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

Tumor Progression02:07

Tumor Progression

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...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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

Cancer-Critical Genes II: Tumor Suppressor Genes

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...
Tumor Progression02:07

Tumor Progression

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

Cancer-Critical Genes II: Tumor Suppressor Genes

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...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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...

You might also read

Related Articles

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

Sort by
Same author

Correction: Yang et al. 5-Methylcytidine RNA Epitranscriptomics in Women's Health and Disease: Mechanisms and Clinical Implications. <i>Cells</i> 2026, <i>15,</i> 847.

Cells·2026
Same author

Dietary fatty acid intake and the risk of pancreatic cancer: a dose-response meta-analysis of observational studies.

Annals of medicine and surgery (2012)·2026
Same author

Trends of blood pressure in the first 12 months post-kidney transplantation: blood pressure trends in kidney transplant patients.

Annals of medicine and surgery (2012)·2026
Same author

Spatial Proteomic Profiling, a Novel Method for Detecting Diagnostic and Prognostic Proteins in Pediatric Sarcoma.

The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society·2026
Same author

Rapid detection of enterotoxigenic <i>Bacillus cereus</i> by loop-mediated isothermal amplification assay from food and feed samples.

Frontiers in cellular and infection microbiology·2026
Same author

Isolation, Characterization, and Optimization of Antimicrobial Proteinaceous Compounds Produced by <i>Bacillus safensis</i> Isolated From Rhizosphere Soil Samples in Bangladesh.

International journal of microbiology·2026

Related Experiment Video

Updated: Jul 5, 2026

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections
05:45

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections

Published on: July 31, 2017

10.2K

TUBB2A and TM4SF1 Methylation Define Prognostic Subgroups in Adult-Type Diffuse Glioma.

Tarek Arabi1, Itika Arora1,2, Arshiya Akbar1

  • 1College of Medicine, Alfaisal University, Riyadh 11533, Saudi Arabia.

Cancers
|February 27, 2026
PubMed
Summary

CpG island methylator phenotype (G-CIMP) gliomas show molecular heterogeneity. Gene-specific methylation, like in TUBB2A and TM4SF1, refines prognostic stratification beyond isocitrate dehydrogenase (IDH) status alone for better glioma classification.

Keywords:
DNA methylationgene-specific methylationglioblastomaglioma-CIMP (G-CIMP)prognostic biomarkers

More Related Videos

Evaluation of Biomarkers in Glioma by Immunohistochemistry on Paraffin-Embedded 3D Glioma Neurosphere Cultures
06:32

Evaluation of Biomarkers in Glioma by Immunohistochemistry on Paraffin-Embedded 3D Glioma Neurosphere Cultures

Published on: January 9, 2019

8.3K
Digital Spatial Profiling for Characterization of the Microenvironment in Adult-Type Diffusely Infiltrating Glioma
09:17

Digital Spatial Profiling for Characterization of the Microenvironment in Adult-Type Diffusely Infiltrating Glioma

Published on: September 13, 2022

2.8K

Related Experiment Videos

Last Updated: Jul 5, 2026

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections
05:45

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections

Published on: July 31, 2017

10.2K
Evaluation of Biomarkers in Glioma by Immunohistochemistry on Paraffin-Embedded 3D Glioma Neurosphere Cultures
06:32

Evaluation of Biomarkers in Glioma by Immunohistochemistry on Paraffin-Embedded 3D Glioma Neurosphere Cultures

Published on: January 9, 2019

8.3K
Digital Spatial Profiling for Characterization of the Microenvironment in Adult-Type Diffusely Infiltrating Glioma
09:17

Digital Spatial Profiling for Characterization of the Microenvironment in Adult-Type Diffusely Infiltrating Glioma

Published on: September 13, 2022

2.8K

Area of Science:

  • Neuro-oncology
  • Epigenetics
  • Genomics

Background:

  • Gliomas are diverse, with isocitrate dehydrogenase (IDH) mutations influencing prognosis.
  • IDH-mutant gliomas often exhibit the CpG island methylator phenotype (G-CIMP), characterized by widespread epigenetic changes.
  • Current G-CIMP classification has limitations due to heterogeneity within G-CIMP gliomas.

Purpose of the Study:

  • To identify gene-level DNA methylation and expression patterns associated with clinical outcomes in gliomas.
  • To investigate molecular heterogeneity within IDH-defined G-CIMP gliomas.
  • To determine if gene-specific methylation can refine prognostic stratification.

Main Methods:

  • Utilized The Cancer Genome Atlas (TCGA) glioblastoma, IDH-wildtype discovery cohort.
  • Identified gene-level DNA methylation and expression patterns, focusing on epigenetically regulated genes like TUBB2A and TM4SF1.
  • Validated findings in an independent TCGA diffuse glioma cohort enriched for IDH-mutant tumors.

Main Results:

  • Identified significant associations between promoter methylation of TUBB2A and TM4SF1 and overall survival.
  • Demonstrated that these gene-specific methylation events are linked to clinical outcomes.
  • Highlighted molecular heterogeneity within IDH-defined G-CIMP gliomas.

Conclusions:

  • Gene-specific methylation events, such as in TUBB2A and TM4SF1, can refine prognostic stratification in gliomas.
  • Findings underscore the importance of considering molecular heterogeneity beyond IDH status for improved glioma classification.
  • Epigenetic alterations provide valuable biomarkers for predicting patient outcomes.