Kidney cancer gene reveals an unexpected weakness and a new path for treatment

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Researchers have discovered that kidney cancer cells deficient in the SETD2 tumor suppressor gene depend on the BCL-xL protein for survival. Targeting this dependency in laboratory models has allowed selective elimination of these cancer cells, suggesting a new potential therapeutic strategy for aggressive kidney cancer types.

A common genetic mutation that helps some kidney cancers survive may also expose an unexpected weakness, one that MUSC Hollings Cancer Center researchers hope to transform into a new treatment strategy. In a study published in Cancer Research, Aguirre de Cubas, Ph.D., and colleagues have discovered that kidney cancer cells lacking the tumor suppressor gene SETD2 become highly dependent on a protein called BCL-xL for survival. By targeting that dependency, the researchers were able to selectively eliminate SETD2-deficient cancer cells in laboratory models while largely sparing cancer cells with intact SETD2. The findings identify a potential new therapeutic strategy for patients with a particularly aggressive subset of kidney cancers.