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Article: Lineage promiscuity in hemopoietic differentiation and leukemia

TitleLineage promiscuity in hemopoietic differentiation and leukemia
Authors
Issue Date1986
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
Citation
Blood, 1986, v. 67 n. 1, p. 1-11 How to Cite?
AbstractAn increasing number of reports document instances in which individual leukemic cells coexpress markers normally believed to be restricted to a single lineage. This has been interpreted by McCulloch and colleagues as aberrant programming or lineage infidelity and contrasts with earlier suggestions that lineage fidelity of gene expression was usually maintained in leukemia. We argue that several examples of infidelity are suspect on technical grounds, whereas others are bona fide and require explanation, eg, partial rearrangements and expression of Ig heavy-chain and/or T cell receptor genes in inappropriate cells and terminal deoxynucleotidyl transferase in leukemic myeloblasts. Individual examples of truly aberrant gene expression may well occur in leukemia but with insufficient regularity to be of general significance. We suggest that verifiable and consistent examples of apparent lineage infidelity do not reflect genetic misprogramming but rather the existence of a transient phase of limited promiscuity of gene expression occurring in normal bipotential or multipotential progenitors and able to be preserved as a relic in leukemic blast cell populations that are in maturation arrest. This alternative explanation has interesting implications for mechanism of hematopoietic differentiation and leads to some testable predictions.
Persistent Identifierhttp://hdl.handle.net/10722/147774
ISSN
2015 Impact Factor: 11.841
2015 SCImago Journal Rankings: 6.395
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorGreaves, MFen_US
dc.contributor.authorChan, LCen_US
dc.contributor.authorFurley, AJWen_US
dc.date.accessioned2012-05-29T06:09:09Z-
dc.date.available2012-05-29T06:09:09Z-
dc.date.issued1986en_US
dc.identifier.citationBlood, 1986, v. 67 n. 1, p. 1-11en_US
dc.identifier.issn0006-4971en_US
dc.identifier.urihttp://hdl.handle.net/10722/147774-
dc.description.abstractAn increasing number of reports document instances in which individual leukemic cells coexpress markers normally believed to be restricted to a single lineage. This has been interpreted by McCulloch and colleagues as aberrant programming or lineage infidelity and contrasts with earlier suggestions that lineage fidelity of gene expression was usually maintained in leukemia. We argue that several examples of infidelity are suspect on technical grounds, whereas others are bona fide and require explanation, eg, partial rearrangements and expression of Ig heavy-chain and/or T cell receptor genes in inappropriate cells and terminal deoxynucleotidyl transferase in leukemic myeloblasts. Individual examples of truly aberrant gene expression may well occur in leukemia but with insufficient regularity to be of general significance. We suggest that verifiable and consistent examples of apparent lineage infidelity do not reflect genetic misprogramming but rather the existence of a transient phase of limited promiscuity of gene expression occurring in normal bipotential or multipotential progenitors and able to be preserved as a relic in leukemic blast cell populations that are in maturation arrest. This alternative explanation has interesting implications for mechanism of hematopoietic differentiation and leads to some testable predictions.en_US
dc.languageengen_US
dc.publisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/en_US
dc.relation.ispartofBlooden_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntibodies, Monoclonal - Immunologyen_US
dc.subject.meshAntigens, Differentiation, T-Lymphocyteen_US
dc.subject.meshAntigens, Surface - Analysisen_US
dc.subject.meshCell Differentiationen_US
dc.subject.meshDna Nucleotidylexotransferase - Analysisen_US
dc.subject.meshHematopoiesisen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunoglobulins - Geneticsen_US
dc.subject.meshLeukemia - Immunology - Pathologyen_US
dc.subject.meshModels, Biologicalen_US
dc.subject.meshPhenotypeen_US
dc.subject.meshReceptors, Antigen, T-Cell - Geneticsen_US
dc.subject.meshRecombination, Geneticen_US
dc.subject.meshTranscription, Geneticen_US
dc.titleLineage promiscuity in hemopoietic differentiation and leukemiaen_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.pmid3079640-
dc.identifier.scopuseid_2-s2.0-0022647730en_US
dc.identifier.volume67en_US
dc.identifier.issue1en_US
dc.identifier.spage1en_US
dc.identifier.epage11en_US
dc.identifier.isiWOS:A1986AYB4500001-
dc.publisher.placeUnited Statesen_US

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