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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.
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,...
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,...

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SGSS05-NS3, a covalent SETD8 inhibitor that activates p53 pathway in neuroblastoma.

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GPC2-CAR T cells have potent preclinical activity against orthotopic medulloblastoma xenografts.

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Cohesin Loading Factor NIPBL Is Essential for MYCN Expression and MYCN-Driven Oncogenic Transcription in Neuroblastoma.

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Corrigendum: Combination of rapamycin and MK-2206 induced cell death via autophagy and necroptosis in MYCN-amplified neuroblastoma cell lines.

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Related Experiment Video

Updated: May 14, 2026

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
10:28

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers

Published on: September 20, 2018

MYCN and the epigenome.

Stanley He1, Zhihui Liu, Doo-Yi Oh

  • 1Cell and Molecular Biology Section, Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute Bethesda, MD, USA.

Frontiers in Oncology
|February 2, 2013
PubMed
Summary

Neuroblastoma (NB) prognosis depends on tumor cell differentiation. Polycomb repressor complex proteins (PRC2) are elevated in undifferentiated NB, suppressing tumor suppressor genes and impacting MYC gene regulation.

Keywords:
EZH2HATHDACMYCNRNA polymerase IIepigeneticsnucleosometranscriptional activation

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Quantification of Global Histone Post Translational Modifications Using Intranuclear Flow Cytometry in Isolated Mouse Brain Microglia
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Quantification of Global Histone Post Translational Modifications Using Intranuclear Flow Cytometry in Isolated Mouse Brain Microglia

Published on: September 15, 2023

Area of Science:

  • Oncology
  • Developmental Biology
  • Epigenetics

Background:

  • Neuroblastoma (NB) prognosis is linked to tumor histology and gene expression, with undifferentiated tumors showing poor outcomes.
  • High-risk NB often presents with genetic alterations like MYCN amplification and exhibits uncontrolled growth.
  • Retinoic acid can induce differentiation and growth control in NB, suggesting dysregulated rather than lost signaling pathways.

Purpose of the Study:

  • To review the role of MYC genes in epigenome regulation during normal development.
  • To explore alterations in MYC gene function during tumorigenesis, specifically in Neuroblastoma.
  • To investigate the role of Polycomb Repressor Complex 2 (PRC2) in NB pathogenesis.

Main Methods:

  • Review of existing literature on MYC genes, epigenetics, and Neuroblastoma.
  • Analysis of the role of Polycomb Repressor Complex proteins (PRC1 and PRC2) in stem cell differentiation.
  • Examination of PRC2 complex levels in NB tumors and its function in suppressing tumor suppressor genes.

Main Results:

  • Undifferentiated NB tumors show elevated PRC2 complex levels.
  • PRC2 functions to suppress critical tumor suppressor genes in NB.
  • MYC genes play a crucial role in regulating the epigenome, with potential alterations during tumorigenesis.

Conclusions:

  • Dysregulation of signaling pathways, not functional loss, contributes to NB progression.
  • PRC2 is implicated in suppressing tumor suppressor genes in undifferentiated NB.
  • Understanding MYC gene regulation of the epigenome is key to unraveling NB tumorigenesis.