A5006867948- Lymphoma Diagnosis and Treatment
- Chronic Lymphocytic Leukemia Research
- Immune Cell Function and Interaction
- T-cell and B-cell Immunology
- Multiple Myeloma Research and Treatments
- Ubiquitin and proteasome pathways
- CAR-T cell therapy research
- Protein Degradation and Inhibitors
- Viral-associated cancers and disorders
- NF-κB Signaling Pathways
- Chromatin Remodeling and Cancer
- Immunotherapy and Immune Responses
- Cancer-related gene regulation
- Immune Response and Inflammation
- Chronic Myeloid Leukemia Treatments
- Immunodeficiency and Autoimmune Disorders
- Nuclear Receptors and Signaling
- Acute Lymphoblastic Leukemia research
- Cancer Genomics and Diagnostics
- Galectins and Cancer Biology
- T-cell and Retrovirus Studies
- Cytokine Signaling Pathways and Interactions
- Cancer Mechanisms and Therapy
- Diabetes and associated disorders
- Single-cell and spatial transcriptomics
National Institutes of Health
2015-2024
National Cancer Institute
2015-2024
Target (United States)
2022-2024
AstraZeneca (United States)
2022-2024
Center for Cancer Research
2013-2023
Government of the United States of America
2022
Johns Hopkins University
1996-2015
Max Planck Institute for Metabolism Research
2008-2010
Dana-Farber Cancer Institute
2008
Boston University
2008
Diffuse large B-cell lymphomas (DLBCLs) are phenotypically and genetically heterogeneous. Gene-expression profiling has identified subgroups of DLBCL (activated B-cell–like [ABC], germinal-center [GCB], unclassified) according to cell origin that associated with a differential response chemotherapy targeted agents. We sought extend these findings by identifying genetic subtypes based on shared genomic abnormalities uncover therapeutic vulnerabilities tumor genetics.
Gene-expression profiling has been used to define 3 molecular subtypes of diffuse large B-cell lymphoma (DLBCL), termed germinal center B-cell-like (GCB) DLBCL, activated (ABC) and primary mediastinal (PMBL). To investigate whether these DLBCL arise by distinct pathogenetic mechanisms, we analyzed 203 biopsy samples high-resolution, genome-wide copy number analysis coupled with gene-expression profiling. Of 272 recurrent chromosomal aberrations that were associated alterations, 30...
The gene encoding the BCL-6 transcriptional repressor is frequently translocated and mutated in diffuse large cell lymphoma. Mice with a disrupted developed myocarditis pulmonary vasculitis, had no germinal centers, increased expression of T helper type 2 cytokines. DNA recognition motif resembled sites bound by STAT (signal transducers activators transcription) transcription factors, which mediate cytokine signaling. could repress interleukin-4 (IL-4)-induced when to site recognized...
Abstract We have identified two intronic regions of mouse prdm1, the gene encoding B lymphocyte-induced maturation protein-1 (Blimp-1), which confer transcriptional repression in response to Bcl-6. The Bcl-6 element intron 5, is conserved between mice and humans, was studied detail. It binds vitro shown by chromatin immunoprecipitation be occupied vivo. Neither functions as a STAT3-response element, showing that STAT3 does not compete with at these sites. Bcl-6−/− confirm biological...
A common V(D)J recombinase that recognizes a conserved recombination signal sequence (RSS) mediates the assembly of immunoglobulin (Ig) and T cell receptor (TCR) genes in B precursors. The rearrangement particular Ig TCR gene segments, however, is tightly regulated with respect to lineage developmental stage. Using an vitro system, we analyzed cleavage RSSs flanking segments nuclei. We found both lineage-specificity temporal ordering reflected accessibility within chromatin cleavage.