Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

B Cell Activation and Differentiation01:24

B Cell Activation and Differentiation

The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...
Cells of the Adaptive Immune Response01:23

Cells of the Adaptive Immune Response

The T and B lymphocytes of the adaptive immune system develop from common lymphoid progenitor cells in the bone marrow. These progenitors give rise to precursors that eventually develop into both T and B lymphocytes. As these precursors mature, they gain the ability to detect and respond to foreign antigens in the body, a process known as immunocompetence. Additionally, these precursors acquire self-tolerance, a process that ensures they do not react to self-antigens. This intricate system...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Antigen Processing Pathways01:31

Antigen Processing Pathways

MHC molecules are key players in the immune response, enabling T cells to recognize and respond to specific antigens. They are present on the surface of all nucleated cells in the body and are instrumental in presenting antigens to T cells and activating them. T cells recognize the MHC-antigen complex and initiate an immune response. MHC class I and MHC class II are two main types of MHC molecules, each associated with a distinct antigen processing pathway.
MHC Class I: Presenting Endogenous...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

SPEN loss drives extra-follicular diffuse large B cell lymphoma with female-specific lethality and therapeutic vulnerabilities.

Cancer discovery·2026
Same author

Enhanced efficacy of a specific HDAC3 inhibitor in combination with 5-azacitidine against diffuse large B-cell lymphoma.

Blood neoplasia·2026
Same author

Elevated levels of TNF and its targets characterize better-risk older acute myeloid leukemia patients.

Leukemia·2026
Same author

CCAAT-enhancer binding protein delta functions as a tumor suppressor gene in acute myeloid leukemia.

Neoplasia (New York, N.Y.)·2026
Same author

Impact of Perforin 1 A91V germ line background in patients with aggressive B-NHL treated with R-CHOP.

Blood advances·2026
Same author

The LMO2-LDB1-TAL1 complex regulates transcription networks in acute myeloid leukemia.

Blood neoplasia·2026

Related Experiment Video

Updated: Jun 6, 2026

Enhancing Tumor Content through Tumor Macrodissection
10:04

Enhancing Tumor Content through Tumor Macrodissection

Published on: February 12, 2022

Pathogenesis of diffuse large B cell lymphoma proteogenotypes.

Julius C Enssle1, Björn Häupl2, Arber Qoku3

  • 1Department of Medicine, Hematology and Oncology, University Hospital, Goethe University Frankfurt, Frankfurt am Main, Germany; German Cancer Consortium (DKTK), Partner Site Frankfurt/Mainz, a Partnership Between DKFZ and UCT Frankfurt-Marburg, Germany, Frankfurt am Main, Germany; Frankfurt Cancer Institute (FCI), Frankfurt am Main, Germany; Lymphoid Malignancies Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

Cancer Cell
|June 4, 2026
PubMed
Summary
This summary is machine-generated.

Researchers identified seven diffuse large B cell lymphoma (DLBCL) proteogenotypes (PGs). PG4 is linked to poor outcomes, regardless of other factors, and reveals common oncogenic pathways for targeted therapies.

Keywords:
B cell receptorMYCgenomicsimmune exhaustionlymphomamulti-omics data integrationprotein translationproteomicssingle cell sequencingtumor microenvironment

More Related Videos

From a 2DE-Gel Spot to Protein Function: Lesson Learned From HS1 in Chronic Lymphocytic Leukemia
10:18

From a 2DE-Gel Spot to Protein Function: Lesson Learned From HS1 in Chronic Lymphocytic Leukemia

Published on: October 19, 2014

Tumor Engraftment in a Xenograft Mouse Model of Human Mantle Cell Lymphoma
10:52

Tumor Engraftment in a Xenograft Mouse Model of Human Mantle Cell Lymphoma

Published on: March 30, 2018

Related Experiment Videos

Last Updated: Jun 6, 2026

Enhancing Tumor Content through Tumor Macrodissection
10:04

Enhancing Tumor Content through Tumor Macrodissection

Published on: February 12, 2022

From a 2DE-Gel Spot to Protein Function: Lesson Learned From HS1 in Chronic Lymphocytic Leukemia
10:18

From a 2DE-Gel Spot to Protein Function: Lesson Learned From HS1 in Chronic Lymphocytic Leukemia

Published on: October 19, 2014

Tumor Engraftment in a Xenograft Mouse Model of Human Mantle Cell Lymphoma
10:52

Tumor Engraftment in a Xenograft Mouse Model of Human Mantle Cell Lymphoma

Published on: March 30, 2018

Area of Science:

  • Oncology
  • Genomics
  • Proteomics

Background:

  • Diffuse large B cell lymphoma (DLBCL) exhibits significant clinical and molecular heterogeneity.
  • Current understanding of DLBCL subtypes and their underlying biology remains incomplete.

Purpose of the Study:

  • To integrate multi-omic data for a deeper understanding of DLBCL heterogeneity.
  • To identify novel molecular subgroups and their clinical implications.
  • To establish a proteogenomic framework for DLBCL classification and treatment.

Main Methods:

  • Integrated analysis of proteomic, transcriptomic, and genomic data from 478 DLBCL tumors.
  • Proteogenomic profiling to define distinct DLBCL subgroups (proteogenotypes).
  • Single-cell sequencing and spatial transcriptomics to investigate cellular phenotypes and microenvironment.

Main Results:

  • Identified seven distinct DLBCL proteogenotypes (PGs) that encompass known molecular subtypes.
  • PG4 emerged as a high-risk subgroup associated with poor outcomes, independent of existing prognostic factors.
  • PG4 tumors exhibit a dark-zone B cell phenotype, enriched BTG1 mutations, activated MYC and TCF3/4 signaling, and an exhausted CD8+ T cell microenvironment.

Conclusions:

  • Proteogenomic profiling provides a refined classification of DLBCL.
  • PG4 represents a high-risk DLBCL subgroup with distinct molecular drivers and microenvironment characteristics.
  • This study offers a foundation for developing novel diagnostic and therapeutic strategies for aggressive DLBCL.