L.V. Filatova (1, 2), M.S. Motalkina (1), E.V. Kharchenko (1), I.V. Ishmatova (1), I.S. Zyuzgin (1), P.S. Shilo (1), Yu.A. Oleinik (1), Yu.A. Chudinovskikh (1), T.Yu. Semiglazova (1, 2)

1 N.N. Petrov National Medical Research Center of Oncology, St. Petersburg, Russia; 2 North-Western State Medical University n.a. I.I. Mechnikov, Saint-Petersburg, Russia
High-dose chemotherapy with autologous hematopoietic stem cell transplantation (HDCT c autoHSCT) is a modern standard for the treatment of primary refractory forms and the first relapses of Hodgkin’s lymphoma (HL). HDCT with autoHSCT is effective for 50–60% of patients with the first late chemosensitive relapse of HL. Chemoresistance is defined as a predictive factor for an unfavorable prognosis. Allogeneic hematopoietic stem cell transplantations (alloHSCT) can be performed in case of recurrence of HL after HDCT with autoHSCT with preserved chemosensitivity, and are preferable for young patients in prospective clinical trials. Among the monoclonal antibodies studied, the greatest therapeutic activity was detected for brentuximab vedotin. Brentuximab vedotin is registered for the treatment of patients with classic HL after failure (progression or early relapse) of HDCT with autoHSCT or patients who are not candidates for high-dose CT, if two or more HT lines fail, for consolidation after HDCT with autoHSCT in HL patients with a high risk for recurrence or progression. The high activity of PD-1/PD-L1 checkpoint inhibitors, activating antitumor immunity (nivolumab, pembolizumab) was noted for patients with recurrence of HL. Promising areas of therapy for HL are associated with further study of new targets of tumor cells and their signaling pathways.

About the Autors

Corresponding author: L.V. Filatova – MD, Leading Researcher at the Scientific Department of Innovative Methods of Therapeutic Oncology and Rehabilitation of the N.N. Petrov NMRCO, Associate Professor at the Department of Oncology, MWSMU n.a. I.I. Mechnikov, St. Petersburg, Russia; e-mail: Larisa_Filatova @, ORCID:

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