Burger's Medicinal Chemistry and Drug Discovery, by Donald J. Abraham

By Donald J. Abraham

This is often quantity five: Chemotherapeutic brokers, of Burger's Medicinal Chemistry and Drug Discovery, sixth version. This new quantity comprises severe new chapters on Molecular Biology of melanoma, artificial Anti-angiogenic brokers and Selective Toxicities.

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Prevention strategies are now focusing on pre-invasive, yet neoplastic lesions. Prevention strategies generally influence one or more of five processes in carcinogenesis (99). One strategy has been to inhibit carcinogen-induced initiation events, which lead to DNA damage. An important caveat to this strategy is that the intervention must be present at the time of carcinogen exposure to be effective. Once irreversible DNA damage has occurred, this type of strategy is ineffective in preventing cancer development.

To circumvent this, cis-acting viral sequences, such as long terminal repeats (LTRs), transfer RNA (tRNA)primer binding sites, and polypurine tracts, have been used for developing packaging systems of retrovirus vectors. Many recombinant retrovirus vectors are designed to express two genes, one of which is often a selectable marker. New strategies for expression, such as splicing, transcription from heterologous promoters, and translation directed by an internal ribosome entry signal (IRES), have been used for expression of the second gene.

Elimination of p53 function leads to increased rates of mutation and resistance to apoptosis. Thus, p53 sits a t the crux of several biochemical pathways that are disrupted during tumorigenesis. Consequently, mutations in p53 are the most frequent genetic change encountered in human cancers. p53 activity can be eliminated by at least three mechanisms. The most common event that leads to a nonfunctioning protein is mutation of the p53 gene, which occurs in about 50% of all sporadic human tumors.

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