Hypermutation of multiple proto-oncogenes in B-cell diffuse large-cell lymphomas

By L. Pasqualucci, P. Neumeister, T. Goossens, G. Nanjangud, R. Chaganti, Ralf Küppers, R. Dalla-Favera. Nature, 2001

1,056 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/fadb3f41dde066a2bd5d726da98c7ee77a3650f5

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Citations in the corpus

Widespread genetic heterogeneity in multiple myeloma: implications for targeted therapy (2014, neutral): “We found that EGR1 mutations were clustered toward the 50 end of the gene (Tables S1 and S2; Figure S1), a pattern of mutation often associated with somatic hypermutation (Pasqualucci et al., 2001).”
Analysis of the Coding Genome of Diffuse Large B-Cell Lymphoma (2011, background): “However, it cannot be excluded that the abnormal and/or ectopic activity of activation-induced cytidine deaminase has a role in the generation of DNA lesions affecting these residues; indeed, activation-induced cytidine deaminase has been shown to target the 5′ portion of multiple genes—mostly nonco”
Somatic mutation of EZH2 (Y641) in Follicular and Diffuse Large B-cell Lymphomas of Germinal Center Origin (2010, neutral): “Assay plates are coated with biotinylated histone H3 (21-44) peptide.”
Integrated genomic analysis identifies recurrent mutations and evolution patterns driving the initiation and progression of follicular lymphoma (2013, neutral): “SHM hotspots typically occur within the 2-kb window downstream of the transcription start site (TSS) and we have focused our analyses on these regions 53 .”
Germinal centres: role in B-cell physiology and malignancy (2008, background): “Finally, what sequences are normally targeted by AID in addition to the immunoglobulin heavy- and light-chain loci? Increasing evidence indicates that multiple loci are targeted by SHM in normal centroblast”
Discovery and prioritization of somatic mutations in diffuse large B-cell lymphoma (DLBCL) by whole-exome sequencing (2012, result): “This is consistent with previous demonstrations of aberrant SHM preferentially occurring closer to the 5′ end (34).”
Mechanisms of B-cell lymphoma pathogenesis (2005, background): “Some of these genes, however, undergo aberrant somatic hypermutation, and therefore acquire DNA strand breaks in the same regions where the chromosomal breakpoints are located (see below”
Pax5: the guardian of B cell identity and function (2007, background): “Aberrant SHM has been shown to target exon 1B of PAX5 in diffuse large B cell lymphomas (DLBCL), which are germinal-center B cell–derived tumor”