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The current curative therapeutic option for the treatment of chronic myeloid leukemia (CML) in the chronic phase is still allogeneic stem cell transplantation (SCT). For the patients who are not candidates for allogeneic SCT, Imatinib is the treatment of choice. It was found that high dose chemotherapy with autologous stem cell rescue prolongs the disease-free survival and may also restore sensitivity to interferon. Here we report the results of Imatinib treatment in three late-phase CML patients who were submitted to autologous SCT following resistance to interferon. Complete cytogenetic response and major molecular response were achieved in the three cases. Imatinib has the potential to induce late molecular remissions during the course of treatment and its effect may be optimized by a previous autologous SCT in this type of patients.

In chronic myeloid leukemia (CML), the occurrence of blastic transformation is rare. Treatment outcome is generally poor. Allogeneic stem cell transplantation (allo‑SCT) is the only potentially curative treatment option for advanced‑phase CML. Infections caused by carbapenem‑resistant Klebsiella pneumoniae (CRKP) isolates are associated with high morbidity and mortality rates, particularly in patients with haematological malignancies. Infection and colonization by these multiresistant bacteria may represent a challenge in SCT recipients for the management of post‑transplantation complications, as well as for the eligibility to receive a transplant in patients who acquire the pathogen prior to the procedure. We herein report the case of a blast‑phase CML patient with a highly resistant, CRKP‑associated tricuspid valve endocarditis, who was treated with a combination of systemic antimicrobial therapy and surgical valve repair, and subsequently underwent a successful allo‑SCT. [ABSTRACT FROM AUTHOR]

In this study, we retrospectively examined 34 donor/recipient transplant pairs fully tested for the alleles HLA-A, B, C, DRB1, DQB1 and DPB1 in two different centers in Istanbul, Turkey. HLA-DPB1 disparity in at least one antigen level was 79.6% and only 20.6% of transplant pairs were fully identical for HLA-DPB1, in our study group. Neutrophil and thrombocyte engraftment successfully occurred in the entire study group. When the occurrence of severe (Grade III-IV) aGVHD was taken into account, we have observed that, non-permissive HLA-DPB1 mismatches were a significant factor for development of severe aGVHD (p= 0.019). There was a trend of increasing significance for the gut (p= 0.006) and liver (p: 0.054) aGVHD but not for skin aGVHD in non-permissive HLA-DPB1 mismatched transplantations. In multivariate analysis, non-permissive HLA-DPB1 mismatches remained as an independent factor for severe aGVHD. Our results did not show a significant impact of HLA-DPB1 mismatches on relapse. In survival analysis, both HLADPB1 disparities and non-permissive mismatches showed a decreasing trend of event free and overall survival times. Considering these results during donor selection may improve transplant outcomes in the setting of unrelated ASCT. [ABSTRACT FROM AUTHOR]