Zheng Ye1, James M Parry. 1. Bioinformatics Group, Centre for Molecular Genetics and Toxicology, School of Biological Sciences,University of Wales Swansea, Singleton Park, Swansea, UK.
Abstract
BACKGROUND: Rapid NAT2 acetylation has been considered as a risk factor for developing colon cancer in a number of studies, however the overall results of such studies are inconsistent. To clarify the influence of NAT2 rapid acetylation status on colon cancer risk, we have performed a meta-analysis of 20 published case-control studies (4431 cases, 4547 controls). MATERIAL/ METHODS: Odd ratio was employed to evaluate the risk of colon cancer and NAT2 rapid acetylation status. To take into account the possibility of heterogeneity across the studies, a statistical test for heterogeneity across the studies was performed. The summary odds ratios were assessed by calculating a weighted average of odds ratios for all of the studies. RESULTS: The pooling of studies based on phenotyping methods indicated that the overall odds ratio of colon cancer risk associated with rapid acetylator was 1.51 (95%CI: 1.07-2.12). However, the risk of colon cancer associated with rapid acetylator from the studies based on genotyping method was lower with a calculated overall odds ratio of 1.06 (95%CI: 0.97-1.15). Pooling studies were also conducted on specific tumour sites and ethnic groups. The results show that effect of rapid acetylator on colon cancer risk was not obviously different. CONCLUSIONS: The results of our meta-analyses do not support the hypothesis that NAT2 alone is an important risk factor for colon cancer and suggests that NAT2 rapid acetylation status has no specific effect on the risk of developing colon cancer.
BACKGROUND: Rapid NAT2 acetylation has been considered as a risk factor for developing colon cancer in a number of studies, however the overall results of such studies are inconsistent. To clarify the influence of NAT2 rapid acetylation status on colon cancer risk, we have performed a meta-analysis of 20 published case-control studies (4431 cases, 4547 controls). MATERIAL/ METHODS: Odd ratio was employed to evaluate the risk of colon cancer and NAT2 rapid acetylation status. To take into account the possibility of heterogeneity across the studies, a statistical test for heterogeneity across the studies was performed. The summary odds ratios were assessed by calculating a weighted average of odds ratios for all of the studies. RESULTS: The pooling of studies based on phenotyping methods indicated that the overall odds ratio of colon cancer risk associated with rapid acetylator was 1.51 (95%CI: 1.07-2.12). However, the risk of colon cancer associated with rapid acetylator from the studies based on genotyping method was lower with a calculated overall odds ratio of 1.06 (95%CI: 0.97-1.15). Pooling studies were also conducted on specific tumour sites and ethnic groups. The results show that effect of rapid acetylator on colon cancer risk was not obviously different. CONCLUSIONS: The results of our meta-analyses do not support the hypothesis that NAT2 alone is an important risk factor for colon cancer and suggests that NAT2 rapid acetylation status has no specific effect on the risk of developing colon cancer.
Authors: Lou qian Zhang; Jian nong Zhou; Jun Wang; Guo dong Liang; Jing ying Li; Yi dan Zhu; Yun tao Su Journal: PLoS One Date: 2012-03-05 Impact factor: 3.240