KRAS

[Cell Reports] Pharmacologic inhibition of CHK1 alone caused apoptotic growth suppression of both PDAC cell lines and organoids, which correlated with loss of MYC expression.

[Critical Reviews in Oncology Hematology] Cell-free DNA biomarkers indicate accelerated progression and decreased survival in PDAC.

[Cell Death & Disease] Researchers investigated whether cetuximab-mediated regulation of p38/Nrf2/HO-1 promoted RSL3-induced ferroptosis and played a pivotal role in overcoming drug resistance in KRAS mutant colorectal cancer.

[Journal of Biological Chemistry] Investigtors established a system-wide profile of the KRAS-regulated kinase signaling network in KRAS-mutant pancreatic ductal adenocarcinoma.

[Scientific Reports] Researchers demonstrated the versatile applicability of the new MMTV-Flp strain and manipulated genes in a temporally and spatially controlled manner in the normal mammary gland, in luminal-type mammary tumors that overexpressed ERBB2, and in a new KRAS-associated mammary cancer model.

[Oncogene] Researchers showed that the restoration of wild type (WT) KRAS expression in human pancreatic ductal adenocarcinoma (PDAC) cell lines with LOH at KRAS significantly attenuated the malignancy of PDAC cells both in vitro and in vivo, demonstrating a tumor-suppressive role of the WT KRAS allele.