Checkpoint inhibition before haploidentical transplantation with posttransplant cyclophosphamide in Hodgkin lymphoma

• Published in: Blood advances 2020-04, Vol.4 (7), p.1242-1249
• Main Authors: De Philippis, Chiara, Legrand-Izadifar, Faezeh, Bramanti, Stefania, Giordano, Laura, Montes de Oca, Catalina, Duléry, Rémy, Bouabdallah, Reda, Granata, Angela, Devillier, Raynier, Mariotti, Jacopo, Sarina, Barbara, Harbi, Samia, Maisano, Valerio, Furst, Sabine, Pagliardini, Thomas, Weiller, Pierre-Jean, Lemarie, Claude, Calmels, Boris, Chabannon, Christian, Santoro, Armando, Mohty, Mohamad, Blaise, Didier, Castagna, Luca
• Format: Article
• Language: English
• Subjects: Cyclophosphamide; Graft vs Host Disease - etiology; Hodgkin Disease - therapy; Humans; Lymphoid Neoplasia; Neoplasm Recurrence, Local; Transplantation, Haploidentical
• ISSN: 2473-9529; 2473-9537
• DOI: 10.1182/bloodadvances.2019001336

We report on 59 Hodgkin lymphoma patients undergoing haploidentical stem cell transplantation (SCT; haplo-SCT) with posttransplant cyclophosphamide (PTCy) as graft-versus-host disease (GVHD) prophylaxis, comparing outcomes based on pretransplant exposure to checkpoint inhibitors (CPIs). Considering pretransplant characteristics, the 2 cohorts (CPI = 29 patients vs no-CPI = 30 patients) were similar, except for the number of prior lines of therapy (6 vs 4; P < .001). With a median follow-up of 26 months (range, 7.5-55 months), by univariate analysis, the 100-day cumulative incidence of grade 2-4 acute GVHD was 41% in the CPI group vs 33% in the no-CPI group (P = .456), whereas the 1-year cumulative incidence of moderate to severe chronic GVHD was 7% vs 8%, respectively (P = .673). In the CPI cohort, the 2-year cumulative incidence of relapse appeared lower compared with the no-CPI cohort (0 vs 20%; P = .054). No differences were observed in terms of overall survival (OS), progression-free survival (PFS), and nonrelapse mortality (NRM) (at 2 years, 77% vs 71% [P = .599], 78% vs 53% [P = .066], and 15% vs 21% [P = .578], respectively). By multivariable analysis, CPI before SCT was an independent protective factor for PFS (hazard ratio [HR], 0.32; P = .037). Stable disease (SD)/progressive disease (PD) was an independent negative prognostic factor for both OS and PFS (HR, 14.3; P < .001 and HR, 14.1; P < .001, respectively) . In conclusion, CPI as a bridge to haplo-SCT seems to improve PFS, with no impact on toxicity profile. •Checkpoint inhibition before haplo-SCT seems to improve PFS in patients receiving haplo-SCT with PTCy as GVHD prophylaxis.•Programmed death 1 blockade as bridge to haplo-SCT with PTCy as GVHD prophylaxis does not increase toxicities and NRM. [Display omitted]