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

Abnormal Proliferation02:23

Abnormal Proliferation

5.4K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.4K
Epigenetic Regulation01:37

Epigenetic Regulation

4.1K
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...
4.1K
Epigenetic Regulation01:46

Epigenetic Regulation

34.2K
Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
34.2K
Epigenetic Regulation01:46

Epigenetic Regulation

26.2K
26.2K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

6.2K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
6.2K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

2.0K
2.0K

You might also read

Related Articles

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

Sort by
Same author

EpiATLAS - a reference for human epigenomic research.

bioRxiv : the preprint server for biology·2026
Same author

A multidisciplinary RNA-guided approach to complement genomic analysis of unsolved patients with an inborn error of immunity.

Frontiers in immunology·2026
Same author

The Growth Supporting Role of ZDHHC11 Is Linked to the MEF2B-BCL6 Regulatory Circuit in Burkitt Lymphoma.

International journal of cancer·2026
Same author

Relevance of Epstein-Barr Virus (EBV) miRNAs in EBV-Infected B Cells and B-Cell Lymphomas.

Cancers·2026
Same author

Multidimensional Characterization of Tumor-Immune Architecture Reveals Clinically Relevant Classic Hodgkin Lymphoma Subtypes.

Cancer discovery·2026
Same author

Dynamics of circulating tumour DNA in relapsed/refractory diffuse large B-cell lymphoma patients.

British journal of haematology·2025

Related Experiment Video

Updated: Mar 21, 2026

In Vitro Selection of Engineered Transcriptional Repressors for Targeted Epigenetic Silencing
10:44

In Vitro Selection of Engineered Transcriptional Repressors for Targeted Epigenetic Silencing

Published on: May 5, 2023

2.0K

SETD2: an epigenetic modifier with tumor suppressor functionality.

Jun Li1, Gerben Duns2, Helga Westers1

  • 1Department of Genetics, University of Groningen, University Medical Center Groningen, The Netherlands.

Oncotarget
|May 19, 2016
PubMed
Summary
This summary is machine-generated.

Set domain containing 2 (SETD2) is a histone modifier implicated in cancer. Inactivating mutations in SETD2 are linked to tumor development, particularly in clear cell Renal Cell Cancer, offering new therapeutic targets.

Keywords:
H3K36me3SETD2ccRCChistone modificationtumor suppressor gene

More Related Videos

An Engineered Split-TET2 Enzyme for Chemical-inducible DNA Hydroxymethylation and Epigenetic Remodeling
08:34

An Engineered Split-TET2 Enzyme for Chemical-inducible DNA Hydroxymethylation and Epigenetic Remodeling

Published on: December 18, 2017

7.1K
Toxicological Assays for Testing Effects of an Epigenetic Drug on Development, Fecundity and Survivorship of Malaria Mosquitoes
10:26

Toxicological Assays for Testing Effects of an Epigenetic Drug on Development, Fecundity and Survivorship of Malaria Mosquitoes

Published on: January 16, 2015

8.9K

Related Experiment Videos

Last Updated: Mar 21, 2026

In Vitro Selection of Engineered Transcriptional Repressors for Targeted Epigenetic Silencing
10:44

In Vitro Selection of Engineered Transcriptional Repressors for Targeted Epigenetic Silencing

Published on: May 5, 2023

2.0K
An Engineered Split-TET2 Enzyme for Chemical-inducible DNA Hydroxymethylation and Epigenetic Remodeling
08:34

An Engineered Split-TET2 Enzyme for Chemical-inducible DNA Hydroxymethylation and Epigenetic Remodeling

Published on: December 18, 2017

7.1K
Toxicological Assays for Testing Effects of an Epigenetic Drug on Development, Fecundity and Survivorship of Malaria Mosquitoes
10:26

Toxicological Assays for Testing Effects of an Epigenetic Drug on Development, Fecundity and Survivorship of Malaria Mosquitoes

Published on: January 16, 2015

8.9K

Area of Science:

  • Epigenetics
  • Molecular Biology
  • Cancer Research

Background:

  • Epigenetic regulatory machinery is crucial in understanding cancer.
  • Genetic aberrations in epigenetic modifiers are linked to various cancers.
  • Targeting the epigenome is a novel cancer treatment strategy.

Purpose of the Study:

  • To review the structural characteristics and functions of Set domain containing 2 (SETD2).
  • To explore the role of SETD2 in cancer development and its association with H3K36 trimethylation.
  • To discuss the prevalence of SETD2 mutations in cancers and their potential contribution to tumorigenesis.

Main Methods:

  • Literature review combining studies on SETD2 function across multiple species (yeast, Drosophila, C. elegans, mice, humans).
  • Analysis of structural characteristics and functional roles of SETD2.
  • Examination of SETD2's role as the primary human gene for H3K36 trimethylation (H3K36me3).

Main Results:

  • SETD2 is the key enzyme responsible for H3K36 trimethylation.
  • H3K36me3 modification is read by specific proteins that regulate transcription elongation, RNA processing, and DNA repair.
  • SETD2-inactivating mutations are prevalent in various cancers, notably clear cell Renal Cell Cancer.

Conclusions:

  • SETD2 mutations are associated with cancer development.
  • Understanding SETD2 function and its inactivation is critical for developing targeted cancer therapies.
  • SETD2-negative tumors represent a potential target for novel therapeutic strategies.