No abstract available.
Genes, ras* ; Humans

No abstract available.
Genes, ras* ; Humans*

A variety of molecules are involved in tumorigenesis,during which the RAS pathway-related molecules play key roles. RAS gene mutations exist in about 30% of human tumors;in some tumors(e.g. pancreatic adenocarcinomas),the mutation rates may rise to 75%-95%. Even in tumors without RAS mutations,the RAS pathway-related molecules can also be highly activated. RAS-GTPase-activating proteins(RASGAPs)are a group of tumor suppressors. They normally turn off RAS pathway by catalyzing the hydrolysis of RAS-GTP. However,the mutation or hypermethylation of their promoters will inactivate their roles and thus provide an alternative mechanism of activating Ras. This article reviews the research advances in the role of RASGAPs in the development of tumors.
Cell Transformation, Neoplastic ; DNA Methylation ; Genes, ras ; Humans ; Mutation ; Neoplasms ; ras GTPase-Activating Proteins

The gene is frequently mutated and abnormally activated in many cancers，and plays an important role in cancer development. Metabolic reprogramming occurs in malignant tumors，which can be one of the key targets for anti-tumor therapy. gene can regulate lipid metabolism through AKT-mTORC1 single axis or multiple pathways，such as lipid synthesis pathways and degradation pathways. Similarly，lipid metabolism can also modify and activate RAS protein and its downstream signaling pathways. This article overviews the current research progress on the interaction between lipid metabolism and ，to provide insight in therapeutic strategies of lipid metabolism for -driven tumors.
Genes, ras ; Humans ; Lipid Metabolism/genetics* ; Neoplasms/genetics* ; Signal Transduction ; ras Proteins/metabolism*

No abstract available.
Genes, ras* ; Humans* ; Lymph Nodes* ; Polymerase Chain Reaction*

The EGFR Tyrosine kinase inhibitors (TKIs) show significant clinical benefit in selected population with no smoking history, adenocarcinoma or mutations in EGFR gene. Mutations of K-ras gene are associated with resistance to EGFR TKIs. Three published studies of gefitinib experience from Korea are reviewed. Mutations of EGFR gene published up to now and correlation with response to EGFR-TKIs is summarized. This review also discusses the suggested mechanisms of acquired resistance to EGFR TKIs
Adenocarcinoma ; Genes, erbB-1 ; Genes, ras ; Korea ; Protein-Tyrosine Kinases* ; Smoke ; Smoking ; Tyrosine*

Animals ; Genes, BRCA2 ; Genes, erbB-1 ; Genes, erbB-2 ; Genes, p16 ; Genes, p53 ; Genes, ras ; Genetic Predisposition to Disease ; genetics ; Humans ; Pancreatic Neoplasms ; classification ; genetics ; pathology

BACKGROUND: ras gene mutations have been described in various human malignancies, suggesting that their activation may play a role in oncogenesis. However, there are few reports concerning ras gene alterations in malignant fibrous histiocytomas. We therefore designed a study to determine the prevalence and type of mutations in the first exons of H-ras and K-ras genes in these tumors. METHODS: Twenty-seven malignant fibrous histiocytomas were investigated by direct sequencing analysis with the automated DNA sequencing of polymerase chain reaction-amplified ras sequences. RESULTS: Twenty-four mutations were found in 18 (67%) of the tumors: GGC to GAC transition mutations at codon 13 of K-ras (coding for aspartic acid instead of glycine) in 18 of the samples and GGC to GTC transversions at codon 12 of H-ras (coding for valine instead of glycine) in six of the lesions. CONCLUSIONS: Our data suggest an involvement of the ras gene mutation in conjunction with other yet unknown events in the tumorigenesis and/or progression of malignant fibrous histiocytomas. The K-ras gene activation predominated in these tumors by a mutation at codon 13. It is noteworthy that H-ras mutations were detected only in association with the lesions containing K-ras mutated genes, the significance of which remains to be determined.
Aspartic Acid ; Carcinogenesis ; Codon ; Exons ; Genes, ras* ; Histiocytoma, Malignant Fibrous* ; Humans ; Prevalence ; Sequence Analysis, DNA ; Valine

Cellular oncogenes are expressed as an intrinsic part of the transformed or neoplastic phenotype. More than 60 of the known cellular oncogenes play a specific role in normal cellular development and differentiation. To examine the correlation between ras oncogene expression and the development of cervical cancer, this study investigated the reactivity of cervical intraepithelial neoplasia(CIN) and carcinoma of the uterine cervix by using anti-ras P21 mouse monoclonal antibody. The expression of ras oncogene significantly increased with the grade of malignancy from 11% in severe dysplasia, 30% in carcinoma in situ, 43% in microinvasive carcinoma, to 53% in invasive cancer. The expression of ras oncogene was not correlated with histologic type, tumor size, and nodal status of cervical cancer. It was concluded that expression of ras oncogene is related to early phase of carcinogenesis and tumor invasion of carcinoma of the uterine cervix.
Animals ; Carcinogenesis ; Carcinoma in Situ ; Cervix Uteri* ; Female ; Genes, ras* ; Mice ; Oncogenes ; Phenotype ; Uterine Cervical Neoplasms

No abstract available.
Colorectal Neoplasms* ; Electrophoresis* ; Genes, ras* ; Humans* ; Point Mutation* ; Polymerase Chain Reaction*