Hodgkin Disease

Abstract

Hodgkin disease is a malignancy of the lymphatic system, affecting predominantly young adults. Radio and chemotherapy have allowed long‐term cure in a large portion of patients. Unfortunately, 15–20% of patients can relapse and eventually die to this disease. CD30+ Reed–Sternberg cells represent the hallmark of this disease and they can be a variable, but usually very small portion of the cellular components of the affected lymph nodes. On the other hand, it is prominent the presence of a tumour microenvironment composed of nonmalignant B cells, T cells, granulocytes, eosinophils and stromal cells. It is thought that this microenvironment can influence the fate of the lymphoma cell growth and finally the clinical outcome of this disease. Recent therapeutic approaches such as chimeric anti‐CD30 antibody‐drug conjugates, chimeric antigen receptor T cells to the CD30 surface molecule and immune checkpoint inhibitors have given a new hope to treat patients with a relapsed/refractory disease. Key Concept Reed–Sternberg cells expressing CD30 membrane surface molecule are the main feature of the Hodgkin disease. Reed–Sternberg cells induce a strong immunosuppressive tumour microenvironment. Fluorodeoxyglucose (FDG) positron emission tomography (PET)–computerised tomography (CT) is essential to define the Hodgkin disease stage and the response to therapy. Combination chemotherapy with ABVD or MOPP followed by X‐ray radiation is the standard treatment for Hodgkin disease. 15–20% of Hodgkin disease patients do not respond to the combination chemotherapy and radiation or can relapse. The salvage therapy consists of high‐dose combination chemotherapy followed by autologous or allogeneic hematopoietic stem‐cell transplantation. Relapsed/refractory patients can be treated with anti‐CD30 drug‐conjugated antibodies or anti‐CD30 chimeric antigen receptor T cells or immune checkpoint inhibitors. Immune checkpoint inhibitors are antibodies to molecules involved in the regulation of immune response.