Near‐haploid acute lymphoblastic leukemia is rare subgroup of the disease, which is very important due to very poor prognosis and resistance to treatment including novel monoclonal antibodies and CAR‐T therapy.
Background/Aim: Classic Hodgkin lymphoma (cHL) is a common B-cell malignancy. Despite the good prognosis, in some patients the standard chemotherapy and radiotherapy-based approach does not lead to long-term remission, and these patients eventually relapse. Moreover, the primary refractory disease is of major concern regarding prognosis. Patients and Methods: We performed a retrospective analysis to evaluate PD-L1 expression in 120 patients with classic Hodgkin lymphoma (cHL). Results: The median follow-up of the entire group of patients was 90 months. After initial therapy, complete remission was achieved in 113 (94.2%) patients. During the follow-up, cHL relapse/refractory disease was reported in 23 (19.2%) cases. A total of five patients died during the follow-up period, all from cHL progression. When determining PD-L1 expression on Hodgkin-Reed-Sternberg (HRS) cells, 37 cases (30.8%) were evaluated as negative, and 83 cases (69.2%) as positive. In the negative PD-L1 group of patients, no cHL relapse/refractory disease was observed during the follow-up period. However, out of 83 patients with positive PD-L1 expression on HRS cells, 23 (28%) showed relapse/refractory cHL. Conclusion: A significantly higher relapse rate was observed in PD-L1-positive patients diagnosed with cHL.Classic Hodgkin lymphoma (cHL) is a common B-cell malignancy with increased incidence in young adults and those over 55 years of age (1, 2). Generally, cHL has a good prognosis; long-term remission is achieved in more than 80% of patients (3). Unfortunately, in some patients, the standard chemotherapy and radiotherapy-based approach does not lead to long-term remission, and these patients eventually relapse. Moreover, the primary refractory disease is of major concern regarding prognosis (4, 5).Compared to other lymphomas, cHL contains only a small portion of malignant cells in the tumor -Hodgkin-Reed-Sternberg (HRS) cells account for only 1% -5% of all cells (6). The tumor microenvironment (TME) mostly consists of inflammatory cells, including macrophages, CD4+ and CD8+ T cells, plasma cells, eosinophils, and other immune cells (7). However, antitumor immune response is limited. Furthermore, studies show that HRS cells produce molecules that limit the efficacy of T cell-mediated antitumor immune responses (6). Primary HRS cells express programmed cell death-1 ligand 1 (PD-L1), while tumor-infiltrating T cells express the coinhibitory receptor, programmed death-1 (PD-1) (7).The function of PD-1 signaling is to abrogate T cellmediated immune responses (8). Normal antigen-presenting cells, dendritic cells, and macrophages express PD-1 ligands that bind PD-1 receptors on activated T cells (8, 9). Then, PD-1 receptor recruits the Src homology 2 domain-containing protein tyrosine phosphatase-2 (SHP2) phosphatase to the 1735
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