The Experts below are selected from a list of 136155 Experts worldwide ranked by ideXlab platform
J. Larry Jameson - One of the best experts on this subject based on the ideXlab platform.
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Mechanisms by Which Thyroid Hormone Receptor Mutations Cause Clinical Syndromes of Resistance to Thyroid Hormone
Thyroid, 1994Co-Authors: J. Larry JamesonAbstract:Resistance to thyroid Hormone (RTH) is an autosomal dominant disorder that is caused by mutations in the thyroid Hormone Receptor β (TRβ) gene. The thyroid Hormone Receptor is a nuclear Receptor th...
Fabrice Andre - One of the best experts on this subject based on the ideXlab platform.
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alpelisib for pik3ca mutated Hormone Receptor positive advanced breast cancer
The New England Journal of Medicine, 2019Co-Authors: Fabrice Andre, G Rubovszky, Ingrid A Mayer, Hiroji Iwata, Hope S Rugo, E. Ciruelos, Pierfranco Conte, Sibylle Loibl, Bella KaufmanAbstract:Abstract Background PIK3CA mutations occur in approximately 40% of patients with Hormone Receptor (HR)–positive, human epidermal growth factor Receptor 2 (HER2)–negative breast cancer. The PI3Kα-sp...
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palbociclib in Hormone Receptor positive advanced breast cancer
The New England Journal of Medicine, 2015Co-Authors: Nicholas C Turner, Hiroji Iwata, Fabrice Andre, Sibylle Loibl, Sherene Loi, Sunil Verma, N Harbeck, Cynthia Huang Bartlett, Ke Zhang, Carla GiorgettiAbstract:BackgroundGrowth of Hormone-Receptor–positive breast cancer is dependent on cyclin-dependent kinases 4 and 6 (CDK4 and CDK6), which promote progression from the G1 phase to the S phase of the cell cycle. We assessed the efficacy of palbociclib (an inhibitor of CDK4 and CDK6) and fulvestrant in advanced breast cancer. MethodsThis phase 3 study involved 521 patients with advanced Hormone-Receptor–positive, human epidermal growth factor Receptor 2–negative breast cancer that had relapsed or progressed during prior endocrine therapy. We randomly assigned patients in a 2:1 ratio to receive palbociclib and fulvestrant or placebo and fulvestrant. Premenopausal or perimenopausal women also received goserelin. The primary end point was investigator-assessed progression-free survival. Secondary end points included overall survival, objective response, rate of clinical benefit, patient-reported outcomes, and safety. A preplanned interim analysis was performed by an independent data and safety monitoring committee af...
John W M Martens - One of the best experts on this subject based on the ideXlab platform.
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characterizing steroid Hormone Receptor chromatin binding landscapes in male and female breast cancer
Nature Communications, 2018Co-Authors: Tesa M Severson, Yongsoo Kim, Stacey E P Joosten, Karianne Schuurman, Petra Van Der Groep, Cathy B Moelans, Natalie D Ter Hoeve, Quirine F Manson, John W M MartensAbstract:Male breast cancer (MBC) is rare and largely hormonally driven. Here, the authors examine the action of steroid Hormone Receptors in male and female breast cancers and find gender selective Hormone Receptor action that associates with the survival of MBC patients.
Mark E Sherman - One of the best experts on this subject based on the ideXlab platform.
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etiology of Hormone Receptor defined breast cancer a systematic review of the literature
Cancer Epidemiology Biomarkers & Prevention, 2004Co-Authors: Michelle D Althuis, Jennifer H Fergenbaum, Montserrat Garciaclosas, Louise A Brinton, Patricia M Madigan, Mark E ShermanAbstract:Breast cancers classified by estrogen Receptor (ER) and/or progesterone Receptor (PR) expression have different clinical, pathologic, and molecular features. We examined existing evidence from the epidemiologic literature as to whether breast cancers stratified by Hormone Receptor status are also etiologically distinct diseases. Despite limited statistical power and nonstandardized Receptor assays, in aggregate, the critically evaluated studies ( n = 31) suggest that the etiology of Hormone Receptor–defined breast cancers may be heterogeneous. Reproduction-related exposures tended to be associated with increased risk of ER-positive but not ER-negative tumors. Nulliparity and delayed childbearing were more consistently associated with increased cancer risk for ER-positive than ER-negative tumors, and early menarche was more consistently associated with ER-positive/PR-positive than ER-negative/PR-negative tumors. Postmenopausal obesity was also more consistently associated with increased risk of Hormone Receptor–positive than Hormone Receptor–negative tumors, possibly reflecting increased estrogen synthesis in adipose stores and greater bioavailability. Published data are insufficient to suggest that exogenous estrogen use (oral contraceptives or Hormone replacement therapy) increase risk of Hormone-sensitive tumors. Risks associated with breast-feeding, alcohol consumption, cigarette smoking, family history of breast cancer, or premenopausal obesity did not differ by Receptor status. Large population-based studies of determinants of Hormone Receptor–defined breast cancers defined using state-of-the-art quantitative immunostaining methods are needed to clarify the role of ER/PR expression in breast cancer etiology.
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etiology of Hormone Receptor defined breast cancer a systematic review of the literature
Cancer Epidemiology Biomarkers & Prevention, 2004Co-Authors: Michelle D Althuis, Jennifer H Fergenbaum, Montserrat Garciaclosas, Louise A Brinton, Patricia M Madigan, Mark E ShermanAbstract:Breast cancers classified by estrogen Receptor (ER) and/or progesterone Receptor (PR) expression have different clinical, pathologic, and molecular features. We examined existing evidence from the epidemiologic literature as to whether breast cancers stratified by Hormone Receptor status are also etiologically distinct diseases. Despite limited statistical power and nonstandardized Receptor assays, in aggregate, the critically evaluated studies ( n = 31) suggest that the etiology of Hormone Receptor–defined breast cancers may be heterogeneous. Reproduction-related exposures tended to be associated with increased risk of ER-positive but not ER-negative tumors. Nulliparity and delayed childbearing were more consistently associated with increased cancer risk for ER-positive than ER-negative tumors, and early menarche was more consistently associated with ER-positive/PR-positive than ER-negative/PR-negative tumors. Postmenopausal obesity was also more consistently associated with increased risk of Hormone Receptor–positive than Hormone Receptor–negative tumors, possibly reflecting increased estrogen synthesis in adipose stores and greater bioavailability. Published data are insufficient to suggest that exogenous estrogen use (oral contraceptives or Hormone replacement therapy) increase risk of Hormone-sensitive tumors. Risks associated with breast-feeding, alcohol consumption, cigarette smoking, family history of breast cancer, or premenopausal obesity did not differ by Receptor status. Large population-based studies of determinants of Hormone Receptor–defined breast cancers defined using state-of-the-art quantitative immunostaining methods are needed to clarify the role of ER/PR expression in breast cancer etiology.
Bella Kaufman - One of the best experts on this subject based on the ideXlab platform.
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alpelisib for pik3ca mutated Hormone Receptor positive advanced breast cancer
The New England Journal of Medicine, 2019Co-Authors: Fabrice Andre, G Rubovszky, Ingrid A Mayer, Hiroji Iwata, Hope S Rugo, E. Ciruelos, Pierfranco Conte, Sibylle Loibl, Bella KaufmanAbstract:Abstract Background PIK3CA mutations occur in approximately 40% of patients with Hormone Receptor (HR)–positive, human epidermal growth factor Receptor 2 (HER2)–negative breast cancer. The PI3Kα-sp...