“…In addition, four of 12 patients experienced chromothripsis/chromoplexy-like events which mediated the deletion of relevant tumor suppressors (e.g., CDKN2C, CHD5, FAS, PTEN, etc.). In full agreement with previously published data, 5 we found that gains within 7q and 17q as well as losses within 1p and 13q were the most common largescale chromosomal imbalances. Our analysis identified a group of bona fide oncogenes and tumor suppressors with central roles in the cell cycle (i.e., CDKN2A/B, MIR34AHG, MYC, RB1, TP53), chromatin regulation (i.e., ARID1A, BAZ1A, EED, EPC1, KMT2D, NCOR1, ZEB1) and the JAK-STAT pathway (i.e., JAK2, JAK3, PTPRC, SH2B3, SOCS1, STAT3, STAT5B) whose copy number, sequence organization and/or nucleotide composition were found to be recurrently altered in our pcAECyTCL cohort.…”