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Article: A novel abl protein expressed in Philadelphia chromosome positive acute lymphoblastic leukaemia

TitleA novel abl protein expressed in Philadelphia chromosome positive acute lymphoblastic leukaemia
Authors
Issue Date1987
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/nature
Citation
Nature, 1987, v. 325 n. 6105, p. 635-637 How to Cite?
AbstractThe Philadelphia (Ph) chromosome breakpoints in chronic myelocytic leukaemia are clustered on chromosome 22 band q11 in a 5.8-kilobase (kb) region designated bcr. The c-abl protooncogene is translocated from chromosome 9 band q34 into bcr and the biochemical consequence of this molecular rearrangement is the production of an abnormal fusion protein bcr-abl p210 with enhanced protein-tyrosine kinase activity compared to the normal p145 c-abl protein. The Ph chromosome translocation is also seen in some acute lymphoblastic leukaemias with B-cell precursor phenotypes some of which have bcr rearrangement (bcr +) and some do not (bcr -). We present evidence that the Ph +, bcr - leukaemias are associated with a novel p190 abl kinase. We propose that acute lymphoblastic leukaemias that are bcr +, p210 + are probably lymphoid blast crises following a clinically silent chronic phase of chronic myelocytic leukaemia arising in multipotential stem cells whereas bcr -, p190 + cases are de novo acute lymphoblastic leukaemias arising in more restricted precursors.
Persistent Identifierhttp://hdl.handle.net/10722/147788
ISSN
2015 Impact Factor: 38.138
2015 SCImago Journal Rankings: 21.936
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChan, LCen_US
dc.contributor.authorKarhi, KKen_US
dc.contributor.authorRayter, SIen_US
dc.date.accessioned2012-05-29T06:09:13Z-
dc.date.available2012-05-29T06:09:13Z-
dc.date.issued1987en_US
dc.identifier.citationNature, 1987, v. 325 n. 6105, p. 635-637en_US
dc.identifier.issn0028-0836en_US
dc.identifier.urihttp://hdl.handle.net/10722/147788-
dc.description.abstractThe Philadelphia (Ph) chromosome breakpoints in chronic myelocytic leukaemia are clustered on chromosome 22 band q11 in a 5.8-kilobase (kb) region designated bcr. The c-abl protooncogene is translocated from chromosome 9 band q34 into bcr and the biochemical consequence of this molecular rearrangement is the production of an abnormal fusion protein bcr-abl p210 with enhanced protein-tyrosine kinase activity compared to the normal p145 c-abl protein. The Ph chromosome translocation is also seen in some acute lymphoblastic leukaemias with B-cell precursor phenotypes some of which have bcr rearrangement (bcr +) and some do not (bcr -). We present evidence that the Ph +, bcr - leukaemias are associated with a novel p190 abl kinase. We propose that acute lymphoblastic leukaemias that are bcr +, p210 + are probably lymphoid blast crises following a clinically silent chronic phase of chronic myelocytic leukaemia arising in multipotential stem cells whereas bcr -, p190 + cases are de novo acute lymphoblastic leukaemias arising in more restricted precursors.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/natureen_US
dc.relation.ispartofNatureen_US
dc.subject.meshAdolescenten_US
dc.subject.meshAdulten_US
dc.subject.meshDna Restriction Enzymes - Metabolismen_US
dc.subject.meshDna, Neoplasm - Analysisen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshLeukemia, Lymphoid - Geneticsen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshNucleic Acid Hybridizationen_US
dc.subject.meshPhiladelphia Chromosomeen_US
dc.subject.meshProtein-Tyrosine Kinases - Metabolismen_US
dc.subject.meshProto-Oncogene Proteins - Analysisen_US
dc.titleA novel abl protein expressed in Philadelphia chromosome positive acute lymphoblastic leukaemiaen_US
dc.typeArticleen_US
dc.identifier.emailChan, LC:chanlc@hkucc.hku.hken_US
dc.identifier.authorityChan, LC=rp00373en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid3027581-
dc.identifier.scopuseid_2-s2.0-0023105320en_US
dc.identifier.volume325en_US
dc.identifier.issue6105en_US
dc.identifier.spage635en_US
dc.identifier.epage637en_US
dc.identifier.isiWOS:A1987F973500061-
dc.publisher.placeUnited Kingdomen_US

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