cocarcinogenesis

cocarcinogenesis

 [ko-kahr″sĭ-no-jen´ĕ-sis]
the development, according to one theory, of cancer only in preconditioned cells as a result of conditions favorable to its growth.
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.
References in periodicals archive ?
Zhitkovich, "Genetic and epigenetic mechanisms in metal carcinogenesis and cocarcinogenesis: nickel, arsenic, and chromium," Chemical Research in Toxicology, vol.
For carcinogenicity potential mechanisms include genotoxicity oxidative stress altered cell proliferation altered DNA methylation cocarcinogenesis and tumor formation (Saha et al.
[171] have demonstrated a dose-dependent accumulation of AP sites as well as inhibition of APE1 activity in AP site incision under Pb exposure, implying an underlying mechanism by which Pb promotes cocarcinogenesis. On the other hand, Scortegagna and Hanbauer [77] have reported the enhanced APE1 accumulation in the nucleus in response to Pb treatment.
From the above studies it is hypothesized that the combined activity of Tag and tag antigens induce Notch-1 and telomerase activity, when acting in concert with the potential mutagenic effects of asbestos fibers closely apposed to or impacted into the mesothelial cells, which leads to the malignant transformation of the mesothelial cells, as observed in the in vitro and in vivo models of SV40-asbestos cocarcinogenesis. (73,74) The fundamentals of this process are schematically represented in the Figure, designed to depict potential "hit-and-run" cocarcinogenic association of SV40 with asbestos in mesothelial cell transformation.
Possible role of acetaldehyde in ethanol-related rectal cocarcinogenesis in the rat.
Arsenite cocarcinogenesis: an animal model derived from genetic toxicology studies.
2007a), and cocarcinogenesis with other environmental toxicants (Rossman et al.
Proposed mechanisms include genotoxicity, oxidative stress, inhibition of DNA repair, tumor promotion, cocarcinogenesis, cell proliferation, and altered signal transduction or DNA methylation (Hughes 2002; Kitchin 2001; Rossman 2003).
The mechanism(s) by which arsenic exposure contributes to human cancer risk is unknown; however, several indirect cocarcinogenesis mechanisms have been proposed.
Mechanisms of Tumor Promotion and Cocarcinogenesis, Vol 2 (Slaga TJ, Sivak A, Boutwell RK, eds).