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Autologous stem cell transplantation (ASCT) remains an important therapeutic strategy for multiple myeloma; however, a proportion of patients fail to mobilize a sufficient number of peripheral blood stem cells (PBSCs) to proceed to ASCT. In the present study, we aimed to clarify the characteristics and outcomes of poor mobilizers. Clinical data on poorly mobilized patients who underwent PBSC harvest for almost 10 years were retrospectively collected from 44 institutions in the Japanese Society of Myeloma (JSM). Poor mobilizers were defined as patients with less than 2 × 10 6 /kg of CD34 + cells harvested at the first mobilization. The proportion of poor mobilization was 15.1%. A sufficient dataset including overall survival (OS) was evaluable in 258 poor mobilizers. Overall, 92 out of 258 (35.7%) poor mobilizers did not subsequently undergo ASCT, mainly due to an insufficient number of PBSCs. Median OS from apheresis was longer for poor mobilizers who underwent ASCT than for those who did not (86.0 vs. 61.9 mon., p = 0.02). OS from the diagnosis of poor mobilizers who underwent ASCT in our cohort was similar to those who underwent ASCT in the JSM database (3y OS rate, 86.8% vs. 85.9%). In this cohort, one-third of poor mobilizers who did not undergo ASCT had relatively poor survival. In contrast, the OS improved in poor mobilizers who underwent ASCT. However, the OS of extremely poor mobilizers was short irrespective of ASCT.

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To the Editor, Rearrangements of PDGFRA, PDGFRB, FGFR1 or JAK2 are established features of myeloid/lymphoid neoplasms with eosinophilia (MLN-Eo). 1 The rearrangement of the fms-related tyrosine kinase 3 (FLT3) gene should also be associated with MLN-Eo, and ETV6, SPTBN1, GOLGB1 and TRIP11 have been identified as FLT3 rearrangement partner genes 2 (Figure S1). Cases of MLN-Eo with FLT3 rearrangement are rare but have a poor outcome.We encountered a patient who achieved a favourable long-term outcome by allogeneic haematopoietic stem cell transplantation (allo-HSCT) and without using tyrosine kinase inhibitors, despite being refractory to conventional chemotherapy. The coiled-coil domain containing an 88C (CCDC88C)-FLT3 translocation was identified in this patient who was diagnosed with myeloid neoplasm with T-cell lymphoblastic lymphoma (T-LBL). Chronic myelomonocytic leukaemia (CMML) was one of the differential diagnoses for the current patient; the criteria of chronic myelomonocytic leukaemia included not having the specific genes, such as PDGFRA, if eosinophilia was present. 1 The current case showed a FLT3 rearrangement, and therefore we considered a diagnosis of MLN-Eo as reasonable. The CCDC88C-FLT3 translocation was identified in T-LBL, CD34-positive haematopoietic stem and multilineage cells.We speculated that FLT3 was associated with the t(13;14)(q12;q32) translocation. Previous reports indicated FLT3 breakpoints in theThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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