By a News Reporter-Staff News Editor at Cancer Gene Therapy Week -- Data detailed on Biotechnology have been presented. According to news reporting from New Orleans, Louisiana, by NewsRx journalists, research stated, "We previously showed that DNA fragmentation factor, which comprises a caspase-3-activated DNase (CAD) and its inhibitor (ICAD), may influence the rate of cell death by generating PARP-1-activating DNA breaks. Here we tested the hypothesis that ICAD-deficient colon epithelial cells exhibiting resistance to death stimuli may accumulate additional genetic modifications, leading to a tumorigenic phenotype."
The news correspondents obtained a quote from the research from Louisiana State University, "We show that ICAD deficiency may be associated with colon malignancy in humans. Indeed, an examination of ICAD expression using immunohistochemistry in an array of both colon cancer and normal tissues revealed that ICAD expression levels were severely compromised in the cancerous tissues. Upon DNA damage caused by a low dose of irradiation, ICAD cells acquire a tumorigenic phenotype. Colon epithelial cells derived from ICAD mice showed a significant resistance to death induced by the colon carcinogen dimethylhydrazine in vitro and in mice. Such resistance was associated with a decrease in PARP-1 activation. In an animal model of dimethylhydrazine-induced colon tumorigenesis, ICAD(-/-) mice developed significantly higher numbers of tumors with markedly larger sizes than the wild-type counterparts. Interestingly, the phenotype of the ICAD(-/-) mice was not associated with a significant increase in the precancerous aberrant crypt foci suggesting a potential link to tumor progression rather than initiation. More importantly, ICAD deficiency was associated with severe genomic instability as assessed by array comparative genomic hybridization. Such genomic instability consisted most prominently of amplifications but with sizable deletions as compared to the wild-type counterparts affecting several cancer-related genes including RAF-1, GSN, LMO3, and Fzd6 independently of p53."
According to the news reporters, the research concluded: "Altogether, our results present a viable case for the involvement of ICAD deficiency in colon carcinogenesis and show that apoptosis and genomic instability may comprise the means by which such deficiency may contribute to the process of increasing susceptibility to carcinogen-induced tumorigenesis."
For more information on this research see: ICAD deficiency in human colon cancer and predisposition to colon tumorigenesis: linkage to apoptosis resistance and genomic instability. Plos One, 2013;8(2):e57871. (Public Library of Science - www.plos.org; Plos One - www.plosone.org)
Our news journalists report that additional information may be obtained by contacting Y. Errami, The Stanley Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, Louisiana, United States. Additional authors for this research include H. Brim, K. Oumouna-Benachour, M. Oumouna, A.S. Naura, H. Kim, J. Ju, C.J. Davis, J.G. Kim, H. Ashktorab, K. Fallon, M. Xu, J. Zhang, L. Del Valle and A.H Boulares (see also Biotechnology).
Keywords for this news article include: Biotechnology, Genetics, Oncology, Louisiana, Apoptosis, New Orleans, United States, Cancer Gene Therapy, North and Central America.
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