Exogenous factors in colonic carcinogenesis
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Exogenous factors in colonic carcinogenesis proceedings of Falk Symposium 128 held in Würzburg, Germany, May 2-3, 2002 by Falk Symposium (128th 2002 WГјrzburg, Germany)

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Published by Kluwer Academic in Dordrecht, London .
Written in English

Subjects:

  • Colon (Anatomy) -- Cancer -- Congresses.,
  • Carcinogenesis -- Congresses.

Book details:

Edition Notes

Includes bibliographical references and index.

Statementedited by W. Scheppach and M. Scheurlen.
GenreCongresses.
SeriesFalk symposium -- 128
ContributionsScheppach, W., Scheurlen, M.
The Physical Object
Paginationxiv, 334 p. :
Number of Pages334
ID Numbers
Open LibraryOL22489295M
ISBN 100792387805

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  It was held in Kaiserslautern in October The remarkable results which have been presented by renouned researchers are documented in this book. There is extensive evidence that diet influences the risk of developing cancer due to carginogens and anti-carcinogens in our food. Abstract The mechanisms for activation of procarcinogens and some of the factors that affect these reactions are considered. It is proposed that the nucleus of the colonic cell may actually be resp Cited by: 9. Potential link between sphingomyelin metabolism and colonic tumorigenesis Duan, Rui-Dong LU () FALK Symposium on Exogenous Factors in Colonic Carcinogenesis p Mark. Organ-specific cancer incidence rates can vary dramatically between low- and high-incidence areas. Such differences are due to (1) heritable susceptibility determinants, (2) risk factors associated with the environmental and local living conditions (e.g., viruses, pollution), and (3) personal life-style factors. For organs showing large differences between cancer registries, exogenous factors.

Active oxygen may be involved in carcinogenesis through two possible mechanisms: induction of gene mutations that result from cell injury, and the effects on signal transduction and transcription factors. Which mechanism it follows depends on factors such as the type of active oxygen species involved and the intensity of stress. Cellular. pancreas, ovary, and colon (4). Wilms' tumor has been recom mended as an index for consistency in tumor registries (5). Even in breast (6) and colon cancers, where a large number of risk factors have been established, they account for only about one-fourth of . such environmental factors have been discov-ered, and molecular targets of environmental factors are increasingly being clarified. 1. Physical factors 1) Ionized radiation It is well known that ionized radiation may cause gene mutation or chromosome aberra-tion. The results of an epidemiological survey of carcinogenesis in atomic bomb victims show. In the approach to the analysis of disease, including, of course, cancer, two major thrusts may be distinguished. These may be referred to, in shorthand, as agents and processes: the causative agents (chemical, microbial, physical, environmental, and psychosocial) and the organismic processes, initiated and furthered by the agents, culminating in observable pathology (at the macromolecular.

  DNA damage and repair system: Mutator genes and cancer • small mutational damage to the dividing cell by exogenous factors (e.g. by radiation, chemical carcinogens etc) is also repaired. • p53 gene is held responsible for detection and repair of DNA damage • if this system of DNA repair is defective as happens in some inherited mutations. @inbook{6ca4beafc27d8b4b0b0, author = {Duan, Rui-Dong}, booktitle = {Exogenous factors in colonic carcinogenesis.}, editor = {Scheppach, W and. Thomas Smyrk, Henry T. Lynch, in Encyclopedia of Cancer (Second Edition), VII Summary. The multistep model of colon carcinogenesis has provided the framework to advance our understanding of the molecular basis of colon cancer. There is an ever-expanding list of genes that are candidates for inclusion in the process, some occurring early and some late. Carcinogenesis in intestinal metaplastic epithelium probably progresses through a series of irreversible genetic mutations in a manner comparable to the development of adenocarcinoma of the colon. The molecular pathway of carcinogenesis in Barrett esophagus is much less understood than that of colonic adenocarcinoma.