The first two authors contributed equally to this paper.
Tumor-specific changes in mtDNA content in human cancer
Article first published online: 26 APR 2005
Copyright © 2005 Wiley-Liss, Inc.
International Journal of Cancer
Volume 116, Issue 6, pages 920–924, 10 October 2005
How to Cite
Mambo, E., Chatterjee, A., Xing, M., Tallini, G., Haugen, B. R., Yeung, S.-C. J., Sukumar, S. and Sidransky, D. (2005), Tumor-specific changes in mtDNA content in human cancer. Int. J. Cancer, 116: 920–924. doi: 10.1002/ijc.21110
- Issue published online: 28 JUL 2005
- Article first published online: 26 APR 2005
- Manuscript Accepted: 31 JAN 2005
- Manuscript Received: 10 NOV 2004
- National Institutes of Health. Grant Numbers: 5 U01 CA084986-04, P01CA077664-07
- mtDNA content;
- thyroid cancer;
- breast cancer
Mitochondrial DNA (mtDNA) alterations are associated with various cancer types, suggesting that the mitochondrial genome may be a critical contributing factor in carcinogenesis. mtDNA alterations have been suggested as a potentially sensitive and specific biomarker for several cancer types. We examined mtDNA content in 25 pairs of normal and tumor breast tissue samples, 37 papillary thyroid carcinoma (PTC), 21 benign thyroid neoplasms and in 20 paired normal and PTC samples. Our results showed that mtDNA content was reduced in 80% of the breast tumors relative to their corresponding normal. mtDNA was increased in papillary thyroid carcinomas, however, when compared to the corresponding normal DNA taken from the same individual. Also, mtDNA content was increased in none-paired PTC samples compared to the normal controls. Our findings indicate that changes in mtDNA content during carcinogenesis may be regulated in a tumor specific manner. Additionally, changes in mtDNA levels did not correlate with tumor grade and metastasis, suggesting that these alterations may occur in the early stages of tumorigenesis. Our findings suggest that mtDNA content can be used as a molecular diagnostic tool to help identify genetic abnormalities in human tumors. © 2005 Wiley-Liss, Inc.