Romidepsin-induced durable remission for relapsed nodal peripheral T-cell lymphoma with T follicular helper phenotype after allogeneic hematopoietic cell transplantation

Patients with recurrent peripheral T-cell lymphoma (PTCL) after allogeneic hematopoietic cell transplantation (HCT) have dismal outcomes. Nodal PTCL with the T follicular helper phenotype (PTCL-TFH) is uniquely sensitive to histone deacetylase inhibitors compared to non-TFH phenotypes. We report the case of a 19-year-old man who experienced recurrence of PTCL-TFH shortly after allogeneic HCT and subsequently achieved durable remission with romidepsin. Before HCT, the patient had refractory disease after CHOP and ESHAP chemotherapies but achieved a partial response after two cycles of romidepsin as salvage treatment. HLA-haploidentical peripheral blood stem cell transplantation was performed using conditioning with fludarabine 180 mg/sqm, melphalan 80 mg/sqm, and total body irradiation 2 Gy, and graft-versus-host disease (GVHD) prophylaxis with post-transplantation cyclophosphamide. One month after HCT, disease progression was observed in the lung. Romidepsin was readministered every 2 weeks at a reduced dose of 12 mg/sqm. After two cycles of romidepsin, the patient achieved a complete metabolic response without severe GVHD or other non-hematological toxicities. Romidepsin was discontinued after seven treatment cycles due to prolonged lymphopenia. The patient remains in complete remission 30 months after the last dose of romidepsin. Our experience suggests that romidepsin could be safely administered soon after allogeneic transplantation.

 

Comments：
Romidepsin is a histone deacetylase inhibitor that has shown activity in the treatment of relapsed or refractory PTCL, especially in PTCL-TFH. The fact that the patient achieved a partial response to romidepsin prior to HCT suggests that this agent was already active in this patient's disease. The use of romidepsin as salvage treatment prior to HCT may have contributed to the patient's favorable response to romidepsin after HCT.

It is also worth noting that the patient received a haploidentical HCT with post-transplantation cyclophosphamide as GVHD prophylaxis. This approach has been shown to be effective in reducing the risk of GVHD and improving outcomes in patients with hematological malignancies, including PTCL.

Overall, this case report suggests that romidepsin could be a safe and effective treatment option for patients with relapsed or refractory PTCL-TFH after allogeneic HCT. However, further studies are needed to confirm these findings and to determine the optimal timing and dosing of romidepsin in this setting.

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