PubMed · 4803327
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R F Crampton. 1973. Editorial: The Delaney Amendment.. https://doi.org/10.1016/0091-7435(73)90020-0
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Cancer may be viewed as a genetic disease characterized by the failure of cellular mechanisms to maintain genomic integrity. Molecular progression models defining genetic damage are being developed for a number of solid tumors including head and neck squamous cell carcinoma. Genetic alteration of certain classes of genes, the tumor suppressor genes and proto-oncogenes, seem to be common events in such models. Host modulation of environmental carcinogens, however, also may be an important disease determinant. Interindividual differences in susceptibility to the genotoxic effects of environmental carcinogens may be genetically determined. With technologic advances in molecular genetics, it is now possible to identify specific genetic alterations that occur in different stages of neoplasia. Correlation of these genetic alterations with susceptibility models for solid tumors has important implications for the field of molecular epidemiology.
Long-term (8-48 h) treatment of SH-SY5Y neuroblastoma cells with phorbol-12,13-dibutyrate (PDBu; 100 nM) promotes the down-regulation of protein kinase C (PKC) subtypes alpha and epsilon and reduces by up to 60% noradrenaline (NA) release evoked via both PKC-dependent (M3-muscarinic receptor activation) and PKC-independent (depolarization) pathways, over similar time courses. A similar effect on release is observed following long-term (16-48 h) incubation with the PKC inhibitor Ro 31-7549 (10 microM), even after removal of the inhibitor, indicating a mechanism which is not rapidly reversible. Evidence is presented which suggests that long-term treatment with PDBu does not (1) affect calcium entry, (2) modulate levels of proteins important in the secretory mechanism or (3) reduce the number of secretory vesicles. Thus, the decrease in NA release in SH-SYSY cells following down-regulation of PKC appears to be the result of a sustained reduction in PKC activity acting on a component of the secretory pathway not involved in the regulation of calcium entry or vesicle number.
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