Tag results:
KRAS
Pancreatic Cell News
ANGPTL4 Accelerates KRASG12D-Induced Acinar to Ductal Metaplasia and Pancreatic Carcinogenesis
[Cancer Letters] Scientists investigated the role of ANGPTL4 in KRASG12D-induced acinar-to-ductal metaplasia, pancreatic intraepithelial neoplasia formation, and pancreatic ductal adenocarcinoma maintenance.
Extracellular Matrix News
Tumor Microenvironment-Adjusted Prognostic Implications of the KRAS Mutation Subtype in Patients with Stage III Colorectal Cancer Treated with Adjuvant FOLFOX
[Scientific Reports] Considering the effect of KRAS mutations on tumor microenvironment, investigators analyzed the prognostic significance of KRAS mutation types after adjusting for the tumor-infiltrating lymphocytes and tumor-stromal percentage statuses.
Intestinal Cell News
Immuno-Genomic Classification of Colorectal Cancer Organoids Reveals Cancer Cells with Intrinsic Immunogenic Properties Associated with Patient Survival
[Journal of Experimental & Clinical Cancer Research] Investigators developed a patient-derived colorectal cancer organoid model and performed pairwise analysis of 87 CCOs and their matched primary tumors. The tumor immune microenvironment type of the primary tumor was classified as immuno-active, immuno-exhausted, or immuno-desert.
Pancreatic Cell News
An Exosome-Mimicking Membrane Hybrid Nanoplatform for Targeted Treatment toward Kras-Mutant Pancreatic Carcinoma
[Biomaterials Science] Scientists constructed a hybrid nanoplatform by fusing Celastrol-Loaded PEGylated lipids with the DC2.4 cell membrane to achieve targeted treatment of Kras-mutant pancreatic cancer.
Pancreatic Cell News
PTHrP Drives Pancreatic Cancer Growth and Metastasis and Reveals a New Therapeutic Vulnerability
[Cancer Discovery] Scientists reported that the parathyroid hormone–related protein (PTHrP) was frequently amplified as part of the KRAS amplicon in patients with pancreatic cancer.
Cancer Stem Cell News
Targeting KRAS4A Splicing through the RBM39/DCAF15 Pathway Inhibits Cancer Stem Cells
[Nature Communications] The authors demonstrated that coordinated regulation of both isoforms through control of splicing was essential for development of Kras mutant tumors. The minor KRAS4A isoform was enriched in cancer stem-like cells, where it responded to hypoxia, while the major KRAS4B was induced by ER stress.