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: We investigated stomach cancers for ras abnormalities and expression of ERK1 and ERK2 to determine their significance in the tumor development and/or progression and to evaluate their potential correlation with clinicopathologic parameters. METHODS: Seventy gastric adenocarcinomas were studied immunohistochemically in paraffin-embedded tissue sections for the expression of ERK1 and ERK2 proteins. All tumors were further analyzed with the use of a polymerase chain reaction technique and a direct sequence analysis procedure for the presence of the mutated ras gene. RESULTS: ERK1 and/or ERK2 was expressed in 65.7% (46/70) of the tumors; overexpression of ERK1 was observed in 38 (54.3%) tumors, whereas ERK2 was detected in 29 (41.4%). Nine (12.8%) samples demonstrated multations in the ras gene: 4 in H-ras and 5 in K-ras. Seven of the 9 (77.8%) mutated tumors were of the intestinal type. No association was established between the ras abnormalities and the overexpression of ERK1 and/or ERK2. However, the correlation between ERK2 and progression (early vs. advanced) was statistically significant (p<0.05). CONCLUSIONS: These data indicate that ras abnormalities are uncommon events in gastric adenocarcinomas. The majority of ras mutations, however, occurred in intestinal-type tumors, supporting the notion of different molecular mechanisms involved between the intestinal-and diffuse-type lesions. Enhanced ERK2 activity may provide assistance in the determination of tumor penetration in these tumors.
Adenocarcinoma ; Genes, ras* ; Polymerase Chain Reaction ; Sequence Analysis ; Stomach Neoplasms* ; Stomach*

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

The present study was carried out to evaluate the correlation of metastasis and prognostic factors in squamous cell carcinoma of head and neck. Examination was performed on a series of thirty-seven patients who were confirmed to squamous cell carcinoma and its lymphatic metastasis by pathologist. Correlations of metastasis and other factors such as angiogenesis, histologic grading, and p53 expression and ras oncogene were studied. The depth of tumors was around 1 to 27mm. Twenty cases were more than 10mm deep, of which seventeen cases were shown lymphatic metastasis. Total score of histologic grading including keratinization, nuclear atypia, growth pattern and intensity of inflammation was ranged from 5 to 10 points. Of these factors, nuclear atypia with intensity of inflammation, and nuclear atypia with growth pattern was correlated with nuclear atypia each. For angiogenesis, number of new-formed vessels were counted 13 to 58 each. Twenty-eight cases were shown to lymphatic metastasis. No correlation with histologic grading and lymphatic metastasis was found. The results of immunohistochemical staining for p53 and ras oncogene revealed that positive cases were 16 and 22, negative for 21 and 15 each. However, both were not correlated with histologic grading and lymphatic metastasis. These results were revealed that angiogenesis was not correlated with lymphatic metastasis of squamous cell carcinoma arising in head and neck. Nuclear atypia with intensity of inflammation and dysplasia with growth pattern were correlated with histologic grading, which suggested that more careful and adequate advice is needed for effective treatment.
Carcinoma, Squamous Cell* ; Genes, ras ; Head* ; Humans ; Inflammation ; Lymphatic Metastasis ; Neck* ; Neoplasm Metastasis*