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Article: Molecular cytogenetic delineation of deletions and translocations involving chromosome band 7q22 in myeloid leukemias

TitleMolecular cytogenetic delineation of deletions and translocations involving chromosome band 7q22 in myeloid leukemias
Authors
Issue Date1997
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
Citation
Blood, 1997, v. 89 n. 6, p. 2036-2041 How to Cite?
AbstractLoss of chromosome 7 (-7) or deletion of its long arm (7q-) are recurring chromosome abnormalities in myeloid disorders, especially in therapy-related myelodysplastic syndrome (t-MDS) and acute myeloid leukemia (t-AML). The association of -7/7q- with myeloid leukemia suggests that these regions contain a novel tumor suppressor gene(s) whose loss of function contributes to leukemic transformation or tumor progression. Based on chromosome banding analysis, two critical regions have been identified: one in band 7q22 and a second in bands 7q32-q35. We analyzed bone marrow and blood samples from 21 patients with myeloid leukemia (chronic myeloid leukemia, n = 2; de novo MDS, n = 4; de novo AML, n = 13: t-AML, n = 2) that on chromosome banding analysis exhibited deletions (n = 19) or reciprocal translocations (n = 2) of band 7q22 using fluorescence in situ hybridization. As probes, we used Alu-polymerase chain reaction products from 22 yeast artificial chromosome (YAC) clones that span chromosome bends 7q21.1-q32, including representative clones from a panel of YACs recognizing a contiguous genomic DNA fragment of 5 to 6 Mb in band 7q22. In the 19 cases with deletions, we identified two distinct commonly deleted regions: one region within band 7q22 was defined by the two CML cases; the second region encompassed a distal part of band 7q22 and the entire band 7q31 and was defined by the MDS/AML cases. The breakpoint of one of the reciprocal translocations was mapped to 7q21.3, which is centromeric to both of the commonly deleted regions. The breakpoint of the second translocation, which was present in unstimulated bone marrow and phytohemagglutinin-stimulated blood of an MDS patient, was localized to a 400-kb genomic segment in 7q22 within the deletion cluster of the MDS/AML cases. In conclusion, our data show marked heterogeneity of 7q22 deletion and translocation breakpoints in myeloid leukemias, suggesting the existence of more than one pathogenetically relevant gene.
Persistent Identifierhttp://hdl.handle.net/10722/44314
ISSN
2015 Impact Factor: 11.841
2015 SCImago Journal Rankings: 6.395
Other Identifiers
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFischer, Ken_HK
dc.contributor.authorFröhling, Sen_HK
dc.contributor.authorScherer, SWen_HK
dc.contributor.authorBrown, JMen_HK
dc.contributor.authorScholl, Cen_HK
dc.contributor.authorStilgenbauer, Sen_HK
dc.contributor.authorTsui, LCen_HK
dc.contributor.authorLichter, Pen_HK
dc.contributor.authorDöhner, Hen_HK
dc.date.accessioned2007-09-12T03:51:14Z-
dc.date.available2007-09-12T03:51:14Z-
dc.date.issued1997en_HK
dc.identifierhttp://bloodjournal.hematologylibrary.org/cgi/reprint/89/6/2036en_HK
dc.identifier.citationBlood, 1997, v. 89 n. 6, p. 2036-2041en_HK
dc.identifier.issn0006-4971en_HK
dc.identifier.urihttp://hdl.handle.net/10722/44314-
dc.description.abstractLoss of chromosome 7 (-7) or deletion of its long arm (7q-) are recurring chromosome abnormalities in myeloid disorders, especially in therapy-related myelodysplastic syndrome (t-MDS) and acute myeloid leukemia (t-AML). The association of -7/7q- with myeloid leukemia suggests that these regions contain a novel tumor suppressor gene(s) whose loss of function contributes to leukemic transformation or tumor progression. Based on chromosome banding analysis, two critical regions have been identified: one in band 7q22 and a second in bands 7q32-q35. We analyzed bone marrow and blood samples from 21 patients with myeloid leukemia (chronic myeloid leukemia, n = 2; de novo MDS, n = 4; de novo AML, n = 13: t-AML, n = 2) that on chromosome banding analysis exhibited deletions (n = 19) or reciprocal translocations (n = 2) of band 7q22 using fluorescence in situ hybridization. As probes, we used Alu-polymerase chain reaction products from 22 yeast artificial chromosome (YAC) clones that span chromosome bends 7q21.1-q32, including representative clones from a panel of YACs recognizing a contiguous genomic DNA fragment of 5 to 6 Mb in band 7q22. In the 19 cases with deletions, we identified two distinct commonly deleted regions: one region within band 7q22 was defined by the two CML cases; the second region encompassed a distal part of band 7q22 and the entire band 7q31 and was defined by the MDS/AML cases. The breakpoint of one of the reciprocal translocations was mapped to 7q21.3, which is centromeric to both of the commonly deleted regions. The breakpoint of the second translocation, which was present in unstimulated bone marrow and phytohemagglutinin-stimulated blood of an MDS patient, was localized to a 400-kb genomic segment in 7q22 within the deletion cluster of the MDS/AML cases. In conclusion, our data show marked heterogeneity of 7q22 deletion and translocation breakpoints in myeloid leukemias, suggesting the existence of more than one pathogenetically relevant gene.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.meshChromosome aberrations - geneticsen_HK
dc.subject.meshChromosome bandingen_HK
dc.subject.meshChromosomes, human, pair 7en_HK
dc.subject.meshGene deletionen_HK
dc.subject.meshLeukemia, myeloid, chronic-phase - geneticsen_HK
dc.titleMolecular cytogenetic delineation of deletions and translocations involving chromosome band 7q22 in myeloid leukemiasen_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.pmid9058725-
dc.identifier.scopuseid_2-s2.0-1842295700en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1842295700&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume89en_HK
dc.identifier.issue6en_HK
dc.identifier.spage2036en_HK
dc.identifier.epage2041en_HK
dc.identifier.isiWOS:A1997WP23100023-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridFischer, K=7403154204en_HK
dc.identifier.scopusauthoridFröhling, S=8847739800en_HK
dc.identifier.scopusauthoridScherer, SW=35374654500en_HK
dc.identifier.scopusauthoridBrown, JM=8747877300en_HK
dc.identifier.scopusauthoridScholl, C=8847739500en_HK
dc.identifier.scopusauthoridStilgenbauer, S=7004928090en_HK
dc.identifier.scopusauthoridTsui, LC=7102754167en_HK
dc.identifier.scopusauthoridLichter, P=7102379763en_HK
dc.identifier.scopusauthoridDöhner, H=35374055900en_HK

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