New understanding of why pancreatic cancer chemotherapy drugs can fail

One of the contributing factors to the poor survival rate for pancreatic cancer is its limited response to conventional chemotherapy. Research published in May 2009 sheds light on why this may be so. Scientists sought to understand why promising drugs generally fail in pancreatic cancer clinical trials. They found that a genetically modified mouse model of pancreatic cancer that closely resembles human cancer was also largely resistant to the drug treatment. Tumours in many other types of cancer develop their own blood supply.

This research, led by Dr. David Tuveson of Cambridge Research Institute, showed that pancreatic cancer tumours have poor blood supply, so limiting the take-up of chemotherapy drugs. Their findings could help overcome resistance to the chemotherapy drug gemcitabine. Dr. Tuveson said: “We’re extremely excited by these results as they may help explain the disappointing response that many pancreatic cancer patients receive from chemotherapy drugs.”

The study also found that the genetically modified mice showed the same resistance to gemcitabine as seen in human pancreatic cancer, whereas the transplantation mouse models traditionally used to develop chemotherapy treatments were sensitive to gemcitabine. This means that the new genetically modified models could prove superior in developing new treatments.

Hear David Tuveson describing the research