Lab study identifies potential drug targets in pancreatic cancer

A cancer cell does not grow on its own: it keeps a set of genes switched on, then copies their instructions into RNA so it can keep multiplying. At Peter Mac, researchers led by Dr. Jennifer Devlin tested drugs against that control system in pancreatic ductal adenocarcinoma cells. The cells were highly sensitive to drugs targeting four proteins in laboratory tests.

The proteins belong to a family called transcriptional cyclin-dependent kinases, or tCDKs. They control crucial stages in the process that copies genetic instructions into RNA. When researchers blocked those stages, the cancer cells produced less new RNA and lost their ability to continue multiplying.

The result matters because pancreatic cancer is still among the hardest cancers to treat. Its overall five-year relative survival rate is approximately 13% to 14%, and outcomes depend heavily on how early the disease is detected and whether it has spread. The study does not show that any of the tested drugs can treat people; it identifies cellular dependencies that future therapies could try to exploit.

The work focused on pancreatic ductal adenocarcinoma, the most common form of pancreatic cancer, and tested a range of drugs aimed at different tCDKs. The researchers found that targeting several of these proteins stopped the cancer cells from growing and multiplying, while pancreatic cancer cells were highly sensitive to drugs targeting CDK9, CDK11, CDK12 and CDK13. Their findings were published in Molecular Cancer Therapeutics.

So what changes in practical terms? For patients, nothing changes yet: the evidence comes from cancer cells in the laboratory, not a clinical trial. For drug researchers, the study narrows the search to four proteins and provides a basis for investigating whether blocking them can become a safe and effective treatment.