Pretransplant imatinib can improve the outcome of nonmyeloablative stem cell transplantation without increasing the morbidity in Philadelphia chromosome-positive chronic myeloid leukemia

Dw, Kim; Chung, Yeun‐Jun; Lee, Sae-Mi; Kim, Yoon Jun; Ng, Chung; Kim, J A; Oh, Iekuni; Tg, Kim; Yl, Kim; Goh, H.T.A.; Sh, Kim; Cho, B; Kim, Hyung Jun; Ck, Min; Lee, Jung Woo; Jin, Jong Youl; Han, Chi Wha; Kim, Jin-Wou; Ws, Min; Hk, Kim; Cc, Kim; Kim, H J

doi:10.1038/sj.leu.2403502

Cited by 15 publications

(12 citation statements)

References 8 publications

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“…To date there are no reports of delayed engraftment in the myeloablative and nonmyeloablative setting for CML and Ph ϩ ALL patients. 34,35,[39][40][41] After adjusting for EBMT score and stemcell source, we found that patients who received IM had slightly faster myeloid engraftment.…”

Section: Discussionmentioning

confidence: 91%

The effects of imatinib mesylate treatment before allogeneic transplantation for chronic myeloid leukemia

Oehler

Gooley

Snyder

et al. 2006

Blood

123

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The impact of imatinib mesylate (IM) treatment for chronic myeloid leukemia (CML) on subsequent allogeneic transplantation is uncertain. To better understand this relationship, we retrospectively compared 145 patients with CML receiving IM for a minimum of 3 months before allogeneic hematopoietic cell transplantation (HCT) to 231 patients with CML who did not. IM treatment was associated with no increase in early hepatotoxicity or engraftment delay after HCT compared with the historical cohort. In addition, there was no statistically significant difference in the IM-treated cohort compared with the historical cohort with regard to overall survival, disease-free survival, relapse, and nonrelapse mortality.

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Section: Discussionmentioning

confidence: 91%

The effects of imatinib mesylate treatment before allogeneic transplantation for chronic myeloid leukemia

Oehler

Gooley

Snyder

et al. 2006

Blood

123

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“…[107][108][109][110] Relationship with alloHSCT Treatment with IM prior to alloHSCT was not reported to be associated with an increase of transplantation-related morbidity and mortality. [111][112][113][114][115] IM was also found to control leukemia in patients relapsing after alloHSCT. 116,117 In a multicentric retrospective study of 128 patients, the CCgR rates were 58% in CP, 48% in AP, and 22% in BC, with molecular negativity in 37%, 33%, and 11% of cases, respectively.…”

Section: Dose Issuesmentioning

confidence: 99%

Evolving concepts in the management of chronic myeloid leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet

