By H. C. Pitot (auth.), Colin S. Cooper Ph.D., Philip L. Grover D.Sc. (eds.)

ISBN-10: 3642747752

ISBN-13: 9783642747755

ISBN-10: 3642747779

ISBN-13: 9783642747779

I were privileged to witness and perform the good progress of information on chemical carcinogenesis and mutagenesis because 1939 whilst I entered graduate tuition in biochemistry on the collage of Wisconsin­ Madison. I instantly began to paintings with the carcinogenic aminoazo dyes un­ der the course of Professor CARL BAUMANN. In 1942 I joined a fellow graduate pupil, ELIZABE1H CAVERT, in marriage and we quickly began a joyous half­ nership in study on chemical carcinogenesis on the McArdle Laboratory for melanoma study within the college of Wisconsin scientific tuition in Madison. This collaboration lasted forty five years. i'm very thankful that this quantity is dedi­ cated to the reminiscence of Elizabeth. the real and sundry issues which are reviewed right here attest to the ongoing development of the fields of chemical automobile­ cinogenesis and mutagenesis, together with their contemporary and fruitful union with viral oncology. i think very positive in regards to the program of information in those fields to the eventual resolution of diverse difficulties, together with the detection and estimation of the hazards to people of environmental chemical cancer causing agents and re­ lated factors.

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Extra resources for Chemical Carcinogenesis and Mutagenesis I

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1985). Thus, the alteration of DNA methylation by chemical carcinogens represents another theoretical pathway by which these agents may induce neoplastic transformation. IV. Aberrations of DNA Repair as Theoretical Mechanisms of Chemical Carcinogenesis In the three theoretical mechanisms of chemical carcinogenesis indicated thus far, changes in the structure of DNA are the end result of each mechanism. Although altered methylation of the 5-position of cytidine in DNA itself is a potential mechanism that alters gene expression, methylation induced by electrophilic (carbonium ion) or free radical methyl groups represents an extension of any or all three of the above mechanisms.

1985; ETHIER and ULLRICH 1982); comparable changes have been noted in humans, at least in mammary tissue (VAN BOGAERT 1984). In the absence of exogenous promotion, the number of identifiable clones derived from spontaneously initiated cells and the total number of cells occupying such clones (volume %) increase with the age of the animal, at least in the liver (SCHULTE-HERMANN et al. 1983; OGAWA et al. 1981). However, when exogenous promoting agents are administered, the number of such focal changes in this organ increases during the first 2 months of life but remains unchanged thereafter (PITOT et al.

Since then, the original two-stage concept has been modified (BOUTWELL 1964; KINZEL et al. 1986). A third stage, termed progression by many investigators, has been demonstrated through the use of protocols that have been altered from the original experiments of 4 decades ago (POTTER 1983; HENNINGS and YUSPA 1985; O'CONNELL et al. 1986). Of even greater significance is the fact that the multistage concept of the development of neoplasia has been found to be a relatively ubiquitous characteristic in the development of neoplasms in most, if not all, tissues under appropriate circumstances (cf.

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Chemical Carcinogenesis and Mutagenesis I by H. C. Pitot (auth.), Colin S. Cooper Ph.D., Philip L. Grover D.Sc. (eds.)

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