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pubmed-article:17180671rdf:typepubmed:Citationlld:pubmed
pubmed-article:17180671lifeskim:mentionsumls-concept:C0021083lld:lifeskim
pubmed-article:17180671lifeskim:mentionsumls-concept:C0023470lld:lifeskim
pubmed-article:17180671pubmed:issue7lld:pubmed
pubmed-article:17180671pubmed:dateCreated2007-4-26lld:pubmed
pubmed-article:17180671pubmed:abstractTextThe treatment of myeloid leukaemia has progressed in recent years with the advent of donor leukocyte infusions (DLI), haemopoietic stem cell transplants (HSCTs) and targeted therapies. However, relapse has a high associated morbidity rate and a method for removing diseased cells in first remission, when a minimal residual disease state is achieved and tumour load is low, has the potential to extend remission times and prevent relapse especially when used in combination with conventional treatments. Acute myeloid leukaemia (AML) and myelodysplastic syndrome (MDS) are heterogeneous diseases which lack one common molecular target while chronic myeloid leukaemia (CML) patients have experienced prolonged remissions through the use of targeted therapies which remove BCR-ABL(+) cells effectively in early chronic phase. However, escape mutants have arisen and this therapy has little effectivity in the late chronic phase. Here we review the immune therapies which are close to or in clinical trials for the myeloid leukaemias and describe their potential advantages and disadvantages.lld:pubmed
pubmed-article:17180671pubmed:languageenglld:pubmed
pubmed-article:17180671pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:17180671pubmed:citationSubsetIMlld:pubmed
pubmed-article:17180671pubmed:statusMEDLINElld:pubmed
pubmed-article:17180671pubmed:monthJullld:pubmed
pubmed-article:17180671pubmed:issn0340-7004lld:pubmed
pubmed-article:17180671pubmed:authorpubmed-author:ThomasN...lld:pubmed
pubmed-article:17180671pubmed:authorpubmed-author:MillsKen IKIlld:pubmed
pubmed-article:17180671pubmed:authorpubmed-author:MohamedaliAzi...lld:pubmed
pubmed-article:17180671pubmed:authorpubmed-author:GuinnBarbara-...lld:pubmed
pubmed-article:17180671pubmed:issnTypePrintlld:pubmed
pubmed-article:17180671pubmed:volume56lld:pubmed
pubmed-article:17180671pubmed:ownerNLMlld:pubmed
pubmed-article:17180671pubmed:authorsCompleteYlld:pubmed
pubmed-article:17180671pubmed:pagination943-57lld:pubmed
pubmed-article:17180671pubmed:dateRevised2007-11-15lld:pubmed
pubmed-article:17180671pubmed:meshHeadingpubmed-meshheading:17180671...lld:pubmed
pubmed-article:17180671pubmed:meshHeadingpubmed-meshheading:17180671...lld:pubmed
pubmed-article:17180671pubmed:meshHeadingpubmed-meshheading:17180671...lld:pubmed
pubmed-article:17180671pubmed:meshHeadingpubmed-meshheading:17180671...lld:pubmed
pubmed-article:17180671pubmed:year2007lld:pubmed
pubmed-article:17180671pubmed:articleTitleImmunotherapy of myeloid leukaemia.lld:pubmed
pubmed-article:17180671pubmed:affiliationDepartment of Haematological Medicine, King's College London School of Medicine, The Rayne Institute, 123 Coldharbour Lane, London, SE5 9NU, UK. barbara.guinn@kcl.ac.uklld:pubmed
pubmed-article:17180671pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:17180671pubmed:publicationTypeReviewlld:pubmed
pubmed-article:17180671pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed