Table of Contents Author Guidelines Submit a Manuscript
Journal of Oncology
Volume 2009 (2009), Article ID 827532, 4 pages
http://dx.doi.org/10.1155/2009/827532
Research Article

Investigation of the miR16-1 ( ) + 7 Substitution in Seven Different Types of Cancer from Three Ethnic Groups

1Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, NewYork, NY 10032, USA
2Department of Basic Oncology, Oncology Institute, University of Istanbul, 34452 Beyazit Istanbul, Turkey
3Department of Hepatobiliary Surgery, First Affiliated Hospital of Guangxi Medical University, Gnangxi 530021, China
4Department of Epidemiology, Mailman School of Public Health, Columbia University, NewYork, NY 10032, USA

Received 17 March 2009; Revised 8 July 2009; Accepted 1 September 2009

Academic Editor: Boffetta Paolo

Copyright © 2009 Hulya Yazici et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. MicroRNAs are a type of small noncoding RNA molecules that have been shown to control gene expression in eukaryotes. Aberrant expression and alteration of miRNAs may be responsible for human diseases including cancer. An miR16-1 ( )  + 7 gene mutation has been previously found in familial chronic lymphocytic leukemia patients, one of which reported a family history of breast cancer. miR16-1 regulates the expression of bcl-2, which is important in retinoblastoma, and is located in a genomic region that is frequently lost in nasopharyngeal and hepatocellular carcinomas (HCCs). Therefore, miR16-1 may be potentially important in the etiology of several solid tumors. To understand the power of the miR16-1 ( )  + 7 mutation as a prognostic and diagnostic risk factor, we investigated the mutation in patients with seven different types of cancer including 188 with breast, 102 with ovarian, and 22 nasopharyngeal carcinomas, 96 HCC, 872 chronic myeloid leukemia (CML), 39 chronic lymphocytic leukemia (CLL), and 46 retinoblastoma cases from three different ethnic groups and of hereditary and sporadic etiology. Methods. Nuclease TaqMan SNP genotyping assay was used to detect the miR16-1 gene substitution. Results. The miR16-1 ( )  + 7 substitution was not detected in any of the groups studied. Conclusions. Considering the large scale of our study, the representation of different ethnicities and levels of hereditary risk, we conclude that the miR-16-1 ( )  + 7 mutation is not a good diagnostic or prognostic indicator of risk for the cancers tested.