The molecular signature of mediastinal large B-cell lymphoma differs from that of other diffuse large B-cell lymphomas and shares features with classical Hodgkin lymphoma.

By K. Savage, Stefano Monti, J. Kutok, G. Cattoretti, D. Neuberg, L. de Leval, P. Kurtin, P. Dal Cin, C. Ladd, F. Feuerhake and 12 more. Blood, 2003

875 citations recorded by the source corpus.

Subfields: Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/1daf04de94d720d8e455cf43167df80add293982

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Citations in the corpus

Analysis of the Coding Genome of Diffuse Large B-Cell Lymphoma (2011, background): “Current understanding of the biology of DLBCL indicates the existence of several disease subgroups reflecting the derivation from B cells at discrete stages of differentiation, namely germinal-center B-cell–like (GCB) DLBCL, activated B-cell–like (ABC) DLBCL and primary mediastinal B-cell lymphoma (”
The 2008 WHO classification of lymphomas: implications for clinical practice and translational research (2009, neutral): “The use of gene expression profiling further confirmed a biological relationship.(35,36) Prior case reports had identified cases of PMBL followed by CHL or vice versa, or other cases in which both lymphomas were composite in the same tumor mass.”
Mutations of multiple genes cause deregulation of NF-kB in diffuse large B-cell lymphoma (2009, neutral): “ABC-DLBCL Non-GC/NC-DLBCL Biallelic deletion Mutation plus deletion Biallelic mutation Heterozygous mutation Monoallelic deletion Normal Mutated Deleted Normal Nonsense mutations (12) Frameshift deletions (7) Frameshift insertions (5) Splice site mutations (2)”
Transcription factor IRF4 controls plasma cell differentiation and class-switch recombination (2006, background): “and is often abnormally expressed in B cell lymphoma”
PD-L1 Expression is Characteristic of a Subset of Aggressive B-Cell Lymphomas and Virus-Associated Malignancies (2013, neutral): “7 CHL is genetically, phenotypically, and/or histologically related to additional large cell lymphomas including primary mediastinal large B-cell lymphoma (PMLBCL), nodular lymphocyte predominant Hodgkin lymphoma (NLPHL), and T-cell rich, histiocyte-rich large B-cell lymphoma (TCRLBCL).(10,11) Simil”
A New Immunostain Algorithm Classifies Diffuse Large B-Cell Lymphoma into Molecular Subtypes with High Accuracy (2009, positive): “Other GEP studies have also characterized primary mediastinal large B-cell lymphoma (PMBL) as distinct from the other subtypes of DLBCL (7, 8), and with a good prognosis similar to GCBDLBCL (7).”
The 2008 WHO classification of lymphoid neoplasms and beyond: evolving concepts and practical applications. (2011, background): “GEP studies further revealed that PMBCL and CHL share a common gene expression signature, supporting a close biological relationship.(96;97)”
GEMS: A system for automated cancer diagnosis and biomarker discovery from microarray gene expression data (2005, methodology): “Based on outputs of Multi-Class SVM methods @BULLETMajority voting @BULLETDecision Trees: CART @BULLETMulti-Class SVM: DAGSVM @BULLETMulti-Class SVM: one-versus-rest @BULLETMulti-Class SVM: one-versus-one Based on outputs of all classifiers @BULLETMajority voting @BULLETDecision Trees: CART”
Mechanisms of B-cell lymphoma pathogenesis (2005, background): “MALT lymphoma API2–MALT1 (30)135, CD95 (5-80)25,140,141‡ Indirect role of – BCL10–IgH (5)136,137, Helicobactor pylori in MALT1–IgH (15-20)138, gastric MALT FOXP1–IgH (10)139 lymphomas85”
Molecular subtypes of diffuse large B-cell lymphoma arise by distinct genetic pathways (2008, positive): “This MCR has been reported previously to occur in both PMBL and Hodgkin’s lymphoma (6, 29), 2 lymphomas that share a common gene-expression signature, clinical presentation in younger patients, and possible origin from thymic B cells (6, 7).”
BIC and miR‐155 are highly expressed in Hodgkin, primary mediastinal and diffuse large B cell lymphomas (2005, positive): “Several studies have reported a close relationship between HL and PMBL cases, based on similar gene expression profiles and common genomic aberrations [27, 28 ].”