Scientists reveal the best way to treat pancreatic cancer

Specific molecular signals released by pancreatic cancer cells have been determined. Pancreatic cancer is usually detected after the disease has spread, and chemotherapy often has no effect on slowing the development of cancer. Even with treatment, most patients can only survive for about six months after being diagnosed with pancreatic cancer.

In pancreatic cancer, fibroblasts are abundant, accounting for nearly 90% of tumor mass. This matrix prevents anticancer drugs from entering the target. In addition, stromal cells secrete factors that contribute to tumor growth. Researchers at Professor David Tuveson’s laboratory at Cold Spring Harbor Laboratory (CSHL) believe that different types of treatments can be better. Part of the problem is that cancer cells in the pancreas are protected by the dense matrix surrounding them. The stroma is a mixture of extracellular components and non-cancerous cells called stroma. All solid tumors contain stroma. Overcoming the protective effects of the matrix is ​​challenging, but as reported in the journal Cancer Discovery on October 26, 2018, the new clue from the Tuveson team points to a promising strategy. The new findings indicate that drugs that target the correct cellular pathway not only prevent tumor-supporting cells in the matrix, they may be recruited into the fight against cancer.

The key to the matrix is ​​fibroblasts, which can produce connective tissue of the matrix, and can also produce factors that promote the growth of cancer cells and prevent the immune system from attacking cancer cells. Last year, Tuveson’s team discovered that pancreatic tumor stroma contains at least two types of fibroblasts. One type shows features that are known to support tumor growth, and the other type shows opposite effects. The good news is that the identity of fibroblasts is not fixed, and tumor-promoting fibroblasts can become tumor limiting factors. Giulia Biffi, a postdoctoral researcher in the Tuveson laboratory, explained, “These cells can transform into each other, depending on the clues they get from the microenvironment and cancer cells. In theory, you can transform tumor-promoting cells into tumor suppressors, It ‘s not just depleting tumor-promoting cells. ”They found that IL-1 drives fibroblasts with tumor-promoting properties. They also discovered how another molecule, TGF-β, covers this signal and keeps fibroblasts in a potentially anti-cancer state. Biffi said patients can benefit most from the combination of treatments targeting cancer cells and the microenvironmental part that supports their growth.