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

CAMBRIDGE, Mass. It is well known that cancers frequently are caused by genetic mutations random alterations along the long chain of molecules that make up the sequence of an organisms DNA. Two studies published this week in Science now point to another culprit in tumor formation, a process that can cause chromosomes to become unstable by affecting changes in the methylation of the DNA, which renders a gene active or inactive by affecting how the DNA is packaged into proteins without changing gene sequences.

The findings are important, researchers say, because some anti-cancer drugs in clinical trials are designed to kill diseased cells by triggering the process under study called hypomethylation which lowers the level of methylation. Previous studies by scientists at Whitehead Institute for Biomedical Research have shown that drug-induced hypomethylation can protect against tumors arising in the intestinal tract (colon cancer). But in this new work, Whitehead scientists found that hypomethylation also may cause tumors in mice, suggesting that such drugs may do harm as well as good, said Rudolf Jaenisch, leader of the team that published these new studies.

You have to know how you interfere with these cancer mechanisms, said Jaenisch, adding that the same alteration of cellular chemistry that controls some cancers is now seen to cause cancer in other tissues. At the moment we have two totally opposite results when we look in two different tissues. In the intestines, hypomethylation protects against cancer, and in the thymus it enhances cancer.

As researchers search for explanations for what prompts cancer cells to proliferate and grow, an increasing number have begun to examine extra-genetic changes problems that affect whether a gene is active or silent not the genes sequence. One process receiving heavy scrutiny is among the most basic events in a cells nucleus during the life of the cell, methylation, during which methyl molecules,
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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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