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Related Concept Videos

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...
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Inheritance of Chromatin Structures03:17

Inheritance of Chromatin Structures

Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying DNA...
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,...
Chromatin Position Affects Gene Expression02:35

Chromatin Position Affects Gene Expression

Chromatin is the massive complex of DNA and proteins packaged inside the nucleus. The complexity of chromatin folding and how it is packaged inside the nucleus greatly influences  access to genetic information. Generally, the nucleus' periphery is considered transcriptionally repressive, while the cell's interior is considered a transcriptionally active area. 
Topologically Associated Domains (TADs)
The 3-dimensional positioning of chromatin in the nucleus influences the timing and level of...
Lineage Commitment01:21

Lineage Commitment

Commitment is the  process whereby stem cells:

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Related Experiment Video

Updated: Jul 20, 2026

Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation
09:02

Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation

Published on: November 26, 2018

Epigenetics and chronic lymphocytic leukemia.

Margaret K Yu1

  • 1Division of Hematology, Department of Internal Medicine, University of Utah, Salt Lake City, UT 84112, USA. margaret.yu@hci.utah.edu

American Journal of Hematology
|August 23, 2006
PubMed
Summary

Chronic lymphocytic leukemia (CLL) patients show lower DNA methylation. Gene promoter hypermethylation silences tumor suppressor genes, but this epigenetic change is reversible with specific drugs.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Patients with chronic lymphocytic leukemia (CLL) typically exhibit global hypomethylation compared to healthy individuals.
  • Despite global decrease, specific gene promoter regions in CLL undergo hypermethylation, leading to the silencing of tumor suppressor genes.
  • Unlike genetic mutations or deletions, DNA methylation is an epigenetic modification that can be reversed.

Purpose of the Study:

  • To explore the role of epigenetic modifications, specifically DNA methylation, in chronic lymphocytic leukemia (CLL).
  • To highlight the potential of DNA methylation modulators as a therapeutic strategy for CLL.
  • To understand how epigenetic changes impact gene expression and clinical outcomes in CLL patients.

Main Methods:

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Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients
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Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients

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A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia
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A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia

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Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation
09:02

Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation

Published on: November 26, 2018

Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients
13:21

Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients

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A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia
09:52

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia

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  • Analysis of DNA methylation levels in CLL patients.
  • Identification of hypermethylated gene promoters and their association with tumor suppressor gene silencing.
  • Review of existing literature and ongoing clinical trials involving DNA methylation inhibitors in myelodysplastic syndrome and CLL.

    • Main Results:

    • Global DNA hypomethylation is observed in CLL, contrasting with regional hypermethylation at gene promoters.
    • Hypermethylated genes often possess tumor suppressor functions, and their silencing contributes to leukemogenesis.
    • Myelodysplastic syndrome serves as a model demonstrating the reversibility of gene demethylation through therapeutic intervention.

    Conclusions:

    • Epigenetic modifications, particularly DNA methylation, play a significant role in the pathogenesis of CLL.
    • DNA methylation inhibitors represent a promising therapeutic avenue for CLL, offering a potentially reversible approach.
    • Future clinical trials correlating treatment response with gene expression will be crucial for risk stratification and predicting patient benefit from DNA methylation inhibitors.