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Integrated Genomic and Transcriptomic Analyses of Diffuse Large B-Cell Lymphoma With Multiple Abnormal Immunologic
Lingshuang Sheng1, Di Fu1, Yiwen Cao1
1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Diffuse large B-cell lymphoma (DLBCL) with abnormal immune markers shows poor prognosis and resembles autoimmune diseases (AIDs). This study reveals genetic and clinical features, guiding targeted therapy for this aggressive lymphoma subtype.
Area of Science:
- Oncology
- Immunology
- Genetics
Background:
- Diffuse large B-cell lymphoma (DLBCL) is an aggressive lymphoma linked to autoimmune diseases (AIDs).
- Primary B-cell receptor-mediated AIDs correlate with poor DLBCL outcomes.
- Investigating immunological alterations is crucial for understanding DLBCL progression.
Purpose of the Study:
- To integrate genomic and transcriptomic analyses of DLBCL with abnormal immunologic markers.
- To determine the role of immunological alterations in DLBCL disease progression.
- To identify clinical and genetic features of DLBCL with multiple abnormal immunologic markers.
Main Methods:
- Collected clinical data from 1,792 newly diagnosed DLBCL patients.
- Performed DNA- and RNA-sequencing on 164 and 127 patients, respectively.
- Analyzed gene mutations, pathways, gene expression, and tumor microenvironment based on immune status.
Main Results:
- DLBCL with abnormal immune markers exhibited elevated LDH, inferior prognosis, and dysregulated cell cycle/immune response.
- Activated oxidative phosphorylation pathway and altered Th1/Th2 and Th17/Treg ratios were observed.
- These findings closely mirrored characteristics seen in autoimmune diseases (AIDs).
Conclusions:
- Pioneered the description of clinical and genetic features in DLBCL with abnormal immunologic markers.
- Illustrated potential mechanisms driving disease progression in this DLBCL subset.
- Provided a clinical rationale for mechanism-based targeted therapy in this DLBCL group.
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