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Article: The occurrence of Philadelphia chromosome (Ph) negative leukemia after hematopoietic stem cell transplantion for Ph positive chronic myeloid leukemia: Implications for disease monitoring and treatment

TitleThe occurrence of Philadelphia chromosome (Ph) negative leukemia after hematopoietic stem cell transplantion for Ph positive chronic myeloid leukemia: Implications for disease monitoring and treatment
Authors
Issue Date2003
PublisherInforma Healthcare. The Journal's web site is located at http://informahealthcare.com/loi/lal
Citation
Leukemia And Lymphoma, 2003, v. 44 n. 7, p. 1121-1129 How to Cite?
AbstractChronic myeloid leukemia (CML) is a clonal neoplastic disorder, characterized by t(9;22)(q34;q11) that results in the formation of the Philadelphia chromosome (Ph) and the BCR/ABL fusion gene. Allogeneic hematopoietic stem cell transplantation (HSCT) is a curative treatment for CML. Much of its therapeutic efficacy is attributed to a graft-versus-leukemia (GVL) effect exerted by donor-derived lymphoid cells against the Ph positive (Ph +) clone. Post-HSCT monitoring by cytogenetic and molecular detection of the Ph + clone is necessary, so that pre-emptive immunologic or pharmacologic treatment may be administered at an early stage of relapse. However, under rare circumstances a second Ph negative (Ph -) leukemia may evolve post-HSCT. The pathogenetic possibilities included leukemia arising from donor-derived hematopoietic stem cells (HSCs), or transformation of residual recipient-derived Ph - HSCs that have survived the conditioning chemotherapy and radiotherapy. Recipient-derived Ph - leukemia may be related to genetic alterations that precede the onset of CML, or myelotoxic effects of the HSCT conditioning regimen. The diagnosis of Ph - relapses requires detailed investigations by conventional karyotyping, fluorescence in-situ hybridization (FISH), and molecular analysis; as well as chimerism studies that help to document the donor or recipient origin of the leukemia. Although uncommonly reported in the past, Ph - relapses may in fact be more frequent if leukemic relapses post-HSCT are more thoroughly evaluated with these investigations. The recognition of Ph - relapses are important in several ways. Ph - relapses cannot be identified by monitoring investigations targeting the Ph + clone, so that the early detection of Ph - leukemia is usually not possible. Furthermore, Ph - relapses will not respond to therapeutic strategies effective against the Ph + CML clone.
Persistent Identifierhttp://hdl.handle.net/10722/162702
ISSN
2015 Impact Factor: 3.093
2015 SCImago Journal Rankings: 1.202
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorAu, WYen_US
dc.contributor.authorMa, SKen_US
dc.contributor.authorKwong, YLen_US
dc.date.accessioned2012-09-05T05:22:31Z-
dc.date.available2012-09-05T05:22:31Z-
dc.date.issued2003en_US
dc.identifier.citationLeukemia And Lymphoma, 2003, v. 44 n. 7, p. 1121-1129en_US
dc.identifier.issn1042-8194en_US
dc.identifier.urihttp://hdl.handle.net/10722/162702-
dc.description.abstractChronic myeloid leukemia (CML) is a clonal neoplastic disorder, characterized by t(9;22)(q34;q11) that results in the formation of the Philadelphia chromosome (Ph) and the BCR/ABL fusion gene. Allogeneic hematopoietic stem cell transplantation (HSCT) is a curative treatment for CML. Much of its therapeutic efficacy is attributed to a graft-versus-leukemia (GVL) effect exerted by donor-derived lymphoid cells against the Ph positive (Ph +) clone. Post-HSCT monitoring by cytogenetic and molecular detection of the Ph + clone is necessary, so that pre-emptive immunologic or pharmacologic treatment may be administered at an early stage of relapse. However, under rare circumstances a second Ph negative (Ph -) leukemia may evolve post-HSCT. The pathogenetic possibilities included leukemia arising from donor-derived hematopoietic stem cells (HSCs), or transformation of residual recipient-derived Ph - HSCs that have survived the conditioning chemotherapy and radiotherapy. Recipient-derived Ph - leukemia may be related to genetic alterations that precede the onset of CML, or myelotoxic effects of the HSCT conditioning regimen. The diagnosis of Ph - relapses requires detailed investigations by conventional karyotyping, fluorescence in-situ hybridization (FISH), and molecular analysis; as well as chimerism studies that help to document the donor or recipient origin of the leukemia. Although uncommonly reported in the past, Ph - relapses may in fact be more frequent if leukemic relapses post-HSCT are more thoroughly evaluated with these investigations. The recognition of Ph - relapses are important in several ways. Ph - relapses cannot be identified by monitoring investigations targeting the Ph + clone, so that the early detection of Ph - leukemia is usually not possible. Furthermore, Ph - relapses will not respond to therapeutic strategies effective against the Ph + CML clone.en_US
dc.languageengen_US
dc.publisherInforma Healthcare. The Journal's web site is located at http://informahealthcare.com/loi/lalen_US
dc.relation.ispartofLeukemia and Lymphomaen_US
dc.rightsLeukemia and Lymphoma. Copyright © Informa Healthcare-
dc.subject.meshHematopoietic Stem Cell Transplantationen_US
dc.subject.meshHumansen_US
dc.subject.meshLeukemia, Myelogenous, Chronic, Bcr-Abl Positive - Diagnosis - Therapyen_US
dc.subject.meshLeukemia, Myeloid, Chronic, Atypical, Bcr-Abl Negative - Etiologyen_US
dc.titleThe occurrence of Philadelphia chromosome (Ph) negative leukemia after hematopoietic stem cell transplantion for Ph positive chronic myeloid leukemia: Implications for disease monitoring and treatmenten_US
dc.typeArticleen_US
dc.identifier.emailKwong, YL:ylkwong@hku.hken_US
dc.identifier.authorityKwong, YL=rp00358en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1080/1042819031000079104en_US
dc.identifier.pmid12916863-
dc.identifier.scopuseid_2-s2.0-0038628023en_US
dc.identifier.hkuros108020-
dc.identifier.hkuros77874-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0038628023&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume44en_US
dc.identifier.issue7en_US
dc.identifier.spage1121en_US
dc.identifier.epage1129en_US
dc.identifier.isiWOS:000182775000004-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridAu, WY=7202383089en_US
dc.identifier.scopusauthoridMa, SK=37020910400en_US
dc.identifier.scopusauthoridKwong, YL=7102818954en_US

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