Researchers identify new mechanisms in pancreatic cancer progression and resistance

Scientists have uncovered two distinct biological mechanisms that contribute to the aggressiveness and treatment resistance of pancreatic cancer.

Researchers at the Karlsruhe Institute of Technology (KIT) identified the CD44 molecule as a key regulator of the tumor microenvironment. In pancreatic cancer, surrounding tissue can account for up to 90% of the tumor mass. The study found that CD44 controls cancer-associated fibroblasts (CAFs), which create a scar-like tissue structure that suppresses the immune response. By inactivating CD44 in laboratory models, researchers observed a reduction in extracellular matrix production and a decreased ability to suppress the immune system, allowing immune cells to attack tumor cells more effectively.

Separately, a study by NYU Langone Health and the Perlmutter Cancer Center examined nearly half a million individual cells to understand how pancreatic ductal adenocarcinoma evolves. The researchers discovered that the cancer utilizes distinct cell populations, or clones, that constantly rewrite their DNA. This genetic reorganization allows certain clones to develop resistance to treatments or gain the ability to invade surrounding tissues and metastasize. This granular view of individual cell evolution helps explain how cancer transitions between less aggressive and more aggressive states.