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Contributions from molecular/biochemical approaches in epidemiology to cancer risk assessment and prevention.
Author(s) -
P.H.M. Lohman,
Bruno Morolli,
F. Darroudi,
A.T. Natarajan,
Jan A. Gossen,
Jaap Venema,
L.H.F. Mullenders,
E. Vogel,
Harry Vrieling,
A.A. van Zeeland
Publication year - 1992
Publication title -
environmental health perspectives
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.257
H-Index - 282
eISSN - 1552-9924
pISSN - 0091-6765
DOI - 10.1289/ehp.9298155
Subject(s) - mutagenesis , cancer genetics , genetics , biology , mutation , cancer , gene
The origin of cancer in the humans is considered to be a complex and multistep process. In all cases, however, the cancer cell contains a genome in which gene(s) are either altered or wrongly expressed. Therefore, alterations in DNA have been thought to be a crucial first step (initiation) in the long chain of events leading to cancer. The occurrence of DNA lesions in cells in the human body is not a rare phenomenon. They can occur due to exposure to many exogenous agents present in our food, environment, and occupational situations. A major additional cause of DNA damage in cells is the action of endogenous factors like the intermediates of metabolic and detoxifying processes in our body (1). In toto the human body contains about 1014 cells; endogenous factors alone may induce around 4000 DNA lesions/day/cell, i.e., 4 x 1017 DNA lesions/body/day. Since the frequency of the transformation of cells into cancerous ones in the body is orders of magnitude lower than that of the formation of DNA lesions, it is obvious that only a limited number of DNA lesions are related to the process of neoplastic transformation. Some of the DNA lesions in cells may be converted to DNA sequence alterations (i.e., mutations),

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