Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0265264 (HOS)
 1,119 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The met oncogene was previously isolated from a chemically transformed human cell line, MNNG-HOS. Recent evidence has demonstrated that two classes of transcripts are expressed from the met proto-oncogene locus. The met oncogene, however, expresses an aberrant RNA which has sequences in common with both transcripts. We now report partial nucleotide sequencing of the human met oncogene and show that met is related to the protein kinase oncogenes and growth factor receptors. The met nucleotide sequence is not identical to that of any published gene, and it is more closely homologous to the tyrosine kinases than to the serine/threonine kinases. Within the tyrosine kinase family, the sequenced met domains are most closely related to the human insulin receptor and the viral abl gene. In situ chromosome hybridization has mapped met to human chromosome 7 band 7q21-q31, a location distinct from that of other kinases. This is also a region associated with nonrandom chromosomal deletions observed in a portion of patients with acute nonlymphocytic leukaemia. The accompanying paper shows that this chromosomal locus is also tightly linked with the human heredity disease cystic fibrosis.
 ...
PMID:The human met oncogene is related to the tyrosine kinase oncogenes. 406 11

The c-met proto-oncogene, encoding the hepatocyte growth factor receptor, can be activated by various mechanisms. These include, among others, gene amplification with concomitant overexpression and the tpr-met oncogenic rearrangement. In the case of gastric cancer, contradictory results on the presence of the tpr-met oncogenic rearrangement have been published. The current study aimed therefore to assess the prevalence of tpr-met expression in Caucasian gastric adenocarcinomas, to evaluate the importance of this oncogene in their carcinogenesis. In addition, the level of c-met expression was determined, to evaluate the role of this alternative mode of activation of the proto-oncogene. A series of Caucasian gastric adenocarcinomas (n=43) and normal gastric mucosal samples (n=14) was analysed for tpr-met and c-met expression. Expression of tpr-met mRNA in the samples was performed by two reverse transcriptase polymerase chain reaction (RT-PCR) assays, with excellent correlation. The specificity of both methods was confirmed by direct sequencing of the PCR products of the MNNG-HOS cell line, which is known to contain the rearrangement. The level of c-met expression was assessed using semi-quantitative RT-PCR assays and immunohistochemistry (IHC). None of the normal gastric mucosal or gastric adenocarcinoma samples expressed tpr-met mRNA, as determined by both RT-PCR assays. Seventy per cent of the adenocarcinomas showed overexpression of c-met, according to elevated c-met mRNA levels, compared with the expression level of normal gastric mucosa. A significant correlation was found between the level of c-met mRNA and protein expression. In conclusion, these results strongly suggest that tpr-met activation does not play a role in Caucasian gastric carcinogenesis, while overexpression of the c-met gene occurs in the majority of Caucasian gastric adenocarcinomas.
 ...
PMID:Absence of tpr-met and expression of c-met in human gastric mucosa and carcinoma. 1152 50