Genetic lesions and impact on clinical and MRD outcome. (A) Relationship of genetic lesions of all patients of the trial population (n = 100) who had mutational analysis available and at least a single mutation and/or 17p/11q deletion present (n = 63). Rows correspond to genes, and columns represent individual patients color-coded according to gene status (white, wild type; red, mutations of NOTCH1; dark green, mutations of SF3B1; dark purple, mutations of TP53; light purple, 17p deletion; light green, 11q deletion). (B, C) OS and EFS according to TP53 mutational status (purple, TP53-mutated with or without 17p- [n = 18]; black, TP53 wild-type with or without 17p- [n = 54]); (D, E) OS and EFS according to SF3B1 and NOTCH1 mutational status (green, SF3B1-mutated [n = 16]; red, NOTCH1-mutated [n = 10]; black, SF3B1 and NOTCH1 wild-type [n = 45]). (F) Durability of MRD-negative remission in 28 patients who had achieved this status at 12 months after HSCT. Both MRD reconversions and clinical relapses without prior MRD reconversion are counted as events. Patients are censored at the time of last available MRD measurement. Upward arrows indicate patients remaining MRD-negative and relapse-free at last measurement; downward arrows indicate patients with MRD reconversion. The patient reconverting to MRD positivity at +29 months is still in clinical CR 63 months post-HSCT; the other 2 relapsed subsequently. Downward double arrows indicate patients with no marker with clinical relapse from MRD negativity (one relapsed extranodally with rapidly fatal Richter’s transformation; the other showed discrete lymph node enlargements that were considered as relapse without histological proof and responded to rituximab). Two patients are censored at 72 months (one 17p- and NOTCH1-mutated, the other without marker).