Abstract: 【Abstract】 CD30 is a transmembrane protein highly expressed on the surface of tumor cells in many lymphomas, making it an important therapeutic target. The antibody-drug conjugate brentuximab vedotin （BV） specifically targets CD30, after which it is subsequently internalized into cells and releases its cytotoxic payload to induce tumor cell apoptosis. It also enhances antitumor immune responses through mechanisms such as the bystander effect and the induction of immunogenic cell death. BV has been approved for the treatment of various CD30-positive lymphomas, and has shown favorable efficacy and safety profiles. However, resistance to BV has emerged in some patients, and the underlying mechanisms remain unclear. This review summarizes the research progress on the mechanisms of action of and resistance to BV in the treatment of CD30-positive cutaneous lymphomas.

Key words: Lymphoma, CD30, Brentuximab vedotin, Action mechanisms, Tumor microenvironment, Drug resistance