Thomas B. Tomasi
State University of New York System
20 Papers
71 Citations
Thomas B. Tomasi is an academic researcher from State University of New York System. The author has contributed to research in topics: Dicer & Biology. The author has an hindex of 15, co-authored 20 publications. Previous affiliations of Thomas B. Tomasi include Roswell Park Cancer Institute.
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Papers
Activation of MHC Class I, II, and CD40 Gene Expression by Histone Deacetylase Inhibitors
William J. Magner,A. Latif Kazim,Carleton C. Stewart,Michelle A. Romano,Geoffrey Catalano,Catherine Grande,Nicholas W. Keiser,Frank Santaniello,Thomas B. Tomasi +8 more
TL;DR: It is shown that histone deacetylase inhibitors that alter the acetylation of histones in chromatin enhance the expression of several genes on tumor cells including: MHC class I, II, and the costimulatory molecule CD40.
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Histone deacetylase inhibitors induce TAP, LMP, Tapasin genes and MHC class I antigen presentation by melanoma cells.
TL;DR: The data indicate that epigenetic modification can convert a tumor cell to an antigen presenting cell capable of activating IFN-γ secreting T cells via the class I pathway and suggest that the abnormalities, observed in some tumors in the expression of MHC class I antigen processing and presentation molecules, may result from epigenetic repression.
miRNA regulation of cytokine genes.
TL;DR: This review discusses specific examples of regulation of cytokine genes and focuses on a new mechanism involving post-transcriptional regulation via miRNAs, a pre-requisite for regulating the half-life of many cytokines and achieving the temporal and spatial distributions required for regulation of these genes.
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Exosomes from plasmacytoma cells as a tumor vaccine.
TL;DR: It is concluded that exosomes can induce tumor-specific immunity and prevent tumor development and are a potential strategy for future therapeutic tumor vaccination.
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Histone deacetylase regulation of immune gene expression in tumor cells
TL;DR: Data is reviewed suggesting that selection of target specific HDACi and combinations with other agents and modalities, including those that activate stress pathways, may further enhance the efficacy of epigenetic therapies.
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