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

OBJECTIVE: Comparative genomic hybridization was performed to evaluate DNA sequence copy number changes in human ovarian carcinomas from paraffin-embedded tissue blocks. PATIENTS AND METHODS: DNA from 20 cases of primary ovarian carcinomas underwent comparative genomic hybridization to evaluate the extent of genetic gains or losses in a test sample. RESULTS: In thirteen cases of 20 samples, varying degree of genetic imbalances was observed. Of the remaining 7 cases, two revealed normal, five failed to yield a result. Most common genetic imbalances are 8q22.2-q24 site amplification and 12p site amplification, where c-myc gene and k-ras gene respectively are included. Second most common site of genetic imbalance is 7p21-pter site deletion. CONCLUSION: Our results have shown many chromosomal alterations in human ovarian carcinomas, and these sites are known previously as oncogene or tumor-suppression gene, and some sites are not known specific cancer associated sites. Our data can be useful for screening chromosomal changes and molecular mechanism of human ovarian carcinogenesis.
Base Sequence ; Carcinogenesis ; Comparative Genomic Hybridization* ; DNA ; Genes, myc ; Genes, ras ; Humans ; Mass Screening ; Oncogenes ; Ovarian Neoplasms

BACKGROUND: Activation of the K-ras oncogene by specific point mutations at codon 12 occurs at a remarkably high frequency in pancreatic adenocarcinomas. Also, inactivation of the p53 suppressor gene function in pancreatic adenocarcinomas leads to the loss of cellular proliferation regulation and to the induction of cell death. Though K-ras mutation and inactivation of the p53 suppresser gene have been considered to be events in the oncogenesis of a pancreatic adenocarcinoma, whether their association with differences or survival in pancreatic adenocarcinoma is controversial. We investigated the presence of K-ras mutation and overexpression of p53 protein in the carcinogenesis of a pancreatic adenocarcinoma. Also, their correlations with tumor grade, stage, and survival were investigated. METHODS: We examined surgically resected, formalin-fixed, paraffin-embedded pancreatic adenocarci nomas from 48 patients. By using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), we detected a K-ras oncogene mutation at codon 12. An overexpression of p53 protein was detected by using an immunohistochemical staining (IHC) method with anti-p53 monoclonal antibody. RESULTS: K-ras oncogene mutation at codon 12 was detected in 64.6% of the cases and p53 protein was overexpressed in 47.9%. Both K-ras oncogene mutation and p53 protein overexpression were detected in 29.2% of the cases. There was no correlation between the rate of K-ras mutation and tumor grade, T category (tumor size or depth of invasion), N category (lymph-node metastasis) and clinical stage. Also, K-ras mutation was not correlated with the survival rate. A positive correlation between p53 protein overexpression and clinical stage was found (p<0.05). The patients with p53 protein overexpression had a shorter survival than the patients without p53 protein overexpression (p>0.05). CONCLUSION: The mutation of the K-ras oncogene and p53 suppresser gene might play an important role in pancreatic carcinogenesis. However, the mutation of the K-ras oncogene is not thought to be related to the progression of a pancreatic adenocarcinoma and the corresponding survival rate. It is suggested that overexpression of the p53 protein seems to be associated with the progression of pancreatic adenocarcinoma.
Adenocarcinoma* ; Carcinogenesis ; Cell Death ; Cell Proliferation ; Codon ; Genes, ras ; Genes, Suppressor ; Humans ; Noma ; Point Mutation ; Prognosis ; Survival Rate

The blast phase in chronic myelogenous leukemia (CML) is associated with mutation of several genes. It is well known that p53 gene mutation plays a key role in the myeloid or lymphoid blast phase of CML. But for the case of the N-ras gene, the association between N-ras mutations and the blast phase of CML is not yet known. We report here on a case of detecting N-ras point mutation without p53 mutation in a 64 year-old man who suffered from the lymphoblastic blast phase of CML.
Blast Crisis ; Genes, p53 ; Genes, ras ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Point Mutation ; Stress, Psychological