Researchers at Fox Chase Cancer Center reported preclinical evidence that ANO6 is a therapeutic target in pancreatic ductal adenocarcinoma by helping tumors acquire nutrients and suppress immune responses. The study, published in Nature Cancer, links ANO6 to lipid transfer from cancer-associated fibroblasts to tumor cells through trogocytosis. In animal and laboratory experiments, blocking ANO6 slowed tumor growth and reduced immune suppression, according to the authors. The work positions fibroblasts as active contributors to tumor metabolism rather than passive bystanders, describing a mechanistic pathway where CAF units acquire cholesterol from circulation and then transfer lipids to nearby cancer cells. The researchers said the findings help explain how PDAC cells survive within a dense tumor microenvironment with limited functional blood vessels. The paper identifies ANO6 blockade as a candidate strategy for future therapeutic development targeting both tumor growth and immune evasion.