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. 2017 Jan 5;8(7):12031–12040. doi: 10.18632/oncotarget.14509

Figure 2. Somatic mutations were present prior to any cytotoxic treatment.

Figure 2

A. A TP53 Y220C mutation was identified in UPN2 in all the available BM-MNC specimens, from APL diagnosis to complete remission, and expanded in the t-MN clone. B. Similarly, in UPN1 the ASXL1 Y591* mutation was identified in all the available BM-MNC specimens, from NHL diagnosis to t-MN. Notably, this mutation was detected at very low levels in the BM NHL specimen (0.3%), significantly increased at 31 months follow-up (7%) and reached the highest VAF at t-MN diagnosis (42%). C. In UPN9, the IDH1 R132H mutation was originally present at a high allele frequency at NHL diagnosis, 9 years before t-MN onset, when the patient was 72 years old, indicating that this mutation could have occurred as a pre-leukemic event. The SRSF2 P95H mutation was acquired later, at the time of t-MN diagnosis. Legend: APL DG: acute promyelocitic leukemia diagnosis; CR: complete remission; NHL DG: non-Hodgkin lymphoma diagnosis; t-MN DG: therapy-related myeloid neoplasm diagnosis; AIDA: ATRA, idarubicine; RT: radiotherapy; ProMACE-CytaBOM: cyclophosphamide, doxorubicin, etoposide, bleomycin, vincristine, methotrexate and prednisone.