As an embryo develops, its cells must learn what to do with the thousands of genes they've been equipped with. That's why each cell comes with a detailed gene-expression manual outlining exactly which genes should be switched on, to what extent, and when. To execute their respective manuals, the cells employ so-called chromatin reader proteins that identify which gene is up for expression. Now, a new study has found that a problem in this gene-regulatory process may cause normal cells to turn malignant and produce Wilms’ tumor, the most common kidney cancer in children. The findings, which were published online on December 18, 2019, in Nature, open up new treatment possibilities for the disease, which is currently treated by surgery and chemotherapy. The article is titled “Impaired Cell Fate Through Gain-of-Function Mutations in a Chromatin Reader.” The findings also raise intriguing questions about other cancer types. The researchers found that the implicated reader protein causes problems by acquiring a new property and being too active. "We have never seen this type of mechanism before," says Liling Wan, PhD, a former postdoctoral associate in the Rockefeller Univeersity lab of Dr. C. David Allis, and now an Assistant Professor at the University of Pennsylvania. "It raises the question whether this type of molecular mechanism is also hijacked in other cancer types." A few years ago, Dr. Wan discovered that a reader protein called ENL is involved in blood cancer leukemia by activating the cancer-causing genes. Her attention was turned to Wilms' tumor recently, when it was discovered that some people with Wilms' tumor carry mutations in the gene that codes for ENL.
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