Table 1.
Lymphomatype | Gene | Genetic aberration | Frequency of mutated cases (%) | Dysregulated biological process or pathway | References |
Hodgkin’s lymphoma | REL | Amplification | ~50 | NF-κB pathway | Barth et al., 2003 |
NFKBIA, NFKBIE, TNFAIP3 | Point mutations, deletions | 50–60 | Weniger et al., 2016 | ||
MDM2 | Gains | 60 | P53-dependent biological processes (e.g., cell cycle arrest and apoptosis) | Küppers, 2009 | |
TP53 | Point mutations, deletions | 10 | |||
Classical Hodgkin’s lymphoma | JAK1, STAT3, STAT5B | Missense mutations | 15 | JAK-STAT pathway | Tiacci et al., 2018 |
JAK2 | Gains | 32 | |||
PTPN1 | Splice-acceptor, missense mutations | 6 | |||
SOCS1 | Frameshift mutations, disruptive in-frame deletions, splice donor, missense | 47 | JAK-STAT5pathway | Weniger et al., 2006;Tiacci et al., 2018 | |
EBV+ Hodgkin’s lymphoma | LMP2A | EBV-encoded LMP2A mediated transcriptional changes | ~50 | Transcriptional signature similar to that of HRS* cells | Portis et al., 2003 |
*: Reed–Sternberg cells of Hodgkin’s lymphoma.