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  • A possible mechanism of the initiation of HSTCL

    2019-04-22

    A possible mechanism of the Nanaomycin A manufacturer of HSTCL is a prolonged immunosuppressive status which generates the expansion of γδ T-cells recognizing multiple pathogens through excessive antigenic stimulation. Our cases did not have any previous illness related to immunosuppression, recurrent infectious episodes or laboratory evidence of HTLV-1 infection which has the potential of causing immunosuppression as well as a T-cell malignancy. The cause of their immunocompromised status was therefore unknown; an age-related decline in the immune function might be responsible for the lymphomagenesis of HSTCL in these cases. In addition, both of the two previous aged Japanese cases (cases 5 and 6) were positive for EBER (Table 2). In Eastern Asia, EBV infection and reactivation are thought to contribute to the tumorigenesis of T-cell or natural killer (NK)-cell posttransplant lymphoproliferative disorder (T-PTLD) and non-hepatosplenic/non-cutaneous γδ peripheral T-cell lymphomas [7]. Although EBER was undetectable in our cases, there might be a potential contribution of EBV infection and reactivation to the development of HSTCL in aged patients as well as other lymphoid malignancies [6,7]. Regarding therapy management, the cases in this study were treated with CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone) or CHOP-like regimens as first-line therapy. The 5-year overall survival (OS) rate has been reported to be 7% [3]. Cases 2–4 in fact had faint responses, and these cases were not rescued by subsequent salvage therapies, autologous HSCT (auto-HSCT) and allogeneic HSCT (allo-HSCT). The survival benefit of HSTCL cases using allo-HSCT has been reported in a limited number of cases [11]; Considerable issues in allo-HSCT include the treatment-related mortality [12]. However, the evaluable sample size in the study was too small to estimate the risk of cytotoxic effects, GVHD and relapse after allo-HSCT. Therefore, large-scale studies are required to determine the indication for and appropriate strategy of allo-HSCT to improve the treatment outcome of HSTCL. Interestingly, Case 1, an exclusive female patient, achieved a CR that was maintained after 6 cycles of CHOP. This result was compatible with a previous retrospective analysis of 15 patients that showed that the overall survival (OS) was significantly prolonged in females than in males [13].
    Author contributions
    Disclosure of potential conflicts of interest
    Introduction Acute promyelocytic leukemia (APL) is driven by an oncogenic chromosomal translocation fusing the promyelocytic leukemia (PML) and retinoic acid receptor alpha (RARA) genes. The PML/RARA fusion protein causes a maturational block at the promyelocyte stage of myeloid differentiation. Differentiation therapy with all-trans retinoic acid (ATRA) alone or in combination with chemotherapy is a major advance in the treatment of APL and is regarded as the first paradigm of molecularly targeted therapy [1]. However, relapse/refractory APL patients demonstrating resistance to ATRA are recognized as a clinically critical problem. Arsenic trioxide (As2O3) is also highly effective in the treatment of APL. Early studies conducted in China and the United States showed that this agent can induce sustained molecular remission when used as a single agent in patients who have a relapse after treatment with ATRA-containing regimens [2,3]. As2O3 acts through specific binding of the PML moiety of the disease-specific RARA oncoprotein, leading to its degradation and resulting in partial differentiation and induction of apoptosis of leukemic promyelocytes. Synergy of As2O3 and ATRA, which binds the RARA moiety of PML/RARA, has been shown at both the biological and the clinical levels. On the other hand, tamibarotene is in the same family of drugs as ATRA, induces the differentiation of APL cells, and is applied to relapsed cases that have previously received ATRA treatment [4]. Tamibarotene has strong differentiation-inducing activity on human promyelocytic leukemia cells and is expected to be more effective and safe than ATRA [5].