Post from Carbone

Sometimes cancer development is not just about a cell having mutations in its DNA, but about when and how those mutations change the cell’s behavior.

UW Carbone Cancer Center member Peter Lewis, PhD, studies how these behavioral changes can lead to cells becoming cancer – and how clinicians and researchers can take advantage of these changes to more effectively target cancers.

In one aspect of his research, Lewis focuses on how genes are turned on and off during embryonic development, and how misregulation in those genes can lead to some childhood cancers.

“In most adult cancers, tumors likely arise from the accumulation of mutations to tumor-suppressing and promoting genes over many years, and in the right context those mutations can lead to cancers,” Lewis said. “But of course children don’t have decades to accumulate mutations, so how do children get tumors early?”

Lewis and his research group at the Wisconsin Institute for Discovery study how mutations in DNA-organizing histone proteins lead to cancer development. For example, in one type of pediatric brain cancer, 85 percent of all tumors have one histone mutation in common. Lewis and his colleagues have shown that, if present at the right time in development, this histone mutation prevents proper gene regulation and causes the stem cells to remain “stuck” in stem cell form, promoting cancer formation. However, if they introduce the mutation into other cells, cancer does not form.

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