Multiple myeloma is the second most common haematological malignancy. Novel therapies have led to improvement in survival. Current myeloma management is matching the progress made in improved survival through disease control while optimising quality of life with effective supportive care. Supportive treatment is an essential part of the therapeutic management of myeloma patients because it is directed towards improving the patient’s quality of life and also can improve survival. The aim of this review is to highlight the relationship among life of quality, supportive care, and improvement in survival. Conflict of interest:None declared.

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Background: Splenectomy impacts hematological, immunological, and metabolic functions of the patient. Since our understanding of its metabolic effects, in particular effects on lipid metabolism, is limited, this study aims to investigate the effects of splenectomy on lipid metabolism. Methods: The data from 316 patients undergoing splenectomy between 2009 and 2019 were retrospectively analyzed. Thirty-eight patients whose serum lipid values were measured both preoperatively and 1 year after surgery were included in this study. Results: Significantly higher levels of total cholesterol, low-density lipoprotein (LDL), and non-high-density lipoprotein (HDL) lipid profile were found in the postsplenectomy measurements. However, no significant differences were recorded in levels of triglyceride, HDL, or very-LDL. Conclusion: We determined that splenectomy does impact lipid metabolism, and that the metabolic effects of splenectomy should further be investigated.

Myeloid or granulocytic sarcoma (GS) is a tumoral lesion consisting of immature granulocytic cells. It is a rare entity during the course of CML patients especially after allogeneic stem cell transplantation (SCT). Relapse without bone marrow involvement is much rarer. We report a case of CML patient who relapsed with isolated granulocytic sarcoma after allogeneic SCT during cytogenetic and molecular remission. 28-year-old male was diagnosed as CML and allogeneic SCT was performed because of refractory disease to tyrosine kinase inhibitors. Complete cytogenetic and molecular response was achieved after allogeneic SCT followed by dasatinib treatment. Approximately 5 years after the transplantation, very rapidly progressive lesion was documented and diagnosed as GS although he was at molecular and cytogenetic remission. The patient died during chemotherapy due to sepsis. GS relapse after allogeneic SCT is a very rare type of relapse in CML patients with molecular and cytogenetic remission. Since it is a very aggressive disease with a poor prognosis, combined chemoradiotherapies with other possible options like DLI or second allogeneic SCT should be considered as soon as the diagnosis is confirmed.

IntroductionChronic myeloid leukemia (CML) is a hematologic malignancy characterized by the presence of a reciprocal chromosomal translocation of the Abelson (ABL1) oncogene on the 9th chromosome and a breakpoint cluster region (BCR) on the 22nd chromosome, resulting in t (9,22). This results in chimeric fusion, producing oncoprotein BCR-ABL with tyrosine kinase activity (Groffen et al., 1984). The subsequent uncontrolled tyrosine kinase activity results in excess activation of multiple signaling pathways such as RAS/RAF/MAPK, PI3K/Akt, JUN, MYC, and Janus kinase/signal transducers and activators of transcription (JAK/STAT), leading to persistent cell proliferation, reduced apoptosis, and malignant expansion of pluripotent stem cells in bone marrow (Steelman et al., 2004).Since CML is due to a well-recognized translocation, it is possible to inhibit the aberrant BCR-ABL tyrosine kinase (TK) activity using molecularly targeted therapies.Imatinib was the first BCR-ABL TK inhibitor (TKI) introduced for the treatment of CML (Kantarjian et al, 2002). Although imatinib and other second-generation (including dasatinib and nilotinib) and third-generation TKIs are generally well tolerated, ensuing resistance remains a major clinical challenge (Apperley, 2007).Cytokines and growth factors can activate the JAK/ STAT signaling pathway, which has been well investigated in CML. Thus, the cascade transmits information from extracellular chemical signals to the nucleus, resulting in DNA transcription and expression of genes involved in immunity, proliferation, cellular migration, angiogenesis, differentiation, apoptosis, and oncogenesis (Rawlings et al., 2004). Therefore, overexpression of STATs, especially STAT5, is associated with leukemogenesis and carcinogenesis (Bowman et al., 2000;Rawlings et al., 2004). BCR/ABL chimeric protein constitutively activates the JAK/STAT cascade and causes antiapoptotic activity and uncontrolled proliferation of the malignant clone