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 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.
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.
Patients with end-stage pancreatic ductal adenocarcinoma achieved unprecedented survival rates after being treated with the Engeneic dream vector nanocells, with 88% of patients doubling the historical survival rates, Engeneic Ltd. co-CEO Jennifer MacDiarmid told BioWorld.
Patients with end-stage pancreatic ductal adenocarcinoma achieved unprecedented survival rates after being treated with the Engeneic dream vector nanocells, with 88% of patients doubling the historical survival rates, Engeneic Ltd. co-CEO Jennifer MacDiarmid told BioWorld.
The traps that neutrophils develop against microorganisms also hold T cells and prevent the success of immunotherapy in pancreatic cancer. To free the immune system from itself, scientists at the Istituto Oncologico Veneto in Italy made a key that unlocked this sticky dungeon from an antibody against arginase-1 (ARG1), an enzyme also present in the trap.
Tumors have a lower interstitial pH compared to healthy tissues, with tumor acidity having emerged as a driver of tumor progression as it can lead to tumor immune evasion. Solute carrier family 4 member 4 (SLC4A4), which encodes a sodium bicarbonate cotransporter involved in pH regulation and homeostasis in normal tissue, was the focus of studies in pancreatic cancer resistance in in vivo preclinical models. Researchers tested the impact of Slc4a4 deletion in cancer cells on tumor growth, anticancer immunity and response to immunotherapy in murine models of pancreatic ductal adenocarcinoma (PDAC).
Immunotherapeutic targeting of stage-specific embryonic antigen-4 has been shown to inhibit pancreatic cancer growth in animal models and cancer cell lines, indicating that this approach has promise for treating pancreatic ductal adenocarcinoma and possibly other SSEA-4-positive cancers, according to new a Taiwan/U.S. collaborative study.
Pretreatment with an experimental focal adhesion kinase inhibitor has been shown to improve chemotherapeutic efficiency and reduce metastasis in preclinical mouse and patient-derived models of pancreatic ductal adenocarcinoma (PDAC), with this priming regimen soon to enter phase II trials for PDAC using a novel, clinically relevant FAK inhibitor.
