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Gary K. Scott

Researcher at Buck Institute for Research on Aging

Publications -  76
Citations -  33574

Gary K. Scott is an academic researcher from Buck Institute for Research on Aging. The author has contributed to research in topics: Estrogen receptor & Cancer. The author has an hindex of 40, co-authored 74 publications receiving 29688 citations. Previous affiliations of Gary K. Scott include Queen's University & University of California, San Francisco.

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Estrogen-dependent, tamoxifen-resistant tumorigenic growth of MCF-7 cells transfected with HER2/neu.

TL;DR: This pattern of hormone-dependent, TAM-resistant growth exhibited by the MCF/HER2–18 tumors in nude mice supports the possibility that p185HER2 overexpression in human breast cancers may be linked to therapeutic resistance.
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Coordinate suppression of ERBB2 and ERBB3 by enforced expression of micro-RNA miR-125a or miR-125b.

TL;DR: The feasibility of using miRNAs as a therapeutic strategy to suppress oncogene expression and function is illustrated by the use of human breast cancer cell line SKBR3 as a model for ERBB2 and ERBB3 dependence.
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Clinical development of histone deacetylase inhibitors as anticancer agents

TL;DR: An improved understanding of the mechanistic role of specific HDACs in human tumorigenesis, as well as the identification of more specificHDAC inhibitors, will likely accelerate the clinical development and broaden the future scope and utility of HDAC inhibitors for cancer treatment.
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Expression of microRNA-146 suppresses NF-κB activity with reduction of metastatic potential in breast cancer cells

TL;DR: Findings implicate miR-146a/b as a negative regulator of constitutive NF-κB activity in a breast cancer setting and suggest that modulating miR/b levels has therapeutic potential to suppress breast cancer metastases.
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Cell surface-bound IL-1α is an upstream regulator of the senescence-associated IL-6/IL-8 cytokine network

TL;DR: It is shown that cell surface-bound IL-1α is essential for signaling the senescence-associated secretion of IL-6 and IL-8, 2 proinflammatory cytokines that also reinforce the senescent growth arrest and regulates the biological effects of these cytokines.