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Presence of myc is required for Gj-to-S transition, as described earlier, via Rb interactions. The protein functions as nuclear transcription factor for DNA replication enzymes. Expression of myc has also been shown to inhibit terminal differentiation and regulate apoptosis, presumably via interactions with gene promoter sequences. Activation of myc in neoplasia has been shown to occur by at least two mechanisms. First, myc amplification commonly occurs in neuroblastoma and small cell lung carcinoma.
Mutation). Some initiators mutate DNA directly. Others do so after being partially metabolized by the target cell's cytochrome p450 oxygenase system, and are thereby indirect acting. The parent compound of indirect acting carcinogens is called the procarcinogen and the active metabolite is called the ultimate carcinogen. Initiating compounds are reactive electrophiles which mutate DNA by nonenzymatic oxidation. Not all carcinogen induced DNA damage leads to initiation since cells are capable of repairing damaged DNA (see later).
Biology of tumour metastasis. Lancet 339, 1453-1457. H. B. (1994). Cell cycle control and cancer. Science 266, 1821-1828. H. (1989). Tumor cell societies. J. Natl. Cancer Inst. 81, 648-649. H. (1991). Cell-to-cell interaction in regulating diversity of neoplasms Scm. Cancer Biol. 2, 97-103. N. (1994). Mammary fibroblasts may influence breast tumor angiogenesis via hypoxia-induced vascular endothelial growth factor up-regulation and protein expression. Cancer Res. 54, 6083-6086. V. (1995). Tumor stroma as a regulator of neoplastic behavior.