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Article: Molecular cytogenetic characterization of a critical region in bands 7q35-q36 commonly deleted in malignant myeloid disorders

TitleMolecular cytogenetic characterization of a critical region in bands 7q35-q36 commonly deleted in malignant myeloid disorders
Authors
Issue Date1998
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
Citation
Blood, 1998, v. 92 n. 11, p. 4031-4035 How to Cite?
AbstractLoss of chromosome 7 (-7) or deletion of the long arm (7q-) are recurring chromosome abnormalities in myeloid leukemias. The association of - 7/7q- with myeloid leukemia suggests that these regions contain novel tumor suppressor gene(s), whose loss of function contribute to leukemic transformation or tumor progression. Based on chromosome banding analysis, two critical regions have been identified, one in band q22 and another in bands q32-q35. Presently there are no data available on the molecular delineation of the distal critical region. In this study we analyzed bone marrow and blood samples from 13 patients with myeloid leukemia (de novo myelodysplastic syndrome [MDS], n=3; de novo acute myeloid leukemia [AML], n=9; therapy-related (t-) AML, n=1) which, on chromosome banding analysis, exhibited deletions (n=12) or in one case a balanced translocation involving bands 7q31-qter using fluorescence in situ hybridization (FISH). As probes we used representative clones from a contig map of yeast artificial chromosome (YAC) clones that spans chromosome bands 7q31.1-qter. In the 12 cases with loss of 7q material, we identified a commonly deleted region of approximately 4 to 5 megabasepairs in size encompassing the distal part of 7q35 and the proximal part of 7q36. Furthermore, the breakpoint of the reciprocal translocation from the patient with t-AML was localized to a 1,300-kb sized YAC clone that maps to the proximal boundary of the commonly deleted region. Interestingly, in this case both homologs of chromosome 7 were affected: one was lost (-7) and the second exhibited the t(7q35). The identification and delineation of translocation and deletion breakpoints provides the first step toward the identification of the gene(s) involved in the pathogenesis of 7q35-q36 aberrations in myeloid disorders.
Persistent Identifierhttp://hdl.handle.net/10722/44347
ISSN
2023 Impact Factor: 21.0
2023 SCImago Journal Rankings: 5.272
Other Identifiers
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDöhner, Ken_HK
dc.contributor.authorBrown, Jen_HK
dc.contributor.authorHehmann, Uen_HK
dc.contributor.authorHetzel, Cen_HK
dc.contributor.authorStewart, Jen_HK
dc.contributor.authorLowther, Gen_HK
dc.contributor.authorScholl, Cen_HK
dc.contributor.authorFröhling, Sen_HK
dc.contributor.authorCuneo, Aen_HK
dc.contributor.authorTsui, LCen_HK
dc.contributor.authorLichter, Pen_HK
dc.contributor.authorScherer, SWen_HK
dc.contributor.authorDöhner, Hen_HK
dc.date.accessioned2007-09-12T03:51:51Z-
dc.date.available2007-09-12T03:51:51Z-
dc.date.issued1998en_HK
dc.identifierhttp://bloodjournal.hematologylibrary.org/cgi/reprint/92/11/4031.pdfen_HK
dc.identifier.citationBlood, 1998, v. 92 n. 11, p. 4031-4035en_HK
dc.identifier.issn0006-4971en_HK
dc.identifier.urihttp://hdl.handle.net/10722/44347-
dc.description.abstractLoss of chromosome 7 (-7) or deletion of the long arm (7q-) are recurring chromosome abnormalities in myeloid leukemias. The association of - 7/7q- with myeloid leukemia suggests that these regions contain novel tumor suppressor gene(s), whose loss of function contribute to leukemic transformation or tumor progression. Based on chromosome banding analysis, two critical regions have been identified, one in band q22 and another in bands q32-q35. Presently there are no data available on the molecular delineation of the distal critical region. In this study we analyzed bone marrow and blood samples from 13 patients with myeloid leukemia (de novo myelodysplastic syndrome [MDS], n=3; de novo acute myeloid leukemia [AML], n=9; therapy-related (t-) AML, n=1) which, on chromosome banding analysis, exhibited deletions (n=12) or in one case a balanced translocation involving bands 7q31-qter using fluorescence in situ hybridization (FISH). As probes we used representative clones from a contig map of yeast artificial chromosome (YAC) clones that spans chromosome bands 7q31.1-qter. In the 12 cases with loss of 7q material, we identified a commonly deleted region of approximately 4 to 5 megabasepairs in size encompassing the distal part of 7q35 and the proximal part of 7q36. Furthermore, the breakpoint of the reciprocal translocation from the patient with t-AML was localized to a 1,300-kb sized YAC clone that maps to the proximal boundary of the commonly deleted region. Interestingly, in this case both homologs of chromosome 7 were affected: one was lost (-7) and the second exhibited the t(7q35). The identification and delineation of translocation and deletion breakpoints provides the first step toward the identification of the gene(s) involved in the pathogenesis of 7q35-q36 aberrations in myeloid disorders.en_HK
dc.languageengen_HK
dc.publisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/en_HK
dc.relation.ispartofBlooden_HK
dc.subject.meshChromosomes, human, pair 7en_HK
dc.subject.meshGenetic markersen_HK
dc.subject.meshLeukemia, myeloid - geneticsen_HK
dc.subject.meshSequence deletionen_HK
dc.subject.meshGenes, tumor suppressoren_HK
dc.titleMolecular cytogenetic characterization of a critical region in bands 7q35-q36 commonly deleted in malignant myeloid disordersen_HK
dc.typeArticleen_HK
dc.identifier.emailTsui, LC: tsuilc@hkucc.hku.hken_HK
dc.identifier.authorityTsui, LC=rp00058en_HK
dc.description.naturelink_to_OA_fulltexten_HK
dc.identifier.doi10.1182/blood.V92.11.4031.423k55_4031_4035-
dc.identifier.pmid9834205-
dc.identifier.scopuseid_2-s2.0-0032402187en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032402187&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume92en_HK
dc.identifier.issue11en_HK
dc.identifier.spage4031en_HK
dc.identifier.epage4035en_HK
dc.identifier.isiWOS:000077194300006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridDöhner, K=6701684371en_HK
dc.identifier.scopusauthoridBrown, J=8747877300en_HK
dc.identifier.scopusauthoridHehmann, U=6504070834en_HK
dc.identifier.scopusauthoridHetzel, C=19434612900en_HK
dc.identifier.scopusauthoridStewart, J=7404791858en_HK
dc.identifier.scopusauthoridLowther, G=7004062420en_HK
dc.identifier.scopusauthoridScholl, C=8847739500en_HK
dc.identifier.scopusauthoridFröhling, S=8847739800en_HK
dc.identifier.scopusauthoridCuneo, A=7006208534en_HK
dc.identifier.scopusauthoridTsui, LC=7102754167en_HK
dc.identifier.scopusauthoridLichter, P=7102379763en_HK
dc.identifier.scopusauthoridScherer, SW=35374654500en_HK
dc.identifier.scopusauthoridDöhner, H=35374055900en_HK
dc.identifier.issnl0006-4971-

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