Reply
We greatly appreciate the comments from Carsten Goessl. In reply to his comments on our article, we put forth the following arguments. Based on the information that is available at present, it seems premature to conclude that mitochondrial mutations are either the cause of cancer or innocent bystanders. However, there is a significant correlation between the occurrence of mutation and disease. Certainly, inherited mutations in nuclear genes with products that are involved in the mitochondrial Krebs tricarboxylic-acid cycle are a known cause of cancer At least a portion of somatic mutations that have been identified in human cancers are predicted to cause severe disruption in mitochondrial function2.
Moreover, new strategies to target the permeability-transition-pore complex in mitochondria to enhance apoptosis and overcome chemoresistance in cancer are emerging3. Although still premature, the proteomic approaches we presented will lead to a better understanding of the role of mitochondrial DNA mutations in cancer, and perhaps one day provide new targets for therapy.
References
Eng, C., Kiuru, M., Fernandez, M. J. & Aaltonen, L. A. A role for mitochondrial enzymes in inherited neoplasia and beyond. Nature Rev. Cancer 3, 193–202 (2003).
Penta, J. S., Johnson, F. M., Wachsman, J. T. & Copeland, W. C. Mitochondrial DNA in human malignancy. Mutat. Res. 488, 119–133 (2001).
Morisaki, T. & Katano, M. Mitochondria-targeting therapeutic strategies for overcoming chemoresistance and progression of cancer. Curr. Med. Chem. 10, 2517–2521 (2003).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Verma, M., Kagan, J., Sidransky, D. et al. Reply to “Proteomic alterations of cancer-cell mitochondria: driver or bystander?”. Nat Rev Cancer 3, 796 (2003). https://doi.org/10.1038/nrc1192-c2
Issue Date:
DOI: https://doi.org/10.1038/nrc1192-c2
