Chemical Induction of Cancer. Structural Bases and by Joseph C. Arcos

By Joseph C. Arcos

Chemical Induction Of melanoma: Structural Bases and organic Mechanisms quantity IIA offers with the natural and biochemical rules at the back of cancer.

This quantity contains half III of the paintings, which covers structure-activity relationships of chemical cancer agents, the impact of chemical reactivity, molecular geometry, and metabolism on carcinogenic task. less than this is often bankruptcy five, which tackles conjugated fragrant structures.

The textual content is suggested for medical professionals, natural chemists, and biochemists with a sophisticated wisdom in biochemistry and natural chemistry and wish to understand extra the biochemical techniques of melanoma.

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3). T h e partial overlap of carcinogenicity and estrogenic activity could perhaps be a reflection of the fact that both classes of substances have in c o m m o n the property of stimulating cell division. Estrogens, as hormones, stimulate cell division, followed by cell differentiation. The action is specific for certain tissues, it is antagonized by other hormones, and is reversible: withdrawal of the h o r m o n e causes a return of the tissue to its original state. ), but this cell division is not followed by differentiation and becomes ultimately nonspecific and irreversible.

It is of particular interest in this regard that carcinogenic activity appears to have been detected in simple ("nonbridged") polyaryls as well. The first such observation was reported in 1936 by Morton, Branch and Clapp who induced fibrosarcomas upon subcutaneous administration of sym-triphenylbenzene XLIX to mice (43). While it is true that subsequent investigators were unable to confirm their finding (44-47), a more recent observation focused new interest on this class of compounds. Dannenberg reported in 1959 that the higher homolog of XLIX, 1,3,5-tris-p-xenylbenzene L, produces papillomas and epitheliomas locally, as well as hepatomas, when assayed in skin painting on mice (48).

Thus, methyl substitution of the highly active F-nor-steranthrene XLVI in a position corresponding to the position 2' on the aromatic 1,2-benzanthracene moiety of the molecule abolishes carcino­ genic activity (52). It is possible, nonetheless, that the deactivating effect of a methyl substitution in the benz ring—which is regarded almost as a tenet— has not a general validity. In fact, Lacassagne et al reported in 1962 that the activity of r,9-dimethyl-1,2-benzanthracene for inducing sarcomas (sarcoma index 1 1 ; ref.

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