A gene expression-based method to diagnose clinically distinct subgroups of diffuse large B cell lymphoma

By George E. Wright, Bruce K. Tan, Andreas Rosenwald, Elaine Hurt, A. Wiestner, Louis Staudt. Proceedings of the National Academy of Sciences of the United States of America, 2003

1,084 citations recorded by the source corpus.

Subfields: Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/d57431d5a575be486db85d52d0cd95e16eb0fcc8

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Citations in the corpus

Confirmation of the molecular classification of diffuse large B-cell lymphoma by immunohistochemistry using a tissue microarray. (2004, neutral): “Negative 57 (39) 58 ( 45-71 ) .29 52 (38-66) .25 Positive 90 (61) 50 (39-61) 48 (36-59)”
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.”
An enhanced International Prognostic Index (NCCN-IPI) for patients with diffuse large B-cell lymphoma treated in the rituximab era. (2014, background): “The search for novel indices using IHC markers or gene expression signatures has not yet led to a robust index for routine clinical use.(8-13,22,23) This is largely the result of intrinsic limitations in the application of these markers related to technical limitations or poor reproducibility.”
Molecular Diagnosis of Primary Mediastinal B Cell Lymphoma Identifies a Clinically Favorable Subgroup of Diffuse Large B Cell Lymphoma Related to Hodgkin Lymphoma (2003, methodology): “Previously, we developed a Bayesian predictor of the distinction between the ABC and GCB DLBCL subgroups (21).”
Clinical drug response can be predicted using baseline gene expression levels and in vitro drug sensitivity in cell lines (2014, background): “The authors of the original clinical study reported that a 100-gene signature model [32], built on two arms of”
Concurrent expression of MYC and BCL2 in diffuse large B-cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone. (2012, methodology): “DLBCL molecular subtype (GCB, ABC, and unclassifiable) and molecular Burkitt’s lymphoma, if present in DLBCL patient cases with high MYC expression, were assigned by GEP according to previously published protocols.(3,24,25) The validation set consisted of 140 patients from the British Columbia Cance”
Prediction error estimation: a comparison of resampling methods (2005, methodology): “We calculate the LDA with the lda function in the MASS library of the statistical package R (Venables and Ripley, 1994; Ihaka and Gentlemen, 1996).”
Ovarian Carcinoma Subtypes Are Different Diseases: Implications for Biomarker Studies (2008, background): “, breast carcinoma and lymphoma [24,25]), and this subtype specific approach to treatment has implications for the design of clinical trials for women with ovarian carcinomas.”
MYC gene rearrangements are associated with a poor prognosis in diffuse large B-cell lymphoma patients treated with R-CHOP chemotherapy. (2009, methodology): “4 It is unclear from this analysis what proportion of cases had a concurrent t(14;18) translocation.”
Molecular subtypes of diffuse large B-cell lymphoma arise by distinct genetic pathways (2008, background): “3A); this finding was noteworthy because high FOXP1 mRNA expression is a hallmark of ABC DLBCL (5, 15).”
MYC/BCL2 protein coexpression contributes to the inferior survival of activated B-cell subtype of diffuse large B-cell lymphoma and demonstrates high-risk gene expression signatures: a report from The International DLBCL Rituximab-CHOP Consortium Program. (2013, methodology): “A Bayesian model was also used to determine the classification probability.(26) The GEP classification method developed from this study was validated with Figure 1.”
A New Immunostain Algorithm Classifies Diffuse Large B-Cell Lymphoma into Molecular Subtypes with High Accuracy (2009, positive): “) was used for GEP study of these 68 cases, along with the Bayesian algorithm (3).”