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Article: Arsenic Trioxide for Non Acute Promyelocytic Leukemia Hematological Malignancies: A New Frontier

TitleArsenic Trioxide for Non Acute Promyelocytic Leukemia Hematological Malignancies: A New Frontier
Authors
KeywordsArsenic trioxide
Leukemia
Mechanisms
Treatment
Issue Date2014
PublisherAustin Publishing Group.
Citation
Journal of Blood Disorders, 2014, v. 1 n. 4, p. 1-9 How to Cite?
AbstractArsenic trioxide (As2 O3 ) has been confirmed to be effective in the treatment of Acute Promyelocytic Leukemia (APL). Also, encouraging results have been reported in preclinical studies and pilot clinical trials of As2 O3 in other hematological malignancies such as Multiple Myeloma (MM), Myeloplastic syndromes (MDS), T-cell leukemia-lymphoma and Chronic Myelogenous Leukemia (CML). However, conflicting findings have been reported in non-APL Acute Myeloid Leukemia (AML). The mechanisms of As2 O3 activity are complex, with multiple modifications of cell growth and apoptosis control regulations of pro-survival and cell defense molecules, cell cycle arrest, glutathione redox system, p53-dependent apoptotic signals; telomerase activity and caspase pathway. It is now known that other mechanisms are also involved including the immunomodulatory and angiogenesis regulation. Recently there is a trend of investigating whether tetra-arsenic tetra-sulphide will be a better alternative for the arsenic trioxide. In summary this review describes emerging information that provides new insights for As2 O3 as a broad spectrum chemotherapeutic agent in the treatment of hematological malignancies beyond APL.
Persistent Identifierhttp://hdl.handle.net/10722/80081
ISSN

 

DC FieldValueLanguage
dc.contributor.authorZhou, L-
dc.contributor.authorHou, J-
dc.contributor.authorChan, GCF-
dc.contributor.authorSze, DMY-
dc.date.accessioned2010-09-06T08:02:11Z-
dc.date.available2010-09-06T08:02:11Z-
dc.date.issued2014-
dc.identifier.citationJournal of Blood Disorders, 2014, v. 1 n. 4, p. 1-9-
dc.identifier.issn2379-8009-
dc.identifier.urihttp://hdl.handle.net/10722/80081-
dc.description.abstractArsenic trioxide (As2 O3 ) has been confirmed to be effective in the treatment of Acute Promyelocytic Leukemia (APL). Also, encouraging results have been reported in preclinical studies and pilot clinical trials of As2 O3 in other hematological malignancies such as Multiple Myeloma (MM), Myeloplastic syndromes (MDS), T-cell leukemia-lymphoma and Chronic Myelogenous Leukemia (CML). However, conflicting findings have been reported in non-APL Acute Myeloid Leukemia (AML). The mechanisms of As2 O3 activity are complex, with multiple modifications of cell growth and apoptosis control regulations of pro-survival and cell defense molecules, cell cycle arrest, glutathione redox system, p53-dependent apoptotic signals; telomerase activity and caspase pathway. It is now known that other mechanisms are also involved including the immunomodulatory and angiogenesis regulation. Recently there is a trend of investigating whether tetra-arsenic tetra-sulphide will be a better alternative for the arsenic trioxide. In summary this review describes emerging information that provides new insights for As2 O3 as a broad spectrum chemotherapeutic agent in the treatment of hematological malignancies beyond APL.-
dc.languageeng-
dc.publisherAustin Publishing Group.-
dc.relation.ispartofJournal of Blood Disorders-
dc.subjectArsenic trioxide-
dc.subjectLeukemia-
dc.subjectMechanisms-
dc.subjectTreatment-
dc.titleArsenic Trioxide for Non Acute Promyelocytic Leukemia Hematological Malignancies: A New Frontier-
dc.typeArticle-
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1568-0096&volume=&spage=&epage=&date=2009&atitle=Arsenic+trioxide+for+non-acute+promyelocytic+leukemia+hematological+malignancies:+a+new+frontier.+en_HK
dc.identifier.emailChan, GCF: gcfchan@hkucc.hku.hk-
dc.identifier.authorityChan, GCF=rp00431-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros163813-
dc.identifier.volume1-
dc.identifier.issue4-
dc.identifier.spage1-
dc.identifier.epage9-
dc.publisher.placeUS-

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