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fordoctors:k-ras [2019/06/11 20:13]
info_firmalab [Specimen Requirements]
fordoctors:k-ras [2019/06/11 21:32] (current)
info_firmalab [K-RAS Exon 2 sequencing K-RAS. Condon 12, 13 and 61 pathological variations found in Colorectal Cancer - Test # 1333]
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 ====== K-RAS Exon 2 sequencing K-RAS. Condon 12, 13 and 61 pathological variations found in Colorectal Cancer - Test # 1333 ====== ====== K-RAS Exon 2 sequencing K-RAS. Condon 12, 13 and 61 pathological variations found in Colorectal Cancer - Test # 1333 ======
  
-Kirsten ras oncogene homolog from the mammalian ras gene family, encodes a protein that is a member of the small GTPase superfamily. A single amino acid substitution is responsible for an activating mutation. The transforming protein that results is implicated in various malignancies,​ including lung adenocarcinoma,​ mucinous adenoma, ductal carcinoma of the pancreas and colorectal carcinoma. Alternative splicing leads to variants encoding two isoforms that differ in the C-terminal region.The RAS proteins are GDP/​GTP-binding proteins that act as intracellular signal transducers. The cellular homologues of the viral Harvey and Kirsten transforming ras sequences were first identified in the rat genome in 1981 (1) and were subsequently found in the mouse2 and human3 genomes. These discoveries revealed that the ras oncogenes behaved, at least superficially,​ like the src oncogene of Rous sarcoma virus (RSV), the origins of which were first reported in 1976 (2). Thus, protooncogenes residing in the genomes of normal cells can be activated into potent oncogenes by retroviruses,​ which acquire these sequences and convert them into active oncogenes. The Harvey sarcoma virus-associated oncogene was named Ha-ras (H-ras in mammals), whereas that of Kirsten sarcoma virus was termed Ki-ras (K-ras in mammals). Mutant alleles of these ras sequences were soon discovered in many human cancer cell lines, including those of the bladder, colon and lungs(3). The most patological ​variations in different codons and its prevalence in cancer cells are in table 1.+Kirsten ras oncogene homolog from the mammalian ras gene family, encodes a protein that is a member of the small GTPase superfamily. A single amino acid substitution is responsible for an activating mutation. The transforming protein that results is implicated in various malignancies,​ including lung adenocarcinoma,​ mucinous adenoma, ductal carcinoma of the pancreas and colorectal carcinoma. Alternative splicing leads to variants encoding two isoforms that differ in the C-terminal region.The RAS proteins are GDP/​GTP-binding proteins that act as intracellular signal transducers. The cellular homologues of the viral Harvey and Kirsten transforming ras sequences were first identified in the rat genome in 1981 (1) and were subsequently found in the mouse2 and human3 genomes. These discoveries revealed that the ras oncogenes behaved, at least superficially,​ like the src oncogene of Rous sarcoma virus (RSV), the origins of which were first reported in 1976 (2). Thus, protooncogenes residing in the genomes of normal cells can be activated into potent oncogenes by retroviruses,​ which acquire these sequences and convert them into active oncogenes. The Harvey sarcoma virus-associated oncogene was named Ha-ras (H-ras in mammals), whereas that of Kirsten sarcoma virus was termed Ki-ras (K-ras in mammals). Mutant alleles of these ras sequences were soon discovered in many human cancer cell lines, including those of the bladder, colon and lungs(3). The most pathological ​variations in different codons and its prevalence in cancer cells are in table 1.
  
  
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