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KRAS

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.

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.

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.

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.

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.

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.

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