A metabolic vulnerability of pancreatic ductal adenocarcinoma (PDAC) could be used to address this type of cancer that often resists treatments. Scientists at the University of Michigan have discovered that inhibiting the PIKfyve enzyme prevented tumor development and reduced tumor growth by altering the lipid synthesis these cells rely on. The KRAS-MAPK pathway is involved in this process, leading the researchers to suggest that dual inhibitors of PIKfyve and KRAS-MAPK could be an effective therapeutic strategy.

The lung and thrombosis may play a key role in cancer and metastasis progression, according to a collaborative study led by Cornell University scientists.

The lung and thrombosis may play a key role in cancer and metastasis progression, according to a collaborative study led by Cornell University scientists. In the nonmetastatic lung microenvironment of several cancer types, the development of a prothrombosis niche promotes metastasis formation through the release of small extracellular vesicles loaded with an integrin protein.

Understanding the mechanisms of resistance to cancer treatments is necessary to find effective therapies at different stages of the disease. Scientists at UT Southwestern Medical Center studied the most frequent mutation in pancreatic ductal adenocarcinoma (PDAC), identified an escape route to a therapy in clinical trials, blocked it with another experimental compound and reduced tumors in mice.

Pancreatic ductal adenocarcinoma (PDAC) has a low 5-year survival rate of <12%. Even though KRAS is mutated in about 88% of PDACs, the KRAS G12C mutation is rare, limiting the use of KRAS G12C inhibitors. Hence, there is a need for pan-RAS inhibitors to cover the broad RAS mutation spectrum in PDAC.

Repeated RNA elements have a virus-like behavior in the cells that express them. Furthermore, they could confer a novel mode of tumor expansion based on changes in cellular states. “About 10 years ago, we had identified that these repetitive elements were highly expressed in pancreas cancer,” co-senior author David Ting, associate professor of medicine and assistant physician at the Mass General Cancer Center at Harvard Medical School, told BioWorld.

The contribution of alternative RNA splicing in the progression of pancreatic ductal adenocarcinoma (PDAC) has not been deeply explored. In a recent study, the RNA-binding protein RNA binding fox-1 homolog 2 (RBFOX2) was investigated, since its role in modulating alternative splicing in PDAC is not well understood.