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

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

4.0K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
4.0K
Tumor Progression02:07

Tumor Progression

6.8K
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...
6.8K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

9.6K
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...
9.6K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

8.5K
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...
8.5K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

6.1K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
6.1K

You might also read

Related Articles

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

Sort by
Same author

Drosophila Eye Development is Compromised by dTet Overexpression through Altered Retinal Determination Gene Expression.

Developmental biology·2026
Same author

Extracellular Vesicles in the Biology and Liquid Biopsy Diagnostics of Pediatric High-Grade Glioma - Emerging Findings and Opportunities.

Journal of extracellular biology·2026
Same author

TRAM-01: A phase 2 study of trametinib for pediatric patients with neurofibromatosis type 1 and plexiform neurofibromas.

Neuro-oncology·2026
Same author

H3K27me3 spreading organizes canonical PRC1 chromatin architecture to regulate developmental programs.

Nature genetics·2026
Same author

Androgen activity in the male embryonic hindbrain drives lethal PFA ependymoma.

Nature·2026
Same author

Clinical Outcomes and Prognostic Features of Diffuse Hemispheric Glioma, H3 G34-Mutant: An International Multi-institutional Study.

Clinical cancer research : an official journal of the American Association for Cancer Research·2026

Related Experiment Video

Updated: Nov 6, 2025

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
09:08

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer

Published on: January 12, 2020

7.0K

Oncohistones: a roadmap to stalled development.

Shriya Deshmukh1, Adam Ptack2, Brian Krug3

  • 1Division of Experimental Medicine, McGill University, Montreal, QC, Canada.

The FEBS Journal
|May 10, 2021
PubMed
Summary

Oncohistones, mutated histone variants, drive cancer by disrupting epigenetic modifications, particularly at lysine residues K27 and K36. Understanding these epigenetic changes offers potential for new cancer therapies.

Keywords:
H3developmentdifferentiationepigenomeoncohistones

More Related Videos

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
10:27

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

7.5K
Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

11.2K

Related Experiment Videos

Last Updated: Nov 6, 2025

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
09:08

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer

Published on: January 12, 2020

7.0K
Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
10:27

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

7.5K
Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

11.2K

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Recurrent mutations in histone H3 variants, termed 'oncohistones,' are implicated in various cancers, especially pediatric brain tumors.
  • Oncohistones are known to induce genome-wide epigenetic alterations, impacting cellular processes like differentiation.

Purpose of the Study:

  • To review the mechanisms by which oncohistones cause epigenetic perturbations.
  • To explore how oncohistones affect post-translational modifications on histone H3 lysine residues (K27 and K36).
  • To discuss the role of these epigenetic changes in tumorigenesis and potential therapeutic strategies.

Main Methods:

  • Review of existing literature on oncohistone function and epigenetic modifications.
  • Analysis of studies investigating histone H3 lysine methylation and chromatin mark distribution.
  • Synthesis of findings on the link between oncohistones, epigenetic changes, and cancer development.

Main Results:

  • Oncohistones alter post-translational modifications at lysine residues K27 and K36 on the H3 tail.
  • These alterations lead to genome-wide epigenetic dysregulation and disruption of chromatin marks.
  • Tumorigenesis is promoted by maintaining a progenitor cell state, hindering differentiation.

Conclusions:

  • Oncohistones promote cancer by inducing widespread epigenetic changes that impair cell differentiation.
  • The epigenetic disruptions caused by oncohistones are potentially reversible.
  • Further understanding of oncohistone pathogenicity can lead to novel therapeutic approaches for cancer treatment.