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...
Epigenetic Regulation01:37

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
Histone Modification02:32

Histone Modification

The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone deacetylase,...
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...
Lineage Commitment01:21

Lineage Commitment

Commitment is the  process whereby stem cells:
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...

You might also read

Related Articles

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

Sort by
Same author

Deep dynamical models of single-cell multiomic velocities predict loss-of-function and rescue perturbations in B cells.

bioRxiv : the preprint server for biology·2026
Same author

Transcriptome sequencing of Hodgkin lymphoma Hodgkin and Reed-Sternberg cells reveals escape from NK cell recognition and an unfolded protein response.

Blood cancer journal·2026
Same author

Author Correction: BCL6 enables Ph<sup>+</sup> acute lymphoblastic leukaemia cells to survive BCR-ABL1 kinase inhibition.

Nature·2026
Same author

PAIRWISE: Deep Learning-based Prediction of Effective Personalized Drug Combinations in Cancer.

Research square·2026
Same author

Real-world data and clinical experience from over 100,000 multi-cancer early detection tests.

Nature communications·2025
Same author

Multiomic analysis reveals a key BCAT1 role in mTOR activation by B cell receptor and TLR9.

The Journal of clinical investigation·2025
Same journal

Dynamic myeloid suppressor states in cancer and inflammation and their therapeutic potential.

Current opinion in hematology·2026
Same journal

Factor XIa inhibition for the prevention of thrombosis: mechanism, clinical trial signals, and indication-specific positioning.

Current opinion in hematology·2026
Same journal

Nutrition as a regulator of hematopoietic stem cell biology and transplantation.

Current opinion in hematology·2026
Same journal

From biomimicry to clinical actionability: rethinking high-shear thrombosis as a mechanobiological system.

Current opinion in hematology·2026
Same journal

Bidirectional relationship between metabolic and thrombotic disease mechanisms.

Current opinion in hematology·2026
Same journal

The dual role of the brain-derived neurotrophic factor as a regulator of hemostasis and thrombotic risk.

Current opinion in hematology·2026
See all related articles

Related Experiment Video

Updated: Jun 1, 2026

In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells
10:26

In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells

Published on: January 20, 2019

Epigenetics and B-cell lymphoma.

Rita Shaknovich1, Ari Melnick

  • 1Department of Pathology, Weill Cornell Medical College, New York, New York 10065, USA.

Current Opinion in Hematology
|May 18, 2011
PubMed
Summary
This summary is machine-generated.

Mutations in epigenetic mechanisms are common in B-cell lymphomas, disrupting gene networks and chromatin. Targeting these epigenetic lesions offers new therapeutic strategies for lymphoma treatment.

More Related Videos

Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation
11:06

Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation

Published on: September 20, 2017

VDJ-Seq: Deep Sequencing Analysis of Rearranged Immunoglobulin Heavy Chain Gene to Reveal Clonal Evolution Patterns of B Cell Lymphoma
15:07

VDJ-Seq: Deep Sequencing Analysis of Rearranged Immunoglobulin Heavy Chain Gene to Reveal Clonal Evolution Patterns of B Cell Lymphoma

Published on: December 28, 2015

Related Experiment Videos

Last Updated: Jun 1, 2026

In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells
10:26

In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells

Published on: January 20, 2019

Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation
11:06

Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation

Published on: September 20, 2017

VDJ-Seq: Deep Sequencing Analysis of Rearranged Immunoglobulin Heavy Chain Gene to Reveal Clonal Evolution Patterns of B Cell Lymphoma
15:07

VDJ-Seq: Deep Sequencing Analysis of Rearranged Immunoglobulin Heavy Chain Gene to Reveal Clonal Evolution Patterns of B Cell Lymphoma

Published on: December 28, 2015

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Epigenetic mechanisms and epigenomic patterning are increasingly recognized as frequently altered in B-cell lymphomas.
  • Understanding these alterations is crucial for deciphering lymphomagenesis.

Purpose of the Study:

  • To review recent findings on epigenetic mutations in B-cell lymphomas.
  • To provide a framework for understanding the role of epigenetic modifications in lymphomagenesis.

Main Methods:

  • Review of current literature on epigenetic alterations in B-cell lymphomas.
  • Analysis of somatic mutations in key epigenetic regulators.
  • Examination of DNA methylation patterns.

Main Results:

  • Recurrent somatic mutations in histone methyltransferases (e.g., EZH2, MLL2), demethylases (e.g., UTX, JMJD2C), and acetyltransferases (e.g., CBP, p300) are common in lymphomas.
  • These mutations disrupt chromatin structure and lead to aberrant transcriptional programming.
  • Widespread cytosine methylation patterning alterations are a hallmark of B-cell lymphomas, with specific patterns distinguishing subtypes.

Conclusions:

  • Newly identified epigenetic lesions offer insights into B-cell lymphoma genesis.
  • Further research is needed to elucidate the biological mechanisms of these epigenetic lesions.
  • Epigenetic alterations present significant opportunities for developing novel biomarkers and therapeutic strategies for lymphoma.