AI Insight
Researchers at MUSC Hollings Cancer Center have discovered that kidney cancer cells lacking the SETD2 tumor suppressor gene become critically dependent on the BCL-xL protein for survival. In laboratory experiments, targeting this dependency allowed scientists to selectively kill SETD2-deficient cancer cells while sparing those with functional SETD2. This finding reveals a potential therapeutic vulnerability in an aggressive subset of kidney cancers characterized by SETD2 loss.
Why it matters
This research identifies a promising new treatment approach for patients with SETD2-deficient kidney cancers, which are typically more aggressive and difficult to treat. The ability to selectively target cancer cells based on their specific genetic mutations could lead to more effective and personalized therapies with fewer side effects on healthy tissue.
Understand the Science
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.
Source: Kidney cancer gene reveals an unexpected weakness and a new path for treatment