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Article: Recurrent KRAS codon 146 mutations in human colorectal cancer

TitleRecurrent KRAS codon 146 mutations in human colorectal cancer
Authors
Issue Date2006
PublisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cbt/index.php
Citation
Cancer Biology And Therapy, 2006, v. 5 n. 8, p. 928-932 How to Cite?
AbstractAn activating point mutation in codon 12 of the HRAS gene was the first somatic point mutation identified in a human cancer and established the role of somatic mutations as the common driver of oncogenesis. Since then, there have been over 11,000 mutations in the three RAS (HRAS, KRAS and NRAS) genes in codons 12, 13 and 61 reported in the literature. We report here the identification of recurrent somatic missense mutations at alanine 146, a highly conserved residue in the guanine nucleotide binding domain. In two independent series of colorectal cancers from Hong Kong and the United States we detected KRAS A146 mutations in 7/126 and 2/94 cases, respectively, giving a combined frequency of 4%. We also detected KRAS A146 mutations in 2/40 (5%) colorectal cell lines, including the NCI-60 colorectal cancer line HCC2998. Codon 146 mutations thus are likely to make an equal or greater contribution to colorectal cancer than codon 61 mutations (4.2% in our combined series, 1% in the literature). Lung adenocarcinomas and large cell carcinomas did not show codon 146 mutations. We did, however, identify a KRAS A146 mutation in the ML-2 acute myeloid leukemia cell line and an NRAS A146 mutation in the NALM-6 B-cell acute lymphoblastic leukemia line, suggesting that the contribution of codon 146 mutations is not entirely restricted to colorectal cancers or to KRAS. ©2006 Landes Bioscience.
Persistent Identifierhttp://hdl.handle.net/10722/88412
ISSN
2015 Impact Factor: 2.921
2015 SCImago Journal Rankings: 1.297
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorEdkins, Sen_HK
dc.contributor.authorO'Meara, Sen_HK
dc.contributor.authorParker, Aen_HK
dc.contributor.authorStevens, Cen_HK
dc.contributor.authorReis, Men_HK
dc.contributor.authorJones, Sen_HK
dc.contributor.authorGreenman, Cen_HK
dc.contributor.authorDavies, Hen_HK
dc.contributor.authorDalgliesh, Gen_HK
dc.contributor.authorForbes, Sen_HK
dc.contributor.authorHunter, Cen_HK
dc.contributor.authorSmith, Ren_HK
dc.contributor.authorStephens, Pen_HK
dc.contributor.authorGoldstraw, Pen_HK
dc.contributor.authorNicholson, Aen_HK
dc.contributor.authorTsun, LCen_HK
dc.contributor.authorVelculescu, VEen_HK
dc.contributor.authorSiu, TYen_HK
dc.contributor.authorSuet, YLen_HK
dc.contributor.authorStratton, MRen_HK
dc.contributor.authorFutreal, PAen_HK
dc.date.accessioned2010-09-06T09:43:02Z-
dc.date.available2010-09-06T09:43:02Z-
dc.date.issued2006en_HK
dc.identifier.citationCancer Biology And Therapy, 2006, v. 5 n. 8, p. 928-932en_HK
dc.identifier.issn1538-4047en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88412-
dc.description.abstractAn activating point mutation in codon 12 of the HRAS gene was the first somatic point mutation identified in a human cancer and established the role of somatic mutations as the common driver of oncogenesis. Since then, there have been over 11,000 mutations in the three RAS (HRAS, KRAS and NRAS) genes in codons 12, 13 and 61 reported in the literature. We report here the identification of recurrent somatic missense mutations at alanine 146, a highly conserved residue in the guanine nucleotide binding domain. In two independent series of colorectal cancers from Hong Kong and the United States we detected KRAS A146 mutations in 7/126 and 2/94 cases, respectively, giving a combined frequency of 4%. We also detected KRAS A146 mutations in 2/40 (5%) colorectal cell lines, including the NCI-60 colorectal cancer line HCC2998. Codon 146 mutations thus are likely to make an equal or greater contribution to colorectal cancer than codon 61 mutations (4.2% in our combined series, 1% in the literature). Lung adenocarcinomas and large cell carcinomas did not show codon 146 mutations. We did, however, identify a KRAS A146 mutation in the ML-2 acute myeloid leukemia cell line and an NRAS A146 mutation in the NALM-6 B-cell acute lymphoblastic leukemia line, suggesting that the contribution of codon 146 mutations is not entirely restricted to colorectal cancers or to KRAS. ©2006 Landes Bioscience.en_HK
dc.languageengen_HK
dc.publisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cbt/index.phpen_HK
dc.relation.ispartofCancer Biology and Therapyen_HK
dc.subject.meshAdenocarcinoma - geneticsen_HK
dc.subject.meshAmino Acid Sequenceen_HK
dc.subject.meshCarcinoma, Large Cell - geneticsen_HK
dc.subject.meshCodon - geneticsen_HK
dc.subject.meshColorectal Neoplasms - geneticsen_HK
dc.subject.meshDNA Mutational Analysisen_HK
dc.subject.meshDNA, Neoplasm - geneticsen_HK
dc.subject.meshGenes, ras - geneticsen_HK
dc.subject.meshHong Kongen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLeukemia, Myeloid, Acute - geneticsen_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshNeoplasm Stagingen_HK
dc.subject.meshPoint Mutation - geneticsen_HK
dc.subject.meshPrecursor Cell Lymphoblastic Leukemia-Lymphoma - geneticsen_HK
dc.subject.meshSequence Homology, Amino Aciden_HK
dc.subject.meshUnited Statesen_HK
dc.titleRecurrent KRAS codon 146 mutations in human colorectal canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1538-4047&volume=5&issue=8&spage=928&epage=932&date=2006&atitle=Recurrent+KRAS+Codon+146+Mutations+in+Human+Colorectal+Canceren_HK
dc.identifier.emailTsun, LC:tlchan@hku.hken_HK
dc.identifier.emailSuet, YL:suetyi@hkucc.hku.hken_HK
dc.identifier.authorityTsun, LC=rp00418en_HK
dc.identifier.authoritySuet, YL=rp00359en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid16969076-
dc.identifier.scopuseid_2-s2.0-33751165545en_HK
dc.identifier.hkuros123809en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33751165545&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume5en_HK
dc.identifier.issue8en_HK
dc.identifier.spage928en_HK
dc.identifier.epage932en_HK
dc.identifier.isiWOS:000242400700013-
dc.publisher.placeUnited Statesen_HK

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