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

Cancers Originate from Somatic Mutations in a Single Cell

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...

Cancer-Critical Genes II: Tumor Suppressor Genes

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 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

A Clinically Integrated Pediatric Patient-Derived Xenograft Program Enables Evaluation of Cohort and Patient-Specific Biology and Therapeutic Strategies.

Cancer research·2026

Same author

Pancreatic Cancer: Translating Tumor Biology into Actionability.

Cancer discovery·2026

Same author

Selective silencing of placental anti-angiogenic factors in invasive trophoblasts via membrane-fusion divalent siRNA delivery for preeclampsia therapy.

Journal of controlled release : official journal of the Controlled Release Society·2026

Same author

Hierarchical classification of immune cell transcriptomes at population-scale.

bioRxiv : the preprint server for biology·2026

Same author

Mutant KRAS-driven selective mRNA translation reveals mechanisms and therapeutic vulnerabilities in cancer.

Cell reports·2026

Same author

Lysosome-directed targeted protein degradation technologies for overcoming cancer drug resistance: mechanisms, design principles, and therapeutic opportunities.

Drug delivery·2026

Search research articles

Related Experiment Video

Updated: Feb 28, 2026

Author Spotlight: Exploring Strategies for Successful Immune Response Against Tumors

Author Spotlight: Exploring Strategies for Successful Immune Response Against Tumors

Published on: August 16, 2024

Tumor diversity and evolution revealed through RADseq.

Elizabeth B Perry^1,2, Alvin Makohon-Moore³, Caihong Zheng⁴

¹Cancer Biology & Genetics, Memorial Sloan Kettering Cancer Center, New York, New York, USA.

|June 15, 2017

Summary

Restriction-site associated DNA sequencing (RADseq) offers a flexible and efficient method for studying tumor evolution. This technique aids in identifying genetic alterations and inferring evolutionary relationships in cancers.

Keywords:

RADseq cancer next-generation sequencing restriction-site associated DNA sequencing tumor evolution

More Related Videos

Detecting Somatic Genetic Alterations in Tumor Specimens by Exon Capture and Massively Parallel Sequencing

Detecting Somatic Genetic Alterations in Tumor Specimens by Exon Capture and Massively Parallel Sequencing

Published on: October 18, 2013

Comparative Lesions Analysis Through a Targeted Sequencing Approach

Comparative Lesions Analysis Through a Targeted Sequencing Approach

Published on: November 5, 2019

Related Experiment Videos

Last Updated: Feb 28, 2026

Author Spotlight: Exploring Strategies for Successful Immune Response Against Tumors

Author Spotlight: Exploring Strategies for Successful Immune Response Against Tumors

Published on: August 16, 2024

Detecting Somatic Genetic Alterations in Tumor Specimens by Exon Capture and Massively Parallel Sequencing

Detecting Somatic Genetic Alterations in Tumor Specimens by Exon Capture and Massively Parallel Sequencing

Published on: October 18, 2013

Comparative Lesions Analysis Through a Targeted Sequencing Approach

Comparative Lesions Analysis Through a Targeted Sequencing Approach

Published on: November 5, 2019

Area of Science:

Evolutionary Biology
Genetics
Oncology

Background:

Cancer is increasingly viewed as an evolutionary process.
Evolutionary biology tools are valuable for understanding cancer progression.
Restriction-site associated DNA sequencing (RADseq) is a tool for evolutionary genetics.

Purpose of the Study:

To apply RADseq for studying tumor evolution.
To overcome limitations of exome or whole-genome sequencing in cancer research.
To assess RADseq's utility in human and zebrafish cancer models.

Main Methods:

Applied RADseq to human pancreatic cancer and zebrafish melanoma.
Utilized low-frequency (SbfI) and high-frequency (NsiI) cutters.
Analyzed single nucleotide substitutions and copy number alterations.

Main Results:

Successfully identified genetic alterations in tumors using RADseq.
Inferred phylogenetic relationships between primary tumors and metastases.
Demonstrated RADseq's capability for detecting somatic mosaicism.

Conclusions:

RADseq provides an unbiased and cost-effective approach for tumor evolution studies.
The method is versatile, applicable to various cancer types and tissues.
RADseq enhances evolutionary studies of cancer, including rates of evolution and lineage relationships.