Cancer

By testing over 4,000 genes in human tumors, Inder Verma’s team found an enzyme responsible for suppressing lung cancer, which affects nonsmokers as well as smokers and is the leading cause of cancer-related deaths worldwide. This enzyme, called EphA2, normally polices a gene responsible for tissue growth. But when EphA2 is mutated, the Salk team discovered, cellular systems can run amok and quickly develop tumors. The research, published the week of November 2, 2015 in PNAS, suggests that EphA2 could be a new target for a subset of lung cancer.

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A person diagnosed with the brain cancer glioblastoma multiforme typically survives 15 months, if given the best care. Inder Verma’s lab discovered a key to how these tumor cells proliferate so quickly —and ways to turn this engine of tumor growth into a target for cancer treatment. The work was published January 8, 2016 in the journal Science Advances.

To study how glioblastoma multiforme spreads, Verma’s team focused on a transcription factor called nuclear factor kB (or NF-kB). A transcription factor is a protein that binds to DNA and controls the fate of gene expression for a particular set of genes. Verma and colleagues ran a battery of tests to show how overzealous NF-kB activity pushed the cancer cells to proliferate, and how stopping NF-kB slowed cancer growth and increased survival in mice. The scientists fed mice a peptide (called NBD) that is known to block NF-kB activity when NF-kB is triggered by cytokines (proteins produced by the immune system). The NBD peptide easily traveled across the central nervous system and successfully penetrated glioblastoma tumor cells. Treating mice with the NBD peptide doubled their typical survival time compared to mice that didn’t get the NBD peptide.

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