Pancreatic Cancer
Study links sympathetic nerve signaling to early pancreatic cancer growth via a fibroblast feedback loop
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Researchers at Cold Spring Harbor Laboratory report that support cells known as myofibroblastic cancer-associated fibroblasts (myCAFs) can recruit sympathetic nerve fibers into early pancreatic lesions, creating a feedback loop that may help pancreatic cancer take hold before full tumors form. In mouse experiments, disrupting sympathetic nerve activity reduced fibroblast activation and was associated with nearly a 50% reduction in tumor growth.
Scientists at Johns Hopkins Medicine have pinpointed the gene KLF5 as a key driver of pancreatic cancer metastasis through epigenetic changes rather than DNA mutations. Using CRISPR technology, researchers found that KLF5 promotes tumor growth and invasion by altering DNA packaging and activating other cancer-related genes. The findings, published in Molecular Cancer, suggest potential new treatment targets.
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Researchers at Cold Spring Harbor Laboratory have identified key proteins and protein complexes that help certain carcinomas shift their cellular identity and potentially evade treatment. Two new studies, focusing on pancreatic cancer and tuft cell lung cancer, highlight molecular structures that could become targets for more precise and selective therapies.