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

Oehler, Vivian G.; Gooley, Ted; Snyder, David S.; Johnston, Laura; Lin, Allen; Cummings, Carrie L.; Chu, Su; Bhatia, Ravi; Forman, Stephen J.; Negrin, Robert S.; Appelbaum, Frederick R.; Radich, Jerald P.

doi:10.1182/blood-2006-06-031682

Cited by 123 publications

(100 citation statements)

References 48 publications

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“…There have been earlier reports describing lower incidences of chronic GVHD in patients who received imatinib therapy earlier, [16][17][18][19] but as for imatinib increasing the incidence of severe acute GVHD (grade 3-4), the literature does not support our finding. These results may have been affected by our relatively small sample size.…”

Section: Imatinib Groupcontrasting

confidence: 91%

“…20,21 The effect imatinib had on the major transplant outcomes (OS, RFS and risk of relapse) for our CML cohort was not statistically significant and was in agreement with earlier reports. 18,19,22 Limitations to this study exist in the lack of standard dosing and/or timing of imatinib therapy in our patients both before and after HCT, the heterogeneous nature and overall small number of patients evaluated and our limited power to observe a difference in cardiac event rates. Despite these limitations, on the basis of this retrospective analysis of a heterogeneous group of CML patients, imatinib use in the peri-transplant period had no effect on either TRM or cardiac toxicity.…”

Section: Imatinib Groupmentioning

confidence: 99%

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Imatinib use either pre- or post-allogeneic hematopoietic cell transplantation (allo-HCT) does not increase cardiac toxicity in chronic myelogenous leukemia patients

Burke

Trotz

Luo

et al. 2009

Bone Marrow Transplant

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Since the introduction of imatinib mesylate, the role of allogeneic hematopoietic cell transplantation (allo-HCT) for CML has essentially been reserved for patients with advanced disease or imatinib resistance. In addition, there have been concerns regarding imatinib associated cardiac toxicity. We investigated the outcome of 61 patients with CML who received a myeloablative allo-HCT at the University of Minnesota between 1999 and 2006. The median age at HCT was 38.4 (range; 6.9-56.9) years. Thirty-seven patients were in first chronic phase and twenty-four patients in a second chronic or accelerated phase at the time of HCT. Twenty-six patients received imatinib therapy before or after HCT, and thirty-five patients either never received imatinib (n ¼ 32) or received it only at the time of relapse after HCT (n ¼ 3). OS and relapse-free survival (RFS) at 2 years was 69 and 55% for the imatinib group, and 57 and 49% for the non-imatinib group (P ¼ 0.57 and 0.95, respectively). There was no difference in the risk of relapse at 2 years between the groups. Symptomatic cardiac toxicity at 1 year was reported in three imatinib group (12%) and two nonimatinib group (6%) patients (P ¼ 0.44). Thus, patients treated with imatinib either before or after myeloablative allo-HCT had no increase in cardiac toxicity.

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Section: Imatinib Groupcontrasting

confidence: 91%

Section: Imatinib Groupmentioning

confidence: 99%

Imatinib use either pre- or post-allogeneic hematopoietic cell transplantation (allo-HCT) does not increase cardiac toxicity in chronic myelogenous leukemia patients

Burke

Trotz

Luo

et al. 2009

Bone Marrow Transplant

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“…Patients with accelerated or blastic phase CML may receive initial therapy with TKIs (newer generation TKIs like dasatinib or ponatinib preferred over imatinib) to reduce the CML burden, and be considered for early alloSCT [76][77][78][79][80]. Response rates with combinations of TKIs and chemotherapy are 40% in nonlymphoid BP CML and 70-80% in lymphoid BP CML [81][82][83].…”

Section: Advanced Stage CMLmentioning

confidence: 99%

Chronic myeloid leukemia: 2014 update on diagnosis, monitoring, and management

2014

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Disease overview: Chronic Myeloid Leukemia (CML) is a myeloproliferative neoplasm with an incidence of 1–2 cases per 100,000 adults, and accounts for ∼15% of newly diagnosed cases of leukemia in adults. Diagnosis: CML is characterized by a balanced genetic translocation, t(9;22)(q34;q11.2), involving a fusion of the Abelson oncogene (ABL) from chromosome 9q34 with the breakpoint cluster region (BCR) gene on chromosome 22q11.2. This rearrangement is known as the Philadelphia chromosome. The molecular consequence of this translocation is the generation of a BCR‐ABL fusion oncogene, which in turn translates into a Bcr‐Abl oncoprotein. Frontline therapy: Three tyrosine kinase inhibitors (TKIs), imatinib, nilotinib, and dasatinib have been approved by the US Food and Drug Administration for the first‐line treatment of patients with newly diagnosed CML in chronic phase (CML‐CP). Clinical trials with second generation TKIs reported significantly deeper and faster responses; their impact on long‐term survival remains to be determined. Salvage therapy: For patients who fail frontline therapy, second‐line options include second and third generation TKIs. Although second and third generation TKIs are potent and specific BCR‐ABL TKIs, they exhibit unique pharmacological profiles and response patterns relative to different patient characteristics, such as patients comorbidities, disease stage, and BCR‐ABL mutational status. Patients who develop the T315I “gatekeeper” mutation display resistance to all currently available TKIs except ponatinib. Allogeneic transplantation remains an important therapeutic option for CML‐CP who have failed at least 2 TKIs, and for all patients in advanced phase disease. Am. J. Hematol. 89:547–556, 2014. © 2014 Wiley Periodicals, Inc.

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“…61,62 Uma vantagem do TCTH é a sua capacidade de produzir uma resposta molecular completa que pode ocorrer em até 75% dos pacientes, e que está associada a um risco menor de recidiva e uma potencial cura da LMC. 14,64,65 Esta resposta molecular completa, entretanto, não é usual no tratamento com o mesilato de imatinibe (IM). 14,63,64 O TCTH tem sido cada vez mais utilizado como tratamento de "salvamento" para pacientes com LMC intolerantes ou resistentes ao IM.…”

Section: Influência Dos Inibidores De Tirosina Quinase No Transplanteunclassified

“…Finalmente, se a presença de mutações no domínio da tirosina quinase (TKD), diagnosticadas antes do transplante, estaria associada a um pior resultado. 65 Como consequência do uso do IM como primeira linha para o tratamento da LMC, a população de pacientes submetida ao TCTH mudou. Muitos pacientes usaram o IM previamente ao transplante e receberão o transplante em FC se forem intolerantes ou falharem ao IM.…”

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

Cited by 123 publications

References 48 publications

Imatinib use either pre- or post-allogeneic hematopoietic cell transplantation (allo-HCT) does not increase cardiac toxicity in chronic myelogenous leukemia patients

Imatinib use either pre- or post-allogeneic hematopoietic cell transplantation (allo-HCT) does not increase cardiac toxicity in chronic myelogenous leukemia patients

Chronic myeloid leukemia: 2014 update on diagnosis, monitoring, and management

Leucemia mieloide crônica e outras doenças mieloproliferativas crônicas

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