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@ARTICLE{Gler:304272,
      author       = {M. Güler$^*$ and F. Canzian$^*$},
      title        = {{C}lustering of lymphoid neoplasms by cell of origin,
                      somatic mutation and drug usage profiles: a multi-trait
                      genome-wide association study.},
      journal      = {Blood cancer journal},
      volume       = {15},
      number       = {1},
      issn         = {2044-5385},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-01813},
      pages        = {147},
      year         = {2025},
      note         = {#EA:C055#LA:C055#},
      abstract     = {Lymphoid neoplasms (LNs) are heterogeneous malignancies
                      arising from lymphoid cells, displaying diverse clinical and
                      molecular features. Although LNs are collectively frequent,
                      individual subtypes are rare, posing challenges for genetic
                      association studies. Indeed, genome-wide association studies
                      (GWAS) explained only a fraction of the heritability. Shared
                      genetic susceptibility and overlapping risk factors suggest
                      a partially common etiology across subtypes. We employed a
                      multi-trait GWAS strategy to improve discovery power by
                      leveraging pleiotropy among LN subtypes. We defined LN
                      phenoclusters based on cell of origin, somatic mutation
                      profiles, and approved therapeutic agents. Using data from
                      three large cohorts-the UK Biobank, Million Veteran Program,
                      and FinnGen-we analyzed 31,937 LN cases and 1.2 million
                      controls across 8 individual subtypes and 7 phenoclusters.
                      We replicated the novel associations in two independent
                      cohorts (All of Us and the Prostate, Lung, Colorectal, and
                      Ovarian Cancer Screening Trial) with 2892 LN cases and
                      165,791 controls. We identified 76 genome-wide significant
                      loci for individual subtypes or subtype clusters, including
                      20 novel associations. We identified the subtypes
                      contributing to each locus, putative candidate causal
                      variants, and genes underlying the associations, and found
                      enrichment of specific cell types, biological processes, and
                      drugs associated with LN risk genes. Overall, this study
                      identified new LN genetic risk loci and candidate genes,
                      providing insights that may inform novel therapeutic
                      approaches.},
      keywords     = {Humans / Genome-Wide Association Study / Mutation / Female
                      / Male / Genetic Predisposition to Disease / Middle Aged /
                      Aged},
      cin          = {C055},
      ddc          = {610},
      cid          = {I:(DE-He78)C055-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40883272},
      pmc          = {pmc:PMC12397487},
      doi          = {10.1038/s41408-025-01351-4},
      url          = {https://inrepo02.dkfz.de/record/304272},
}