New drug could double survival time in patients with advanced pancreatic cancer

· News-Medical

How does this new drug work?

The medication, called daraxonrasib, is the first drug that targets cancer-causing mutations in pancreas cells.

The drug targets a mutation in the KRAS gene, part of the RAS genetic family. KRAS mutations are present in 92% of pancreatic cancers. KRAS genes normally act as an "on-off" switch for cell growth. Mutated KRAS genes are stuck in the "on" position and send out a signal that causes cells to divide and grow uncontrollably, allowing cancer to form.

Daraxonrasib blocks the KRAS signal by fitting into a keyhole-type spot on the gene. That spot has a complex shape and is difficult to reach within the cell. The drug gets around this problem by using a "passenger protein" as a Trojan horse. When the cell allows this protein in, daraxonrasib tags along.

Why are these clinical trial results so groundbreaking?

What comes next?

We are now testing the drug in patients with earlier-stage pancreatic cancer, prescribing it while their tumors are still operable and before their cancer spreads.

Could daraxonrasib be effective against other cancer types?

RAS mutations are one of the most common cancer-causing genetic mutations, and the drug is now being studied in several cancer types. I think it's going to work especially well in tumors that are primarily RAS driven, including colon cancer and lung cancer. It might also work in other cancer types in combination with drugs targeting other genetic mutations, but further research is needed.

How will this discovery change cancer science?

This is a win for the field. Until now, we have been focused on immune therapies that might make tumors more vulnerable to the body's immune system, and on finding new chemotherapy combinations that kill cancer cells.

This new treatment has given us a new focus, and I think it will spur a lot of scientific discovery over the next few years. There have only been a handful of KRAS researchers and their relevance to therapy was always questioned. That is about to change.

The most important next step for the field is to better understand the biology of cancer. We know that many pancreatic tumors will eventually become resistant to daraxonrasib, and we need to understand how this happens. We also need to identify additional genetic pathways and treatments that can target them. That's how we will turn pancreas cancer from a deadly, deadly cancer into something we can manage-and one day, even cure.

Source:

Cedars-Sinai