Baccarani

Saglio

Goldman

et al. 2006

Blood

1,166

1,023

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The introduction of imatinib mesylate (IM) has revolutionized the treatment of chronic myeloid leukemia (CML). Although experience is too limited to permit evidence-based evaluation of survival, the available data fully justify critical reassessment of CML management. The panel therefore reviewed treatment of CML since 1998. It confirmed the value of IM (400 mg/day) and of conventional allogeneic hematopoietic stem cell transplantation (alloHSCT). It recommended that the preferred initial treatment for most patients newly diagnosed in chronic phase should now be 400 mg IM daily. A dose increase of IM, alloHSCT, or investigational treatments were recommended in case of failure, and could be considered in case of suboptimal response. IntroductionAfter the initial descriptions of chronic myeloid leukemia (CML) more than 150 years ago, little meaningful progress was made in its treatment for more than a century. Radiation therapy and busulfan contributed more to improving quality of life than to prolonging survival. Survival prolongation was first achieved with hydroxyurea (HU), much more with allogeneic hematopoietic stem cell transplantation (alloHSCT) and, later, in a minority of patients, with recombinant interferon-alpha (rIFN␣). 1 Understanding the pathogenesis of the disease began with the discovery of the Philadelphia (Ph) chromosome followed by appreciation of its molecular counterpart, the BCR-ABL fusion gene. 2,3 Recognition of the tyrosine kinase (TK) activity of the Bcr-Abl proteins led to the discovery of a new series of compounds targeted against BCR-ABL-encoded proteins, which inhibited the TK activity, thus aborting the signals controlling the leukemic phenotype. 4 One of the TK inhibitors, imatinib mesylate (IM), was found to have a high and relatively specific biochemical activity and an acceptable pharmacokinetic and toxicity profile, and was thus rapidly introduced into clinical practice. [5][6][7] This resulted in a revolutionary step in the management of CML and by extension a shift in paradigm for the management of cancer in general.The most recent comprehensive analysis of CML treatment was an evidence-based guideline developed in 1998 by an expert panel convened by the American Society of Hematology (ASH) covering conventional chemotherapy, rIFN␣, and alloHSCT. 8 TK inhibitors were not considered at that time but were subsequently the subjects of editorials and preliminary reviews. 7,[9][10][11][12][13][14] Although it is premature at this time to perform an evidence-based analysis of the effects of IM, the implications and consequences of the introduction of TK inhibitors are so important that it is not too early to review the available data and to discuss how the treatment of CML could be managed and further progress could be pursued based upon expert opinion. Therefore, the European LeukemiaNet appointed a panel of experts to review the current situation. This report constitutes its opinion. For personal use only. on May 10, 2018. by guest www.bloodjournal.org From Methods Panel compos...

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“…65,68,69 Do mesmo modo, não existem relatos de atraso da pega, tanto nos transplantes com condicionamento mieloablativos ou não mieloablativos, em pacientes com LMC e leucemia linfoblástica Ph positiva . [68][69][70][71][72] Oehler et al, 65 inclusive, mostraram que os pacientes que receberam IM tiveram uma pega mieloide ligeiramente mais rápida.…”

Section: Influência Dos Inibidores De Tirosina Quinase No Transplanteunclassified

Leucemia mieloide crônica e outras doenças mieloproliferativas crônicas

Funke¹,

Bitencourt²,

Vigorito³

et al. 2010

Rev. Bras. Hematol. Hemoter.

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Leucemia Mieloide Crônica: histórico, tratamento com inibidores de tirosino-quinase e recomendações da Leukemia NetOs primeiros casos de leucemia mieloide crônica (LMC) foram descritos em 1845. Em 1960 foi descrito o cromossomo Filadélfia (Ph), depois identificado como uma translocação recíproca entre os cromossomos 9 e 22. Em 1983, demonstrou-se que esta translocação justapõe a região BCR no cromossomo 22, ao gene c-ABL localizado no cromossomo 9, resultando num gene híbrido -o BCR-ABL. Em seguida verificou-se que o produto deste oncogene era uma proteína de 210 KD, com atividade de tirosina quinase. Em 1990, foi demonstrado em um modelo murino, que a presença do gene híbrido induzia uma doença mieloproliferativa semelhante à LMC vista em humanos, estabelecendo relação de causalidade entre o BCR-ABL e a LMC. 1,2 A irradiação corporal total ou esplênica, o uso de derivados de arsênico (licor de Fowley), o bussulfano e a hidroxiureia, tratamentos utilizados inicialmente, resultavam em controle hematológico, mas não havia mudança da histó-ria natural da doença, com uma inexorável progressão para

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Pretransplant imatinib can improve the outcome of nonmyeloablative stem cell transplantation without increasing the morbidity in Philadelphia chromosome-positive chronic myeloid leukemia

Cited by 15 publications

References 8 publications

The effects of imatinib mesylate treatment before allogeneic transplantation for chronic myeloid leukemia

The effects of imatinib mesylate treatment before allogeneic transplantation for chronic myeloid leukemia

Evolving concepts in the management of chronic myeloid leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet

Leucemia mieloide crônica e outras doenças mieloproliferativas crônicas

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