Researchers have described an unusual mechanism at work in certain types of B-cell lymphomas that requires the joint activities of normal and mutant forms of an enzyme.
In a linkurl:paper;http://www.pnas.org/content/early/2010/11/08/1012525107.abstract published this week in the __Proceedings of the National Academy of Sciences__, a team of scientists from the pharmaceutical company Epizyme describes how in cells heterozygous for a mutation in EZH2—an enzyme that induces epigenetic changes in one of the histone proteins—the normal and mutant form of the enzyme work together to silence genes involved in suppressing tumors."It's a fascinating paper," said linkurl:Olivier Elemento,;http://physiology.med.cornell.edu/faculty/elemento/lab/ a cancer biologist at Weill Cornell Medical College in New York City who was not involved in the study. To his knowledge, it's the first time such a mechanism has been described in cancer. "It is definitely a very unusual situation where you have a mutated gene...
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Image: Wikimedia commons, Zephyris |
C.J. Sneeringer, et al., "Coordinated activities of wild-type plus mutant EZH2 drive tumor-associated hypertrimethylation of lysine 27 on histone H3 (H3K27) in human B-cell lymphomas," PNAS, doi:10.1073/pnas.1012525107, 2010.
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