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Process triggered by some anti-cancer drugs causes tumors in mice, study finds

s; when methylation was reduced in such mice, Eden found that they developed soft-tissue sarcomas earlier when compared to similarly mutated mice with normal methylation levels. In these mice, Eden could show that hypomethylation-induced chromosomal instability caused an increase in tumor formation.

The instability could be an asset to a cancer cell looking to multiply and cause trouble, Jaenisch said. There seems to be a selective advantage for tumor cells to be hypomethylated, because its chromosomes are more unstable.

The data offer real food for thought about the role of losing methylation in cancer, noted Stephen Baylin, a scientist at John Hopkins University in Baltimore, Md. But Baylin also cautioned that these findings in mice may not be seen in people. In the mice engineered at Whitehead Institute, the level of methylation likely was more reduced than in most human tumors. Moreover, he cautioned that unlike hypomethylation induced in cancers that develop in human adults, these hypomethylated mice carry a reduced methylation capacity for their entire lives, starting at the embryonic stage.

Jaenisch may be right, Baylin said, but you have to be very careful about equating the situation that hes looking at experimentally with whats going on in human tumors, an assertion also made by Jaenisch.

It is very important to assess whether findings made in animal models apply to patients, Jaenisch said.

Jaenischs lab plans to extend this work by looking at other tumors, such as those of the pancreas, breast and liver, changing methylation levels and observing the results. I think it will reveal metabolic differences between tissues, he said, and may lead to a deeper understanding why reducing methylation levels seems to harm some cancers and benefit others.


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Contact: Kelli Whitlock or Melissa Withers
newsroom@wi.mit.edu
617-258-5183
Whitehead Institute for Biomedical Research
17-Apr-2003


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