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Reply to 'AIDS, aneuploidy and oncogenes'

Nature Biotechnology volume 22, pages 1077–1078 (2004)Cite this article

George Miklos responds:

The very first serial analysis of gene expression (SAGE) data on colorectal cancer from Kinzler and Vogelstein's laboratory1 revealed that overexpression of oncogenes as the cause of human cancers could not be a generality. Subsequent microarray expression data on other solid tumors reinforce this finding, as do breast cancer tissue microarray data, where only a minority of tumors overexpress the oncogene HER2, and where tumor aggressiveness is independent of HER2 protein levels2. The centrality of oncogenes is further called into question by data from Hanafusa3, who highlights the ongoing failure to repeat Weinberg's oncogene-mediated transformation of normal diploid human cells. Furthermore, Klein and Riethmuller's4 single cell analyses demonstrate that mutations in the p53 tumor suppressor gene generally occur after aneuploidogenic changes, molecularly buttressing the pioneering work of Harris5 on the contributions of aneuploidy to the etiology of tumor suppression. In the best-studied clinical case of cervical carcinoma, it is well known that aneuploidy precedes the development of cancer. Given this abundance of high-profile clinical and molecular literature, it is amusing that Gordon leaves “it to others” to refute the aneuploidy-cancer link.

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Reply to 'AIDS, aneuploidy and oncogenes'. Nat Biotechnol 22, 1077–1078 (2004). https://doi.org/10.1038/nbt0904-1077c

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