PRDM1 and neoplasm: Interestingly, these two cases had very different clinical courses: one was a chemotherapy refractory patient whose tumor rapidly progressed to a leukemic phase and contained additional genetic abnormalities (TP53 loss, cMYC amplification, PRDM1/Blimp1 loss) that may have contributed to the aggressiveness of the malignancy while the second was an 11-year-old whose ALCL lacked these genetic abnormalities and who had a remarkable anti-tumor response to conventional chemotherapy and remains in clinical remission.