Multicenter phase 2 study of oral azacitidine (CC-486) plus CHOP as initial treatment for PTCL.

TitleMulticenter phase 2 study of oral azacitidine (CC-486) plus CHOP as initial treatment for PTCL.
Publication TypeJournal Article
Year of Publication2023
AuthorsRuan J, Moskowitz A, Mehta-Shah N, Sokol L, Chen Z, Kotlov N, Nos G, Sorokina M, Maksimov V, Sboner A, Sigouros M, Van Besien K, Horwitz S, Rutherford SC, Mulvey E, Revuelta MV, Xiang J, Alonso A, Melnick A, Elemento O, Inghirami G, Leonard JP, Cerchietti L, Martin P
JournalBlood
Volume141
Issue18
Pagination2194-2205
Date Published2023 May 04
ISSN1528-0020
KeywordsAntineoplastic Combined Chemotherapy Protocols, Azacitidine, Cyclophosphamide, Doxorubicin, Humans, Immunologic Factors, Lymphoma, T-Cell, Peripheral, Prednisone, Tumor Microenvironment, Vincristine
Abstract

Peripheral T-cell lymphomas (PTCL) with T-follicular helper phenotype (PTCL-TFH) has recurrent mutations affecting epigenetic regulators, which may contribute to aberrant DNA methylation and chemoresistance. This phase 2 study evaluated oral azacitidine (CC-486) plus cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) as initial treatment for PTCL. CC-486 at 300 mg daily was administered for 7 days before C1 of CHOP, and for 14 days before CHOP C2-6. The primary end point was end-of-treatment complete response (CR). Secondary end points included safety and survival. Correlative studies assessed mutations, gene expression, and methylation in tumor samples. Grade 3 to 4 hematologic toxicities were mostly neutropenia (71%), with febrile neutropenia uncommon (14%). Nonhematologic toxicities included fatigue (14%) and gastrointestinal symptoms (5%). In 20 evaluable patients, CR was 75%, including 88.2% for PTCL-TFH (n = 17). The 2-year progression-free survival (PFS) was 65.8% for all and 69.2% for PTCL-TFH, whereas 2-year overall survival (OS) was 68.4% for all and 76.1% for PTCL-TFH. The frequencies of the TET2, RHOA, DNMT3A, and IDH2 mutations were 76.5%, 41.1%, 23.5%, and 23.5%, respectively, with TET2 mutations significantly associated with CR (P = .007), favorable PFS (P = .004) and OS (P = .015), and DNMT3A mutations associated with adverse PFS (P = .016). CC-486 priming contributed to the reprograming of the tumor microenvironment by upregulation of genes related to apoptosis (P < .01) and inflammation (P < .01). DNA methylation did not show significant shift. This safe and active regimen is being further evaluated in the ALLIANCE randomized study A051902 in CD30-negative PTCL. This trial was registered at www.clinicaltrials.gov as #NCT03542266.

DOI10.1182/blood.2022018254
Alternate JournalBlood
PubMed ID36796016
PubMed Central IDPMC10356559
Grant ListP30 CA008748 / CA / NCI NIH HHS / United States
Related Faculty: 
Giorgio Inghirami, M.D. Andrea Sboner, Ph.D.

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