Differential acetylation of histones and transcription factors plays an important regulatory role in developmental processes, proliferation and differentiation. Aberrant acetylation or deacetylation leads to such diverse disorders as leukemia, epithelial cancers, fragile X syndrome and Rubinstein-Taybi syndrome. The various groups of histone acetyltransferases (CBP/p300, GNAT, MYST, nuclear receptor coactivators and TAFII250) and histone deacetylases are surveyed with regard to their possible or known involvement in cancer progression and human developmental disorders. Current treatment strategies are discussed, which are still mostly limited to histone deacetylase inhibitors such as trichostatin A and butyrate.

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A simple and inexpensive method of condensing and linktransfection complexes deliver plasmid DNA to cells by the ing plasmid DNA to carrier adenovirus particles is adenovirus infectious route without interference from virus described. The synthetic polycation polyethylenimine is gene expression because psoralen-inactivated virus is used to condense plasmid DNA into positively charged 100 employed. The PEI-DNA-adenovirus complexes display nm complexes. These PEI-DNA complexes are then DNA delivery comparable to more sophisticated DNA virus bound to adenovirus particles through charge interactions complexes employing streptavidin/biotin linkage, but require with negative domains on the viral hexon. The resulting no special reagents and are much easier to prepare.

Single base pair mutations that alter the function of tumor suppressor genes and oncogenes occur frequently during oncogenesis. The guardian of the genome, p53, is inactivated by point mutation in more than 50% of human cancers. Synthetic small inhibiting RNAs (siRNAs) can suppress gene expression in mammalian cells, although their degree of selectivity might be compromised by an amplification mechanism. Here, we demonstrate that a single base difference in siRNAs discriminates between mutant and WT p53 in cells expressing both forms, resulting in the restoration of WT protein function. Therefore, siRNAs may be used to suppress expression of point-mutated genes and provide the basis for selective and personalized antitumor therapy.