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By Donald J. Abraham

This can be quantity five: Chemotherapeutic brokers, of Burger's Medicinal Chemistry and Drug Discovery, sixth variation. This new quantity includes serious new chapters on Molecular Biology of melanoma, man made Anti-angiogenic brokers and Selective Toxicities.

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88) found that when APC expression was induced in stably transfected APC-'colon cancer cells (using an inducible metallothionine promoter linked to the APC gene), they observed a time-dependent decrease in the RNA and protein levels of c-myc. This suggested that c-myc may be regulated by AF'C through the p-cateninlT-cell factor-4 (Tcf-4) transcription complex. They also showed that constitutive expression of mutant P-catenin (mutated so that it is insensitive to APC) in embryonic kidney cells resulted in a significant increase of c-myc expression.

Comprised of the serinelthereonine kinases. The best studied of these serine-threonine protein kinases is the raf oncogene, which is activated when it is recruited to the plasma membrane by . Raf then initiates a cas" ras (77). cade of mitogen-induced protein kinases (MAPKs), which culminate in the nucleus with the activation of genes containing Elk-1 transcription factor binding sites. Raf can also directly activate protein kinase C, which signals another set of kinases that phosphorylate the c-jun transcription factor.

10. Cell cycle control by the retinoblastoma (Rb)tumor suppressor protein. Unphosphorylated Rb negatively regulates progression into the S phase of the cell cycle by binding to the E2F transcription factor. In this complex, E2F is prevented from activating transcription of its target genes. During late G1, Rb is phosphorylated by the cyclin D/Cdk4 complex and can no longer sequester the E2F transcription factor. E2F then binds to its target S-phase genes, promoting their transcription and allowing the cell cycle to progress.

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