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Regulatory cytokine gene polymorphisms and risk of colorectal carcinoma.
Ann N Y Acad Sci 2006; 1089:98-103AN

Abstract

It is well established that cancer arises in chronically inflamed tissue, and this is particularly notable in the gastrointestinal tract. Classic examples include Helicobacter pylori-associated gastric cancer, hepatocellular carcinoma, and inflammatory bowel disease-associated colorectal cancer. Growing evidence suggests that these associations might be not casual findings. Focusing on individual cytokines has generated evidence that anti-inflammatory cytokine interleukin (IL)-10 and transforming growth factor-beta1 (TGF-beta1) may have a complex role in gastrointestinal carcinogenesis. As an example, IL-10-deficient mice develop severe atrophic gastritis and a chronic enterocolitis, developing colorectal cancer similar to human inflammatory bowel disease-associated neoplasia. TGF-beta1 is a multifunctional signaling molecule with a wide array of roles. Animal experiments suggest that TGF-beta1 plays a biphasic role in carcinogenesis by protecting against the early formation of benign epithelial growths, but promoting a significant stimulation of tumor growth invasion and metastasis during tumor progression. We assessed association of functional polymorphisms (-1082G/A; -592C/A) and TGF-beta1 (-509C/T; +869C/T) influencing the IL-10 production to colorectal cancer risk in a case-control study of 62 patients and 124 matched controls. No significant differences were observed among cancer patients and controls for IL-10 -1082G/A; -592C/A genotype frequencies. Evaluation of odds ratios (OR) for the TGF-beta1 +869C/T genotypes showed a significant increased risk for individuals bearing +869CC genotype compared to +869CT- and +869TT-positive individuals. These results suggest that the +869C allele, responsible for a Leu-->Pro substitution in the signal peptide sequence of the TGF-beta1 protein, may have a predisposing role in the development of colorectal cancer.

Authors+Show Affiliations

Patologia Clinica, Dipartimento di Biopatologia e Metodologie Biomediche, University of Palermo, Palermo, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17261758

Citation

Crivello, Antonino, et al. "Regulatory Cytokine Gene Polymorphisms and Risk of Colorectal Carcinoma." Annals of the New York Academy of Sciences, vol. 1089, 2006, pp. 98-103.
Crivello A, Giacalone A, Vaglica M, et al. Regulatory cytokine gene polymorphisms and risk of colorectal carcinoma. Ann N Y Acad Sci. 2006;1089:98-103.
Crivello, A., Giacalone, A., Vaglica, M., Scola, L., Forte, G. I., Macaluso, M. C., ... Palmeri, S. (2006). Regulatory cytokine gene polymorphisms and risk of colorectal carcinoma. Annals of the New York Academy of Sciences, 1089, pp. 98-103.
Crivello A, et al. Regulatory Cytokine Gene Polymorphisms and Risk of Colorectal Carcinoma. Ann N Y Acad Sci. 2006;1089:98-103. PubMed PMID: 17261758.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulatory cytokine gene polymorphisms and risk of colorectal carcinoma. AU - Crivello,Antonino, AU - Giacalone,Antonio, AU - Vaglica,Marina, AU - Scola,Letizia, AU - Forte,Giusi Irma, AU - Macaluso,Maria Catena, AU - Raimondi,Cristina, AU - Di Noto,Laura, AU - Bongiovanni,Alberto, AU - Accardo,Angela, AU - Candore,Giuseppina, AU - Palmeri,Laura, AU - Verna,Roberto, AU - Caruso,Calogero, AU - Lio,Domenico, AU - Palmeri,Sergio, PY - 2007/1/31/pubmed PY - 2007/3/14/medline PY - 2007/1/31/entrez SP - 98 EP - 103 JF - Annals of the New York Academy of Sciences JO - Ann. N. Y. Acad. Sci. VL - 1089 N2 - It is well established that cancer arises in chronically inflamed tissue, and this is particularly notable in the gastrointestinal tract. Classic examples include Helicobacter pylori-associated gastric cancer, hepatocellular carcinoma, and inflammatory bowel disease-associated colorectal cancer. Growing evidence suggests that these associations might be not casual findings. Focusing on individual cytokines has generated evidence that anti-inflammatory cytokine interleukin (IL)-10 and transforming growth factor-beta1 (TGF-beta1) may have a complex role in gastrointestinal carcinogenesis. As an example, IL-10-deficient mice develop severe atrophic gastritis and a chronic enterocolitis, developing colorectal cancer similar to human inflammatory bowel disease-associated neoplasia. TGF-beta1 is a multifunctional signaling molecule with a wide array of roles. Animal experiments suggest that TGF-beta1 plays a biphasic role in carcinogenesis by protecting against the early formation of benign epithelial growths, but promoting a significant stimulation of tumor growth invasion and metastasis during tumor progression. We assessed association of functional polymorphisms (-1082G/A; -592C/A) and TGF-beta1 (-509C/T; +869C/T) influencing the IL-10 production to colorectal cancer risk in a case-control study of 62 patients and 124 matched controls. No significant differences were observed among cancer patients and controls for IL-10 -1082G/A; -592C/A genotype frequencies. Evaluation of odds ratios (OR) for the TGF-beta1 +869C/T genotypes showed a significant increased risk for individuals bearing +869CC genotype compared to +869CT- and +869TT-positive individuals. These results suggest that the +869C allele, responsible for a Leu-->Pro substitution in the signal peptide sequence of the TGF-beta1 protein, may have a predisposing role in the development of colorectal cancer. SN - 0077-8923 UR - https://www.unboundmedicine.com/medline/citation/17261758/Regulatory_cytokine_gene_polymorphisms_and_risk_of_colorectal_carcinoma_ L2 - https://doi.org/10.1196/annals.1386.002 DB - PRIME DP - Unbound Medicine ER -