Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Tumor Progression

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...

You might also read

Related Articles

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

Sort by

Same author

SAA1 Promotes Pro-inflammatory Macrophage-mediated Bone Invasion in Silent Corticotroph Adenomas.

Genomics, proteomics & bioinformatics·2026

Same author

EpiATLAS - a reference for human epigenomic research.

bioRxiv : the preprint server for biology·2026

Same author

MET-associated immune prognostic signature predicts survival and guides personalized therapy in glioma.

Acta neuropathologica communications·2026

Same author

Blood transcriptomic endotyping of COPD identifies a neutrophil-driven inflammatory endotype reflected by the neutrophil-to-lymphocyte ratio.

Respiratory research·2026

Same author

Extracellular Matrix-Related Gene Signature Implied Immunosuppressive Status and Adverse Survival in Diffuse Glioma Patients.

Cancers·2026

Same author

T2Pdecoder enables protein-centric analyses from transcriptomic data.

Nature communications·2026

Search research articles

Related Experiment Video

Updated: Jul 15, 2025

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

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

Published on: January 9, 2019

Identifying predictors of glioma evolution from longitudinal sequencing.

Quanhua Mu^1,2, Ruichao Chai^1,3,4, Bo Pang^3,4

¹Department of Chemical and Biological Engineering, Division of Life Science, State Key Laboratory of Molecular Neuroscience, Hong Kong University of Science and Technology, Hong Kong, SAR 999077, China.

Science Translational Medicine

|October 4, 2023

Summary

Early molecular changes in diffuse gliomas predict cancer evolution and treatment resistance. MYC amplification at diagnosis drives temozolomide resistance by promoting hypermutation, offering new therapeutic targets.

More Related Videos

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections

Published on: July 31, 2017

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma

Published on: February 22, 2015

Related Experiment Videos

Last Updated: Jul 15, 2025

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

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

Published on: January 9, 2019

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections

Published on: July 31, 2017

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma

Published on: February 22, 2015

Area of Science:

Oncology
Genomics
Cancer Evolution

Background:

Clonal evolution is a key driver of cancer progression and therapeutic resistance in gliomas.
Understanding early molecular features that guide post-treatment cancer evolution is crucial but remains unclear.

Purpose of the Study:

To identify early molecular predictors of tumor evolution in adult diffuse gliomas.
To develop a predictive model for glioma evolution and patient stratification.
To elucidate the mechanism by which MYC influences treatment resistance and hypermutation.

Main Methods:

Multivariate analysis of sequencing and clinical data from 544 initial-recurrent adult diffuse glioma pairs.
Development and validation of the machine learning model CELLO2 (Cancer EvoLution for LOngitudinal data version 2).
In vitro experiments using glioma cell lines and patient-derived gliomaspheres to study temozolomide resistance and MYC function.

Main Results:

CDKN2A deletion predicted later tumor necrosis in IDH-mutant gliomas; Ki67 predicted hypermutation in IDH-wild-type gliomas.
MYC gain or MYC-target activation at diagnosis predicted treatment-induced hypermutation in all glioma subtypes.
CELLO2 model stratified patients, identifying a high-risk group with MYC gain and poor survival.
MYC drives temozolomide resistance by promoting hypermutation via increased vulnerability of mismatch repair genes.

Conclusions:

Early molecular events, particularly MYC alterations, are significant predictors of diffuse glioma evolution and therapeutic resistance.
The CELLO2 model offers a tool for predicting glioma progression and stratifying patients for precision oncology.
Targeting MYC-driven hypermutation presents a potential strategy to overcome temozolomide resistance in gliomas.