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.
Pancreatic ductal adenocarcinom a (PDAC), frequently detected at advanced stages, has a 5-year survival rate of 12%. Metastases are common, including hepatic metastasis, which is particularly lethal due to the liver’s immune-tolerant environment and rich blood supply that facilitate tumor growth.
RAS G12D is one of the most frequent mutations in RAS, and when it occurs, it leaves RAS in a permanently active state, causing the cell to proliferate uncontrollably. Examples of the so-called RAS-addicted cancers are colorectal cancer or pancreatic ductal adenocarcinoma.
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.
Researchers from University of Athens and National Centre For Scientific Research “Demokritos” have reported preclinical data from a study that aimed to assess the novel cryptochrome-2 (CRY2) stabilizer TH-301 in models of pancreatic ductal adenocarcinoma (PDAC). It was seen that treatment with TH-301 led to significant dose-, time- and cell type-dependent decreases in viability.
Cancervax Inc. has selected pancreatic ductal adenocarcinoma (PDAC) as one of its first targets for preclinical development using its novel universal cancer treatment (UCT) platform.
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.
Pancreatic cancer is among the most lethal cancers and the fourth leading cause of cancer deaths worldwide, where 90% of cases fall into the pancreatic ductal adenocarcinoma (PDAC) type.
Pancreatic ductal adenocarcinoma (PDAC) is still one of the most aggressive cancers, with a high mortality rate among patients. Previous findings have pointed to chitinase 3-like 1 (CHI3L1) as being behind PDAC resistance to gemcitabine, and thus a promising therapeutic target.
