title: Histone modifications as a platform for cancer therapy.
abstract: Tumorigenesis and metastasis are a progression of events resulting from alterations in the processing of the genetic information. These alterations result from stable genetic changes (mutations) involving tumor suppressor genes and oncogenes (e.g., ras, BRAF) and potentially reversible epigenetic changes, which are modifications in gene function without a change in the DNA sequence. Mutations of genes coding for proteins that directly or indirectly influence epigenetic processes will alter the cell's gene expression program. Epigenetic mechanisms often altered in cancer cells are DNA methylation and histone modifications (acetylation, methylation, phosphorylation). This article will review the potential of these reversible epigenetic processes as targets for cancer therapies.
authors.affiliation: Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Manitoba, R3E 0V9, Canada.
authors.forename: Paula S
authors.initials: PS
authors.lastname: Espino
authors.forename: Bojan
authors.initials: B
authors.lastname: Drobic
authors.forename: Katherine L
authors.initials: KL
authors.lastname: Dunn
authors.forename: James R
authors.initials: JR
authors.lastname: Davie
mesh_terms: D002843:Chromatin / Q000378:metabolism; D019175:DNA Methylation; D004791:Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D056572:Histone Deacetylase Inhibitors; D006657:Histones / Q000737:chemistry*; D006801:Humans; D008745:Methylation; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009369:Neoplasms / Q000628:therapy*; D010766:Phosphorylation; D015398:Signal Transduction
chemical_list: D002843:Chromatin; D004791:Enzyme Inhibitors; D056572:Histone Deacetylase Inhibitors; D006657:Histones; D020928:Mitogen-Activated Protein Kinases