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The improvement in outcome may partly be a result of all our patients receiving TKIs at some stage, although the influence of TKIs on transplant outcomes has been inconsistent (Kebriaei et?al, 2011; Rives et?al, 2011). With treatment-related mortality comparable to that associated with intensive chemotherapy (Arico et?al, 2000), CR1 transplant, therefore, remains a legitimate option for sub-groups of Ph+ ALL who have a high risk of relapse due to resistance or intolerance to chemotherapy and TKIs. If so, should the eligibility http://www.selleckchem.com/products/Rapamycin.html for alternative donor transplant be restricted to a cohort with a higher risk of relapse than would be eligible for a related donor transplant? Our experience would suggest otherwise, given that the nine patients in our cohort who received an unrelated donor transplant remain alive and in CR, one after DLI and imatinib for post-transplant relapse. Furthermore, 70% of eligible patients lack a related donor and there http://www.selleck.cn/products/Bleomycin-sulfate.html is tentative evidence for a more potent graft-versus-leukaemia effect from unrelated donor transplants (Cornelissen et?al, 2001) resulting in a comparable outcome despite a higher TRM. TRM is not the sole consideration when comparing the merits of transplant versus chemotherapy for high-risk paediatric leukaemia and the late side effects of total body irradiation (TBI) remain a major disadvantage of transplant over chemotherapy. Most chemotherapy protocols recommend cranial radiotherapy as standard central nervous system-directed treatment for all patients with Ph+ ALL not eligible for transplant (Schultz et?al, 2009), but the burden of late side effects is considerably higher following TBI than cranial radiotherapy. However, just as the availability of TKIs might allow cranial radiotherapy to be omitted from future chemotherapy protocols for Ph+ ALL, their use before and after transplant might permit the development of novel http://www.selleckchem.com/products/MG132.html reduced-intensity conditioning regimens that do not contain TBI (Ram et?al, 2011). AV designed the study, analysed the data and wrote the paper. AG, AS and JW analysed the data. All authors contributed to care of the patients included in this study and helped write the paper. ""MLLT11, an MLL fusion partner, is a poor prognostic biomarker for paediatric acute myeloid leukaemia (AML), adult normal cytogenetics AML, and adult myelodysplastic syndrome. MLLT11 is highly regulated during haematopoietic progenitor differentiation and development but its regulatory mechanisms have not been defined. In this study, we demonstrate by transfection experiments that MIR29B directly regulates MLLT11 expression in vitro. MIR29B expression level was also inversely related to MLLT11 expression in a cohort of 56 AML patients (P?