Case report: The utilization of crizotinib and brentuximab vedotin as a bridge to autologous stem cell transplantation and followed by CD30-directed CAR-T cell therapy in relapsed/refractory ALK+ ALCL

Front Immunol. 2024 Feb 5:15:1346001. doi: 10.3389/fimmu.2024.1346001. eCollection 2024.

Abstract

Background: Anaplastic lymphoma kinase-positive anaplastic large cell lymphoma (ALK+ ALCL) is a rare, mature T-cell non-Hodgkin lymphoma. The prognosis of patients with relapsed or refractory ALCL following first-line chemotherapy is extremely poor. NCCN guidelines recommend intensified chemotherapy with or without ASCT consolidation for r/r ALCL, however, this is not an effective treatment for all ALK+ALCL.

Case report: Herein, we report a patient with relapsed/refractory ALK+ ALCL who received crizotinib and brentuximab vedotin as bridging therapy, followed by autologous stem cell transplantation and sequential anti-CD30 CAR T cell therapy.

Conclusion: The patient achieved complete remission and long-term disease-free survival of months and continues to be followed up. The combination therapy model in this case may provide guidance for the management of relapsed/refractory ALK+ ALCL, and further prospective trials are needed to confirm its effectiveness.

Keywords: CAR T cell therapy; T-cell non-Hodgkin lymphoma; anaplastic large cell lymphoma; autologous stem cell transplantation; crizotinib.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Brentuximab Vedotin / therapeutic use
  • Crizotinib / therapeutic use
  • Hematopoietic Stem Cell Transplantation*
  • Humans
  • Immunoconjugates* / therapeutic use
  • Immunotherapy, Adoptive
  • Lymphoma, Large-Cell, Anaplastic* / drug therapy
  • Lymphoma, Large-Cell, Anaplastic* / pathology
  • Neoplasm Recurrence, Local / drug therapy
  • Receptor Protein-Tyrosine Kinases / genetics
  • Receptors, Chimeric Antigen* / therapeutic use
  • Transplantation, Autologous

Substances

  • Brentuximab Vedotin
  • Crizotinib
  • Receptors, Chimeric Antigen
  • Immunoconjugates
  • Receptor Protein-Tyrosine Kinases

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by the National Natural Science Foundation of China (No. 82270183 and 82370196).