TY - JOUR
T1 - CHOP 5'UTR-c.279TC and +nt30CT variants are not associated with overweight condition or with tumors/cancer in Italians-a case-control study
AU - Meenakshisundaram, Ramachandran
AU - Piumelli, Nunzia
AU - Pierpaoli, Laura
AU - Gragnoli, Claudia
N1 - Funding Information:
This study was made possible by the Penn State University Physician-Scientist Stimulus Award and by the Dean's Pilot and Feasibility Grant, number D1BTH06321-01 from the Office for the Advancement of Tele health (OAT), Health Resources and Services Administration, DHHS. This project is funded, in part, under a grant from the Pennsylvania Department of Health using Tobacco Settlement Funds. The Department specifically disclaims responsibility for any analyses, interpretations or conclusions.
PY - 2009
Y1 - 2009
N2 - Background. Type 2 diabetes (T2D) is associated with obesity and has been shown recently to be associated with tumors/cancer. HNF1-beta and JAZF1 genes are associated with T2D and prostate cancer. We have previously shown that CHOP 5'UTR-c.279TC and +nt30CT haplotype variants contribute to T2D. CHOP deficiency causes obesity in mice, thus CHOP gene variants may contribute to human obesity. Furthermore, CHOP mediates apoptosis and is implicated in cancer pathogenesis. Hence, we aimed at identifying any potential association of CHOP 5'UTR-c.279TC and +nt30CT genotypes and corresponding haplotypes with overweight condition/pre-obesity and tumors/cancer in an Italian dataset. Methods. We recruited from Italy 45 overweight subjects (body mass index (BMI) 25) and 44 control subjects (BMI < 25) as well as 54 cases with at least one cancer or at least one tumor and 43 control subjects without tumors/cancer from the general population. We excluded allelic departure from Hardy-Weinberg equilibrium in cases and control subjects, separately. Results. We assessed the power to detect risk odds ratios by association tests in our datasets. We tested the hypothesis of association of CHOP 5'UTR-c.279TC and +nt30CT genotypes and haplotypes with tumors/cancer and, separately, with overweight condition. Both associations were not significant. Conclusion. From our study, we may conclude that CHOP 5'UTR-c.279TC and +nt30CT genotypes and corresponding haplotypes are not associated with tumors/cancer and pre-obesity. However, more studies are warranted to establish the role of CHOP variants in tumor/cancer predisposition and in overweight condition.
AB - Background. Type 2 diabetes (T2D) is associated with obesity and has been shown recently to be associated with tumors/cancer. HNF1-beta and JAZF1 genes are associated with T2D and prostate cancer. We have previously shown that CHOP 5'UTR-c.279TC and +nt30CT haplotype variants contribute to T2D. CHOP deficiency causes obesity in mice, thus CHOP gene variants may contribute to human obesity. Furthermore, CHOP mediates apoptosis and is implicated in cancer pathogenesis. Hence, we aimed at identifying any potential association of CHOP 5'UTR-c.279TC and +nt30CT genotypes and corresponding haplotypes with overweight condition/pre-obesity and tumors/cancer in an Italian dataset. Methods. We recruited from Italy 45 overweight subjects (body mass index (BMI) 25) and 44 control subjects (BMI < 25) as well as 54 cases with at least one cancer or at least one tumor and 43 control subjects without tumors/cancer from the general population. We excluded allelic departure from Hardy-Weinberg equilibrium in cases and control subjects, separately. Results. We assessed the power to detect risk odds ratios by association tests in our datasets. We tested the hypothesis of association of CHOP 5'UTR-c.279TC and +nt30CT genotypes and haplotypes with tumors/cancer and, separately, with overweight condition. Both associations were not significant. Conclusion. From our study, we may conclude that CHOP 5'UTR-c.279TC and +nt30CT genotypes and corresponding haplotypes are not associated with tumors/cancer and pre-obesity. However, more studies are warranted to establish the role of CHOP variants in tumor/cancer predisposition and in overweight condition.
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U2 - 10.1186/1756-9966-28-90
DO - 10.1186/1756-9966-28-90
M3 - Article
C2 - 19558691
AN - SCOPUS:68249147998
VL - 28
JO - Journal of Experimental and Clinical Cancer Research
JF - Journal of Experimental and Clinical Cancer Research
SN - 0392-9078
IS - 1
M1 - 90
ER -