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Article: The correlation of breakpoint cluster region rearrangement and p210 phl/abl expression with morphological analysis of Ph-negative chronic myeloid leukemia and other myeloproliferative diseases

TitleThe correlation of breakpoint cluster region rearrangement and p210 phl/abl expression with morphological analysis of Ph-negative chronic myeloid leukemia and other myeloproliferative diseases
Authors
Issue Date1988
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
Citation
Blood, 1988, v. 71 n. 2, p. 349-355 How to Cite?
AbstractThe chromosome 22 derivative, the Philadelphia (Ph) chromosome, results from a reciprocal translocation t(9;22)(q34;q11) and is associated with chronic myeloid leukemia (CML). The translocation can be identified at the DNA level in Ph-positive CML by using a probe to the breakpoint cluster region (bcr). In addition, as a result of this translocation an abl-related 210-kd protein with protein tyrosine kinase (PTK) activity is produced. We analyzed 28 cases of Ph-negative CML for rearrangement of the chromosome 22 sequences and found that eight of the 28 show rearrangement of the bcr. When 12 of the Ph-negative cases were independently reviewed, five were indistinguishable from Ph-positive CML on the basis of morphology, peripheral blood film and clinical details. These five also showed bcr rearrangement. The other seven were reclassified as six atypical CML (aCML) and one chronic myelomonocytic leukemia (CMML). None of these seven showed bcr rearrangement. In addition 11 cases of bcr- CML were assayed for abl-related PTK, and no detectable activity was present, whereas p210 phl/abl PTk was observed both in Ph-positive (three cases examined) and Ph-negative, bcr+ (four cases examined) CML. Therefore, bcr+ CML, whether or not the Ph chromosome is cytogenetically apparent, involves a similar molecular alteration and produces the 210-kd protein with enhanced PTK activity. Furthermore, these cases can be distinguished from Ph-negative bcr- CML by careful evaluation of clinical and hematologic data.
Persistent Identifierhttp://hdl.handle.net/10722/147814
ISSN
2015 Impact Factor: 11.841
2015 SCImago Journal Rankings: 6.395
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWiedemann, LMen_US
dc.contributor.authorKarhi, KKen_US
dc.contributor.authorShivji, MKKen_US
dc.contributor.authorRayter, SIen_US
dc.contributor.authorPegram, SMen_US
dc.contributor.authorDowden, Gen_US
dc.contributor.authorBevan, Den_US
dc.contributor.authorWill, Aen_US
dc.contributor.authorGalton, DAGen_US
dc.contributor.authorChan, LCen_US
dc.date.accessioned2012-05-29T06:09:21Z-
dc.date.available2012-05-29T06:09:21Z-
dc.date.issued1988en_US
dc.identifier.citationBlood, 1988, v. 71 n. 2, p. 349-355en_US
dc.identifier.issn0006-4971en_US
dc.identifier.urihttp://hdl.handle.net/10722/147814-
dc.description.abstractThe chromosome 22 derivative, the Philadelphia (Ph) chromosome, results from a reciprocal translocation t(9;22)(q34;q11) and is associated with chronic myeloid leukemia (CML). The translocation can be identified at the DNA level in Ph-positive CML by using a probe to the breakpoint cluster region (bcr). In addition, as a result of this translocation an abl-related 210-kd protein with protein tyrosine kinase (PTK) activity is produced. We analyzed 28 cases of Ph-negative CML for rearrangement of the chromosome 22 sequences and found that eight of the 28 show rearrangement of the bcr. When 12 of the Ph-negative cases were independently reviewed, five were indistinguishable from Ph-positive CML on the basis of morphology, peripheral blood film and clinical details. These five also showed bcr rearrangement. The other seven were reclassified as six atypical CML (aCML) and one chronic myelomonocytic leukemia (CMML). None of these seven showed bcr rearrangement. In addition 11 cases of bcr- CML were assayed for abl-related PTK, and no detectable activity was present, whereas p210 phl/abl PTk was observed both in Ph-positive (three cases examined) and Ph-negative, bcr+ (four cases examined) CML. Therefore, bcr+ CML, whether or not the Ph chromosome is cytogenetically apparent, involves a similar molecular alteration and produces the 210-kd protein with enhanced PTK activity. Furthermore, these cases can be distinguished from Ph-negative bcr- CML by careful evaluation of clinical and hematologic data.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.meshChromosomes, Human, Pair 22en_US
dc.subject.meshChromosomes, Human, Pair 9en_US
dc.subject.meshDna, Neoplasm - Geneticsen_US
dc.subject.meshHumansen_US
dc.subject.meshLeukemia, Myeloid - Genetics - Pathologyen_US
dc.subject.meshMyeloproliferative Disorders - Geneticsen_US
dc.subject.meshNeoplasm Proteins - Genetics - Metabolismen_US
dc.subject.meshPhiladelphia Chromosomeen_US
dc.subject.meshProtein-Tyrosine Kinases - Geneticsen_US
dc.subject.meshProto-Oncogene Proteins - Geneticsen_US
dc.subject.meshProto-Oncogenesen_US
dc.titleThe correlation of breakpoint cluster region rearrangement and p210 phl/abl expression with morphological analysis of Ph-negative chronic myeloid leukemia and other myeloproliferative diseasesen_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.pmid3276362-
dc.identifier.scopuseid_2-s2.0-0023851442en_US
dc.identifier.volume71en_US
dc.identifier.issue2en_US
dc.identifier.spage349en_US
dc.identifier.epage355en_US
dc.identifier.isiWOS:A1988L922400012-
dc.publisher.placeUnited Statesen_US

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