Classical Hodgkin Lymphoma (CHL)
Overview
Classical Hodgkin Lymphoma (cHL) is a Hodgkin Lymphoma (parent HL) characterized by Hodgkin and Reed-Sternberg (HRS) cells.
Cohorts in the corpus
- chl_sccc_2023: 25 cHL cases profiled by WGS on FACS-isolated HRS cells plus 36 additional cases by WES, for a combined 61-patient driver-gene cohort PMID:36723991.
- Two age peaks represented: ped/AYA (ages 7–27, n=19 WGS) and older adults (ages 55–85, n=6 WGS); 22/25 samples from diagnosis, 3/25 from relapse PMID:36723991.
Recurrent alterations
- 26 mutated driver genes/hotspots identified; 8 newly described in cHL PMID:36723991.
- Top drivers: SOCS1 62%, TNFAIP3 36%, B2M ~32–33%, ITPKB 28%, GNA13 26%, STAT6 20%, BCL7A 18%, NFKBIE 15%, PTPN1 8%, TP53 8%, XPO1 8% PMID:36723991.
- APOBEC mutagenesis (SBS2/SBS13) highly prevalent, exceeding non-Hodgkin lymphoma and CLL (P<0.00001) PMID:36723991.
- AID off-target activity concentrated on noncoding footprints of BCL7A, SOCS1, TMSB4X, IL4R, and ITPKB PMID:36723991.
- Complex SVs including chromothripsis; SV breakpoints enriched for RAG recombination motifs PMID:36723991.
- High ploidy typically achieved via multiple independent chromosomal gains including whole-genome duplication (WGD) rather than a single event PMID:36723991.
Subtypes
- Ped/AYA cases carried significantly higher genome-wide SBS+indel burden than older adults (median 6,270 vs 3,723, Wilcoxon P=0.0033) PMID:36723991.
Therapeutic landscape
- Paper does not evaluate specific drug responses; treatment implications are inferential only PMID:36723991.
Sources
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