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Article: Acute myeloid leukemia after azathioprine treatment for autoimmune diseases: Association with -7/7q-

TitleAcute myeloid leukemia after azathioprine treatment for autoimmune diseases: Association with -7/7q-
Authors
Issue Date1998
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene
Citation
Cancer Genetics And Cytogenetics, 1998, v. 104 n. 2, p. 94-97 How to Cite?
AbstractAzathioprine is used as an immunosuppressant in a variety of clinical situations, and its prolonged use is associated with an increased risk of solid malignancies. Three patients (one with rheumatoid arthritis and two with systemic lupus erythematosus) treated with azathioprine for 3 to 7 years developed acute myeloid leukemia (AML). The total cumulative doses of azathioprine varied from 89-260 g. An antecedent prolonged pancytopenic phase suggestive of myelodysplasia developed in all the cases. Morphological analysis showed AML with trilineage myelodysplastic features in residual marrow cells in all the cases. Karyotypic analysis showed deletion of the long arm of chromosome 7 (7q-) in one case and monosomy 7 (-7) in two cases. These were chromosomal aberrations typically associated with mutagen- or therapy-related AML. Fluorescence in situ hybridization with a chromosome-7- specific DNA probe was used to investigate the distribution of the monosomy 7 clone in two cases. Monosomy 7 was demonstrated in both the leukemic blasts and the residual myeloid cells of various stages of differentiation. This finding indicated that the leukemia had evolved from a mutated clone that was capable of terminal differentiation, which was consistent with the biological characteristics of the myelodysplastic syndromes. These cases represented therapy-related AML, as evidenced by clincopathological features, karyotypic aberrations of 7q-/-7, and demonstration of leukemic evolution from an underlying clonal myeloid disorder. The data support the hypothesis that azathioprine might be directly mutagenic.
Persistent Identifierhttp://hdl.handle.net/10722/162265
ISSN
2012 Impact Factor: 1.929
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKwong, YLen_US
dc.contributor.authorAu, WYen_US
dc.contributor.authorLiang, RHSen_US
dc.date.accessioned2012-09-05T05:18:30Z-
dc.date.available2012-09-05T05:18:30Z-
dc.date.issued1998en_US
dc.identifier.citationCancer Genetics And Cytogenetics, 1998, v. 104 n. 2, p. 94-97en_US
dc.identifier.issn0165-4608en_US
dc.identifier.urihttp://hdl.handle.net/10722/162265-
dc.description.abstractAzathioprine is used as an immunosuppressant in a variety of clinical situations, and its prolonged use is associated with an increased risk of solid malignancies. Three patients (one with rheumatoid arthritis and two with systemic lupus erythematosus) treated with azathioprine for 3 to 7 years developed acute myeloid leukemia (AML). The total cumulative doses of azathioprine varied from 89-260 g. An antecedent prolonged pancytopenic phase suggestive of myelodysplasia developed in all the cases. Morphological analysis showed AML with trilineage myelodysplastic features in residual marrow cells in all the cases. Karyotypic analysis showed deletion of the long arm of chromosome 7 (7q-) in one case and monosomy 7 (-7) in two cases. These were chromosomal aberrations typically associated with mutagen- or therapy-related AML. Fluorescence in situ hybridization with a chromosome-7- specific DNA probe was used to investigate the distribution of the monosomy 7 clone in two cases. Monosomy 7 was demonstrated in both the leukemic blasts and the residual myeloid cells of various stages of differentiation. This finding indicated that the leukemia had evolved from a mutated clone that was capable of terminal differentiation, which was consistent with the biological characteristics of the myelodysplastic syndromes. These cases represented therapy-related AML, as evidenced by clincopathological features, karyotypic aberrations of 7q-/-7, and demonstration of leukemic evolution from an underlying clonal myeloid disorder. The data support the hypothesis that azathioprine might be directly mutagenic.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergeneen_US
dc.relation.ispartofCancer Genetics and Cytogeneticsen_US
dc.rightsCancer Genetics and Cytogenetics. Copyright © Elsevier Inc.-
dc.subject.meshAcute Diseaseen_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshArthritis, Rheumatoid - Complications - Drug Therapyen_US
dc.subject.meshAzathioprine - Adverse Effectsen_US
dc.subject.meshChromosomes, Human, Pair 7en_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunosuppressive Agents - Adverse Effectsen_US
dc.subject.meshIn Situ Hybridization, Fluorescenceen_US
dc.subject.meshLeukemia, Myeloid - Chemically Induced - Complications - Geneticsen_US
dc.subject.meshLupus Erythematosus, Systemic - Complications - Drug Therapyen_US
dc.subject.meshMutagensen_US
dc.titleAcute myeloid leukemia after azathioprine treatment for autoimmune diseases: Association with -7/7q-en_US
dc.typeArticleen_US
dc.identifier.emailKwong, YL:ylkwong@hku.hken_US
dc.identifier.emailLiang, RHS:rliang@hku.hken_US
dc.identifier.authorityKwong, YL=rp00358en_US
dc.identifier.authorityLiang, RHS=rp00345en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0165-4608(97)00456-1en_US
dc.identifier.pmid9666800en_US
dc.identifier.scopuseid_2-s2.0-0032527868en_US
dc.identifier.hkuros41946-
dc.identifier.hkuros33083-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032527868&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume104en_US
dc.identifier.issue2en_US
dc.identifier.spage94en_US
dc.identifier.epage97en_US
dc.identifier.isiWOS:000074589100004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKwong, YL=7102818954en_US
dc.identifier.scopusauthoridAu, WY=7202383089en_US
dc.identifier.scopusauthoridLiang, RHS=26643224900en_US
dc.identifier.issnl0165-4608-

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