Histone Deacetylase Inhibitors as Cancer Therapeutics, by Steven Grant

By Steven Grant

Advances in melanoma Research offers priceless info at the intriguing and fast-moving box of melanoma examine. This thematic quantity seems at "Histone Deacetylase Inhibitors as melanoma Therapeutics."

  • Provides necessary details at the interesting and fast-moving box of melanoma research
  • This thematic quantity seems to be at "Histone Deacetylase Inhibitors as melanoma Therapeutics"
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Extra info for Histone Deacetylase Inhibitors as Cancer Therapeutics, Volume 116

Sample text

W. (2007). Propagation of centromeric chromatin requires exit from mitosis. The Journal of Cell Biology, 176, 795–805. , Antinore, M. , Lung, F. , et al. (2000). The GADD45 inhibition of Cdc2 kinase correlates with GADD45-mediated growth suppression. The Journal of Biological Chemistry, 275, 16602–16608. Histone Deacetylase Inhibitors Disrupt the Mitotic Spindle Assembly Checkpoint 31 Kasuboski, J. , Bader, J. , Vaughan, P. , Tauhata, S. , Morrissey, M. , et al. (2011). Zwint-1 is a novel Aurora B substrate required for the assembly of a dynein-binding platform on kinetochores.

Et al. (2004). Class I histone deacetylase-selective novel synthetic inhibitors potently inhibit human tumor proliferation. Clinical Cancer Research, 10, 5271–5281. Peart, M. , Smyth, G. , van Laar, R. , Bowtell, D. , Richon, V. , Marks, P. , et al. (2005). Identification and functional significance of genes regulated by structurally different histone deacetylase inhibitors. Proceedings of the National Academy of Sciences of the United States of America, 102, 3697–3702. Peart, M. , Tainton, K.

S. , 2010; Marks & Breslow, 2007). Over 20 chemically different HDAC inhibitors are in clinical trials for hematological malignancies and solid tumors. This review considers the mechanisms of resistance to HDAC inhibitors that have been identified which account for the selective effects of these agents in inducing cancer but not normal cell death. These mechanisms, such as functioning Chk1, high levels of thioredoxin, or the prosurvival BCL-2, may also contribute to resistance of cancer cells to HDAC inhibitors.

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