| These results suggest that loss of Sirt2, as well as increased age, enhanced the immune response to pancreatic injury and induced an inflammatory phenotype permissive for the accumulation of cells carrying oncogenic Kras mutations. | pancreatic, |
| Mutational activation of the K-ras oncogene. A possible pathogenetic factor in adenocarcinoma of the lung. | lung, |
| ras p21 oncoprotein expression in human colonic neoplasia--an immunohistochemical study with monoclonal antibody RAP-5. | colorectal, |
| Incidence and possible clinical significance of K-ras oncogene activation in adenocarcinoma of the human lung. | lung, |
| introducing a rapid and sensitive microarray-based assay for the multiplex detection of minority mutations of oncogenes (KRAS, NRAS and BRAF) with relevant diagnostics implications in tissue biopsies and plasma samples in metastatic colorectal cancer patients | colorectal, |
| NK sensitivity, H-2, c-K-ras proto-oncogene expression and metastases: analysis of the metastatic potential of H-2 gene transfected fibrosarcoma cells. | fibrosarcoma, |
| Results indicate that oncogene addiction can be targeted for therapy in colon cancer cells harboring the KRAS-mutant. | colorectal, |
| Memory T cells targeting oncogenic mutations in KRAS, SMAD5, and MUC4 detected in peripheral blood of colon cancer patients have been isolated. | colorectal, |
| In this study using an inducible kras transgenic zebrafish models for Hepatocellular carcinoma, transcriptomic profiles of oncogenic hepatocytes from larvae, male and female adult fish following a brief induction of oncogenic kras were investigated. Male oncogenic hepatocytes have more severe features than female counterparts. | liver, |
| These data highlight a pivotal role of the cooperative interaction between obesity-ensuing high fat diet and oncogenic KRAS in driving the heightened aerobic glycolysis during pancreatic tumorigenesis. | pancreatic, |
| Our findings suggest that mutant K-Ras plays an oncogenic role through downregulating miR-199b in NSCLC and that overexpression of miR-199b is a novel strategy for the treatment of K-Ras-mutated NSCLC. | lung, |
| Identification of an activated c-Ki-ras oncogene in rat liver tumors induced by aflatoxin B1. | liver, |
| Oncogenic ERBB2 aberrations and KRAS mutations cooperate to promote pancreatic ductal adenocarcinoma progression. | pancreatic, |
| deletion of the Atdc (Trim29) gene, whose human homolog is upregulated in the majority of pancreatic adenocarcinoma, prevents pancreatic adenocarcinoma development in the context of oncogenic KRAS; findings show ATDC (Trim29) promotes acinar-ductal metaplasia progression to pancreatic intraepithelial neoplasia through activation of beta-catenin signaling and subsequent SOX9 up-regulation | pancreatic, |
| We observed frequent duplication of the Kras oncogene with loss of the normal allele, which has potential therapeutic implications that merit further investigation in human leukemia and in other preclinical models | leukemia, |
| Results present evidence that KRAS-mutant pancreatic ductal adenocarcinoma cells can channel their glucose metabolism away from the mitochondria by a previously unappreciated means: programmed mitophagy via the mediator BNIP3L/NIX. Oncogenic KRAS induces NIX expression and suppression of mitochondrial content in a MAPK pathway-dependent fashion. | pancreatic, |
| APEH knockdown abrogated RAS-RAF-MAPK signaling in cells expressing the constitutively active (oncogenic) mutant of KRAS (KRASG12V), and selectively inhibited the proliferation of KRAS-transformed pancreatic cancer cells. Taken together, these results identify APEH as a novel drug target for a potential anti-KRAS therapeutic. | pancreatic, |
| Dual-luciferase reporter assay in pancreatic ductal adenocarcinoma (PDAC) cells validated that TP53TG1 and 3_UTR of KRAS oncogene mRNA competitively bind with miR-96. Data further indicate that TP53TG1 could effectively function as a sponge for miR-96 to modulate the derepression of KRAS, thus promoting PDAC development. | pancreatic, |
| Oncogenic KRAS reduces expression of FGF21 in pancreatic acinar cells, promoting pancreatic tumorigenesis in mice on a high-fat diet. | pancreatic, |
| Cooperation between KRAS and TP53 oncogenic mutations in pancreatic ductal carcinoma activates the ARF6-AMAP1 pathway to promote tumor malignancies and evade the immune system. KRAS primarily acts to promote eIF4A/4E-dependent mRNA translation to up-regulate ARF6 and AMAP1 protein expression, whereas, TP53 facilitates ARF6 activation by platelet-derived growth factor receptor(PDGFR). | pancreatic, |