P
Paul A. Marks
Researcher at Memorial Sloan Kettering Cancer Center
Publications - 101
Citations - 23770
Paul A. Marks is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: Histone deacetylase & Vorinostat. The author has an hindex of 54, co-authored 101 publications receiving 22861 citations. Previous affiliations of Paul A. Marks include Kettering University & Cornell University.
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Journal ArticleDOI
Histone deacetylases and cancer: causes and therapies.
Paul A. Marks,Richard A. Rifkind,Victoria M. Richon,Ronald Breslow,Thomas E. Miller,William Kevin Kelly +5 more
TL;DR: Together, histone acetyltransferases and histone deacetylases determine the acetylation status of histones, and inhibitors of HDACs have been found to cause growth arrest, differentiation and/or apoptosis of many tumours cells by altering the transcription of a small number of genes.
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Structures of a histone deacetylase homologue bound to the TSA and SAHA inhibitors.
Michael S. Finnin,Jill R. Donigian,Alona Cohen,Victoria M. Richon,Richard A. Rifkind,Paul A. Marks,Ronald Breslow,Nikola P. Pavletich +7 more
TL;DR: The structure of the histone deacetylase catalytic core is described, as revealed by the crystal structure of a homologue from the hyperthermophilic bacterium Aquifex aeolicus, and it is established that the residues that make up the active site and contact the inhibitors are conserved across the HDAC family.
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Histone deacetylase inhibitors: molecular mechanisms of action
TL;DR: This review focuses on the mechanisms of action of histone deacetylase ( HDAC) inhibitors (HDACi), a group of recently discovered ‘targeted’ anticancer agents that induces different phenotypes in various transformed cells.
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Histone Deacetylase Inhibitors: Inducers of Differentiation or Apoptosis of Transformed Cells
TL;DR: The working hypothesis is that inhibition of HDAC activity leads to the modulation of expression of a specific set of genes that, in turn, result in growth arrest, differentiation, and/or apoptotic cell death.
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Histone deacetylase inhibitor selectively induces p21WAF1 expression and gene-associated histone acetylation.
TL;DR: The present findings indicate that the induction of p21(WAF1) by SAHA is regulated, at least in part, by the degree of acetylation of the gene-associated histones and that this induced increase in acetylations is gene selective.