Chemical carcinogenesis cell proliferation

Ghanayem Bl, Maronpot RR, Matthews HB. 1986. Association of chemically-induced forestomach cell proliferation and carcinogenesis. Cancer Lett 32 271-278. 

Goldsworthy Chemically induced cell proliferation in carcinogenesis in Mechanisms of carcinogenesis in 27A30... 

If enzymes responsible for DNA repair are unable to remove the DNA adduct, or if an error takes place in the repair, then the error in the genetic code remains when the cell divides. Thus, cellular proliferation is also required, in addition to a mutation, for there to be a permanent effect of a chemical compound. Accumulation of genetic errors, i.e., mutations, has been suspected to be an important factor in chemical carcinogenesis. ... 

Chemically induced cell proliferation also may be a mechanism of epigenetic carcinogenesis. 

Protein kinase C (PKC) actually constitutes a family of several isozymes that are activated by diacylglycerol (DG). The potent tumor promoter, TPA, binds to, and activates PKC, in competition with DG. PKC stimulation results in phosphorylation of regulatory proteins that affect cell proliferation. There is evidence that carcinogenesis may be suppressed by inhibiting this enzyme. Phorbol tumor promoters such as TPA can replace DG in activating PKC. Chemicals that inhibit PKC also inhibit TPA-induced tumor promotion in mouse skin [23]. 

Monticello TM, Morgan KT. 1997. Chemically-induced nasal carcinogenesis and epithelial cell proliferation a brief review. Mutat Res 380 33-41. 

Chemical carcinogenesis may involve several mechanisms (i) interaction with DNA (ii) activation of cellular oncogenes (iii) DNA repair (iv) epigenetic mechanisms (v) cell proliferation. 

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