| [Evaluation of K-ras 12 oncogene mutations in Venezuelan patients with Helicobacter pylori infection]. | None |
| External imaging of CCND1, MYC, and KRAS oncogene mRNAs with tumor-targeted radionuclide-PNA-peptide chimeras. | None |
| Multiple oncogenic changes (K-RAS(V12), p53 knockdown, mutant EGFRs, p16 bypass, telomerase) are not sufficient to confer a full malignant phenotype on human bronchial epithelial cells. | None |
| The bovine papillomavirus E5 oncogene can cooperate with ras: identification of p21 amino acids critical for transformation by c-rasH but not v-rasH. | None |
| [Point mutation of c-k-ras oncogene at codon 12 in mucin-producing cystic tumor of the pancreas]. | None |
| In this study, we provide evidence that the ras oncogene, targeted to a specifically sensitive cell compartment within the salivary glands, can trigger a series of event that are sufficient for full carcinogenesis. | None |
| A nuclease hypersensitive polypurine-A polypyrimidine element within the promoter of the KRAS proto-oncogene regulates transcription. | None |
| G-quadruplex formation within the promoter of the KRAS proto-oncogene and its effect on transcription. | None |
| [E1A oncogene effect on the ability of p21(Waf1) to regulate G1/S arrest in E1A-expressing transformants following irradiation]. | None |
| Physiological analysis of oncogenic K-ras. | None |
| Data suggest that c-MYC and Wnt1 select for the outgrowth of cells with mutations in specific ras isoforms such as Kras2, and that these mutations determine the extent of ras/MAPK pathway activation and the potential for oncogene-independent growth. | None |
| RAS oncogene induces RECK gene silencing through DNMT3b-mediated promoter methylation which may be useful in treatment of cancer metastasis | None |
| Loss of Apc allows phenotypic manifestation of the transforming properties of an endogenous K-ras oncogene in vivo. | None |
| Expression of transforming K-Ras oncogene affects mitochondrial function and morphology in mouse fibroblasts. | None |
| observed increase in intestinal tumor multiplicity and malignant transformation is caused by the synergistic activation of Wnt signaling in cells with oncogenic KRAS and loss-of-function Apc mutations | None |
| Expression of oncogenic K-ras from its endogenous promoter leads to a partial block of erythroid differentiation and hyperactivation of cytokine-dependent signaling pathways. | None |
| Results define a mediating role of Nox1-redox signaling for Ras oncogene-induced actin cytoskeletal changes. | None |
| Advances in cancer biomarkers as applied to chemical exposures: the ras oncogene and p21 protein and pulmonary carcinogenesis. | None |
| RNA aptamers targeting the carboxyl terminus of KRAS oncoprotein generated by an improved SELEX with isothermal RNA amplification. | None |
| N-ras oncogene-induced gene expression in human hematopoietic progenitor cells: upregulation of p16INK4a and p21CIP1/WAF1 correlates with myeloid differentiation. | None |