Chemical Carcinogenesis: Interactions of Carcinogens with Nucleic Acids

Sarma, D.S.R.; Rajalakshmi, S.; Farber, Emmanuel

doi:10.1007/978-1-4613-4449-0_8

Cited by 24 publications

(5 citation statements)

References 246 publications

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“…Although the interactions of various chemical carcinogens with cellular macromolecules have been studied extensively [20,21], their specific interactions and involvement in carcinogenesis are poorly understood. One possible approach to this problem is to discern the mode of action of various chemicals at the gene level.…”

Section: Discussionmentioning

confidence: 99%

Incidence of p53 and Ha-ras gene mutations in chemically induced rat mammary carcinomas

et al. 1996

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To determine whether p53 alterations, which are frequent in human breast cancers, are also common in rat mammary tumors, we examined 40 tumors from 24 rats treated with 7,12-dimethylbenz[a]anthracene (DMBA) and 34 tumors from 14 rats treated with N-nitroso-N-methylurea (NMU) (an N-nitroso compound). DMBA and NMU are known genotoxic mutagens. The entire coding regions of the p53 and Ha-ras genes were examined for mutations by polymerase chain reaction single-strand conformational polymorphism analysis and by direct sequencing. One of the 40 DMBA-induced mammary tumors had a p53 mutation, a single-base substitution (AGC-->GGC) at codon 307, resulting in an amino-acid change from Ser to Gly. No mutations were found in NMU-induced tumors. The incidence of Ha-ras gene mutation was 79% (27 of 34) at codon 12 in the NMU group and 23% (nine of 40) at codon 61 in the DMBA group. Thus, p53 mutation, in contrast to Ha-ras mutation, did not seem to be a prerequisite for carcinogenesis in chemically induced rat mammary tumors.

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Section: Discussionmentioning

confidence: 99%

Incidence of p53 and Ha-ras gene mutations in chemically induced rat mammary carcinomas

et al. 1996

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“…The mechanism by which carcinogens produce cellular changes or anticarcinogens inhibit them is not well understood. Carcinogens may produce their effect by disrupting cellular processes or structures (Poste, 1977;Svoboda & Reddy, 1975), by interacting with and changing DNA and RNA (Kanazir, 1969;Sarma, Rajalakshmi, & Farber, 1975), or by debilitating those mechanisms necessary for DNA repair (Fox & Lajtha, 1973;Urbach, 1975). Anticarcinogens may inhibit any of these actions.…”

Section: Phases Of Tumor Developmentmentioning

confidence: 99%

Stress and cancer.

Sklar¹,

Anisman²

1981

Psychological Bulletin

320

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Consistent with the findings of human research suggesting that stress may influence the carcinogenic process, data derived from infrahuman experimentation have revealed that aversive insults may potentiate or inhibit tumorigenicity. The nature of the change, however, is dependent on a number of psychological, experiential, and organismic variables. Exacerbation of tumor growth is evident following acute exposure to uncontrollable, but not controllable, stress. Moreover, the effects of aversive stimuli vary as a function of the organism's prior stress history as well of social housing conditions. The fact that stress influences neurochemical, hormonal, and immunological functioning and that these changes are subject to many of the same manipulations that influenced the carcinogenic process suggests a relation between these three mechanisms and the stress-induced alterations of tumor growth. This contention is supported by the findings that pharmacological manipulations that modify these endogenous substrates have predictable effects on tumorigenesis.

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“…Since then, more than 150 compounds have been shown to undergo a covalent binding to biological macromolecules in vivo or in vitro and a nurober of reviews are available: a recent and very extensive one by Lawley [139], others by Irving (103], Sarma [228] and, for N-nitroso compounds only, by Lijinsky [149]. Brookes has published two classical short reviews [22,24] and a short discussion on the importance of DNA as the most critical target for a covalent binding [ 2 5].…”

Section: Covalent Binding Of Chemical Carcinogens To Biological Macromentioning

confidence: 99%

In vivo covalent binding of organic chemicals to DNA as a quantitative indicator in the process of chemical carcinogenesis

Lutz

1979

Mutation Research/Reviews in Genetic Toxicology

398

124

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Chemical Carcinogenesis: Interactions of Carcinogens with Nucleic Acids

Cited by 24 publications

References 246 publications

Incidence of p53 and Ha-ras gene mutations in chemically induced rat mammary carcinomas

Incidence of p53 and Ha-ras gene mutations in chemically induced rat mammary carcinomas

Stress and cancer.

In vivo covalent binding of organic chemicals to DNA as a quantitative indicator in the process of chemical carcinogenesis

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