Clofarabine in the treatment of poor risk acute myeloid leukaemia.

Hdl Handle:
http://hdl.handle.net/10147/217638
Title:
Clofarabine in the treatment of poor risk acute myeloid leukaemia.
Authors:
Krawczyk, Janusz; Ansar, Naeem; Swords, Ronan; Murphy, Tracy; MacDonagh, Barry; Meenaghan, Teresa; Hayden, Patrick; Hayad, Amjad; Murray, Margaret; O'Dwyer, Michael
Affiliation:
Department of Haematology, Galway University Hospital and National University of Ireland, Galway, Ireland.
Citation:
Clofarabine in the treatment of poor risk acute myeloid leukaemia. 2010, 28 (3):118-23 Hematol Oncol
Journal:
Hematological oncology
Issue Date:
Sep-2010
URI:
http://hdl.handle.net/10147/217638
DOI:
10.1002/hon.922
PubMed ID:
19768694
Abstract:
Clofarabine is a second generation nucleoside analogue. It inhibits DNA repair and activates the mitochondrial apoptotic pathway leading to cell death. In vitro clofarabine has demonstrated synergy with daunorubicin and Ara-C and in phase II clinical trials has shown promising activity in poor risk Acute myeloid leukaemia (AML) patients. In our institution over a 24 month period 22 AML patients (11 M, 11 F) with poor risk features, deemed unsuitable for standard therapy, were treated with clofarabine, alone (eight patients) or in combination (14 patients) for up to three cycles of treatment. The median age was 67.5 years (24-76) with 16 patients > 60 years. At the time of treatment 18 patients had active AML. Four patients intolerant of standard induction received clofarabine as consolidation. The overall response rate (ORR) for the 18 patients with active AML was 61%, nine patients (50%) achieving a complete response (CR). Induction and consolidation were well tolerated with no unexpected toxicities. Predictably, all patients developed grade 4 neutropenia but the median duration was only 20 days (17-120). Induction mortality was acceptable at 17%. In conclusion, clofarabine (alone or in combination) is active in poor risk AML with an acceptable safety profile and should be considered a potential option in poor risk AML patients.
Language:
en
MeSH:
Adenine Nucleotides; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Arabinonucleosides; Female; Humans; Leukemia, Myeloid, Acute; Male; Middle Aged; Retrospective Studies; Risk Factors; Young Adult
ISSN:
1099-1069
Ethical Approval:
N/A

Full metadata record

DC FieldValue Language
dc.contributor.authorKrawczyk, Janusz-
dc.contributor.authorAnsar, Naeem-
dc.contributor.authorSwords, Ronan-
dc.contributor.authorMurphy, Tracy-
dc.contributor.authorMacDonagh, Barry-
dc.contributor.authorMeenaghan, Teresa-
dc.contributor.authorHayden, Patrick-
dc.contributor.authorHayad, Amjad-
dc.contributor.authorMurray, Margaret-
dc.contributor.authorO'Dwyer, Michael-
dc.date.accessioned2012-04-04T11:34:40Z-
dc.date.available2012-04-04T11:34:40Z-
dc.date.issued2010-09-
dc.identifier.citationClofarabine in the treatment of poor risk acute myeloid leukaemia. 2010, 28 (3):118-23 Hematol Oncol-
dc.identifier.issn1099-1069-
dc.identifier.pmid19768694-
dc.identifier.doi10.1002/hon.922-
dc.identifier.urihttp://hdl.handle.net/10147/217638-
dc.description.abstractClofarabine is a second generation nucleoside analogue. It inhibits DNA repair and activates the mitochondrial apoptotic pathway leading to cell death. In vitro clofarabine has demonstrated synergy with daunorubicin and Ara-C and in phase II clinical trials has shown promising activity in poor risk Acute myeloid leukaemia (AML) patients. In our institution over a 24 month period 22 AML patients (11 M, 11 F) with poor risk features, deemed unsuitable for standard therapy, were treated with clofarabine, alone (eight patients) or in combination (14 patients) for up to three cycles of treatment. The median age was 67.5 years (24-76) with 16 patients > 60 years. At the time of treatment 18 patients had active AML. Four patients intolerant of standard induction received clofarabine as consolidation. The overall response rate (ORR) for the 18 patients with active AML was 61%, nine patients (50%) achieving a complete response (CR). Induction and consolidation were well tolerated with no unexpected toxicities. Predictably, all patients developed grade 4 neutropenia but the median duration was only 20 days (17-120). Induction mortality was acceptable at 17%. In conclusion, clofarabine (alone or in combination) is active in poor risk AML with an acceptable safety profile and should be considered a potential option in poor risk AML patients.-
dc.language.isoen-
dc.rightsArchived with thanks to Hematological oncologyen_GB
dc.subject.meshAdenine Nucleotides-
dc.subject.meshAdult-
dc.subject.meshAged-
dc.subject.meshAntineoplastic Combined Chemotherapy Protocols-
dc.subject.meshArabinonucleosides-
dc.subject.meshFemale-
dc.subject.meshHumans-
dc.subject.meshLeukemia, Myeloid, Acute-
dc.subject.meshMale-
dc.subject.meshMiddle Aged-
dc.subject.meshRetrospective Studies-
dc.subject.meshRisk Factors-
dc.subject.meshYoung Adult-
dc.titleClofarabine in the treatment of poor risk acute myeloid leukaemia.en_GB
dc.contributor.departmentDepartment of Haematology, Galway University Hospital and National University of Ireland, Galway, Ireland.-
dc.identifier.journalHematological oncology-
dc.type.qualificationlevelN/Aen
cr.approval.ethicalN/Aen
dc.description.provinceConnacht-
dc.description.provinceConnachten

Related articles on PubMed

All Items in Lenus, The Irish Health Repository are protected by copyright, with all rights reserved, unless otherwise indicated.