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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

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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...
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Epigenetic Regulation01:46

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Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Chromatin Modification in iPS Cells01:32

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Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
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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. 
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Inheritance of Chromatin Structures03:17

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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...
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The process of chromosome duplication during cell division requires genome-wide disruption and re-assembly of chromatin. The chromatin structure must be accurately inherited, reassembled, and maintained in the daughter cells to ensure lineage propagation.
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Updated: Feb 26, 2026

Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients
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Impact of Chromosomal Rearrangement upon DNA Methylation Patterns in Leukemia.

Hyang-Min Byun1, Shahrooz Eshaghian2, Dan Douer2

  • 1Human Nutrition Research Centre, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, NE4 5PLUnited Kingdom.

Open Medicine (Warsaw, Poland)
|July 22, 2017
PubMed
Summary

Cancer development involves genomic instability and aberrant DNA methylation. This study found that DNA methylation profiles reflect the cell of origin, not the BCR-ABL gene translocation, in various cancers.

Keywords:
5-azacytidineAcute Lymphoblastic LeukemiaAcute Promyelocytic LeukemiaChronic Myelogenous LeukemiaDNA methylationGastrointestinal Stromal TumorPhiladelphia Chromosome

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Area of Science:

  • Oncology
  • Epigenetics
  • Genomics

Background:

  • Genomic instability and aberrant DNA methylation are hallmarks of cancer.
  • The BCR-ABL translocation, specifically t(9:22), is a key driver in certain leukemias.

Purpose of the Study:

  • To investigate the impact of the BCR-ABL translocation on DNA methylation profiles in cancer.
  • To determine if chromosomal lesions or cell of origin dictates cancer DNA methylation patterns.

Main Methods:

  • Compared DNA methylation of 1,505 promoter CpGs across chronic myelogenous leukemia (CML), Philadelphia chromosome-positive (Ph+) and negative acute lymphoblastic leukemia (ALL), and other cancers (APL, GIST).
  • Included CD34+ hematopoietic stem cells transfected with BCR-ABL for mechanistic insights.

Main Results:

  • DNA methylation profiles of CML were more similar to acute promyelocytic leukemia (APL) than to Ph+ ALL.
  • DNA methylation profiles were consistent within tumor types but not significantly influenced by the BCR-ABL gene translocation.
  • BCR-ABL translocation did not appear to be a primary determinant of overall DNA methylation profiles.

Conclusions:

  • DNA methylation profiles in cancer are more likely to reflect the cell of origin.
  • Chromosomal lesions like BCR-ABL translocation may not be the main drivers of global DNA methylation patterns in these cancers.