ArticleBlood cancer discovery2023
Molecular Evolution of Classic Hodgkin Lymphoma Revealed Through Whole-Genome Sequencing of Hodgkin and Reed Sternberg Cells.
Article in Blood cancer discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
34 citing papers in PubMed, 55 citations in OpenAlex.
- Genomic characterization of therapy-associated polyposis reveals an alkylating mutational signature from prior treatment.The Journal of clinical investigation · 2026Article
- Structure and molecular function of the BCL7 proteins.Biochemical Society transactions · 2026Review
- Clonal evolution and mutational trajectories of metastatic colorectal cancer shaped by anticancer therapies.Nature communications · 2026Article
- Exome sequencing of Hodgkin and non-Hodgkin composite lymphomas identifies shared somatic mutations indicative of common founding precursors.Cancer genetics · 2026Article
- Genetic risk and immune dysregulation of classic Hodgkin lymphoma transformation of chronic lymphocytic leukemia/small lymphocytic lymphoma: a multicentric study.medRxiv : the preprint server for health sciences · 2026Article
- Predictors of sensitivity to immune therapies in classic Hodgkin lymphoma.Blood neoplasia · 2026Review
- Article
- Aging cells, young patients: senescence in Hodgkin lymphoma.Blood advances · 2026Article
- Disordered differentiation and cellular senescence in pediatric Hodgkin Reed-Sternberg cells.Blood advances · 2026Article
- Transcriptome sequencing of Hodgkin lymphoma Hodgkin and Reed-Sternberg cells reveals escape from NK cell recognition and an unfolded protein response.Blood cancer journal · 2026Article
- Targeting inflammatory microenvironments: overcoming therapy resistance and immunosuppression.Molecular cancer · 2026Review
- Genome-scale spatial mapping of the Hodgkin lymphoma microenvironment identifies tumor cell survival factors.Nature communications · 2025Article
- Whole Exome Sequencing for the Identification of Mutations in Bone Marrow CD34+Cells in Hodgkin Lymphoma.Current issues in molecular biology · 2025Article
- Temporal genomic dynamics shape clinical trajectory in multiple myeloma.Nature genetics · 2025Article
- The long-term effects of chemotherapy on normal blood cells.Nature genetics · 2025Article
- Genomic landscape of virus-associated cancers.Nature communications · 2025Article
- Newly Diagnosed Classical Hodgkin Lymphoma: Optimizing Outcomes in a New Therapeutic Era.Hematological oncology · 2025Review
- Circulating tumor DNA in lymphoma: technologies and applications.Journal of hematology & oncology · 2025Review
- The mutational landscape and its longitudinal dynamics in relapsed and refractory classic Hodgkin lymphoma.Annals of hematology · 2025Article
- Molecular profiling of cell-free DNA from classic Hodgkin lymphoma patients identifies potential prognostic clusters and corresponds with disease dynamics.Annals of hematology · 2025Article
Corrections and comments
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Authors and funding
32 authors at 12 institutions in 3 countries.
Funding
Abstract
The rarity of malignant Hodgkin and Reed Sternberg (HRS) cells in classic Hodgkin lymphoma (cHL) limits the ability to study the genomics of cHL. To circumvent this, our group has previously optimized fluorescence-activated cell sorting to purify HRS cells. Using this approach, we now report the whole-genome sequencing landscape of HRS cells and reconstruct the chronology and likely etiology of pathogenic events leading to cHL. We identified alterations in driver genes not previously described in cHL, APOBEC mutational activity, and the presence of complex structural variants including chromothripsis. We found that high ploidy in cHL is often acquired through multiple, independent chromosomal gains events including whole-genome duplication. Evolutionary timing analyses revealed that structural variants enriched for RAG motifs, driver mutations in B2M, BCL7A, GNA13, and PTPN1, and the onset of AID-driven mutagenesis usually preceded large chromosomal gains. This study provides a temporal reconstruction of cHL pathogenesis. SIGNIFICANCE: Previous studies in cHL were limited to coding sequences and therefore not able to comprehensively decipher the tumor complexity. Here, leveraging cHL whole-genome characterization, we identify driver events and reconstruct the tumor evolution, finding that structural variants, driver mutations, and AID mutagenesis precede chromosomal gains. This article is highlighted in the In This Issue feature, p. 171.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.