-Initiating Cells in Triple-Negative Breast Cancer Cells.Histone deacetylase inhibitor entinostat reverses epithelial to mesenchymal transition of breast cancer cells by reversing the repression of E-cadherin.Effect of selumetinib on the growth of anastrozole-resistant tumors.The importance of HER2 signaling in the tumor-initiating cell population in aromatase inhibitor-resistant breast cancer.Understanding resistance to endocrine agents: molecular mechanisms and potential for intervention.Progress in aromatase research and identification of key future directions.Design, synthesis, and evaluation of novel mutual prodrugs (hybrid drugs) of all-trans-retinoic acid and histone deacetylase inhibitors with enhanced anticancer activities in breast and prostate cancer cells in vitro.Synergistic effect of a novel antiandrogen, VN/124-1, and signal transduction inhibitors in prostate cancer progression to hormone independence in vitro.Xenograft models for aromatase inhibitor studies.Inhibition of the phosphatidylinositol 3-kinase/Akt pathway improves response of long-term estrogen-deprived breast cancer xenografts to antiestrogens.Role of androgens on MCF-7 breast cancer cell growth and on the inhibitory effect of letrozole.Activation of mitogen-activated protein kinase in xenografts and cells during prolonged treatment with aromatase inhibitor letrozole.The role of growth factor receptor pathways in human breast cancer cells adapted to long-term estrogen deprivation.Seribantumab, an Anti-ERBB3 Antibody, Delays the Onset of Resistance and Restores Sensitivity to Letrozole in an Estrogen Receptor-Positive Breast Cancer Model.Model systems: mechanisms involved in the loss of sensitivity to letrozole.
P50
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P50
description
hulumtuese
@sq
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Gauri J Sabnis
@ast
Gauri J Sabnis
@en
Gauri J Sabnis
@es
Gauri J Sabnis
@nl
Gauri J Sabnis
@sl
type
label
Gauri J Sabnis
@ast
Gauri J Sabnis
@en
Gauri J Sabnis
@es
Gauri J Sabnis
@nl
Gauri J Sabnis
@sl
prefLabel
Gauri J Sabnis
@ast
Gauri J Sabnis
@en
Gauri J Sabnis
@es
Gauri J Sabnis
@nl
Gauri J Sabnis
@sl
P106
P21
P31
P496
0000-0001-8703-9394
P569
2000-01-01T00:00:00Z