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Related Concept Videos

Cancers Originate from Somatic Mutations in a Single Cell02:21

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...
Cancers Originate from Somatic Mutations in a Single Cell02:21

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...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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,...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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,...
Cancer02:18

Cancer

Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
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...

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  3. Extrachromosomal Dna Gives Cancer A New Evolutionary Pathway.
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  3. Extrachromosomal Dna Gives Cancer A New Evolutionary Pathway.

Related Experiment Video

Genome-wide Purification of Extrachromosomal Circular DNA from Eukaryotic Cells
14:26

Genome-wide Purification of Extrachromosomal Circular DNA from Eukaryotic Cells

Published on: April 4, 2016

Extrachromosomal DNA Gives Cancer a New Evolutionary Pathway.

Elizabeth Brunk1, Yue Wang2, Oliver Cope3

  • 1Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27516.

Research Square
|May 7, 2026

View abstract on PubMed

Summary
This summary is machine-generated.

Tumors with extrachromosomal DNA (ecDNA) maintain a spectrum of oncogene levels, enabling rapid adaptation. This ecDNA dosage variation is actively regulated, driving tumor evolution and treatment resistance.

Keywords:
Extrachromosomal DNAecDNAevolutionpopulation heterogeneitysingle cellsingle-cell multi-omics sequencing

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

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Area of Science:

  • Cancer Biology
  • Genomics
  • Tumor Evolution

Background:

  • Tumor progression typically involves dominant clones with advantageous mutations.
  • Cancers driven by extrachromosomal DNA (ecDNA) present a unique model with cellular heterogeneity.
  • ecDNA variation may confer adaptive advantages through bet-hedging strategies.

Purpose of the Study:

  • To systematically characterize ecDNA levels and their functional consequences across single cells.
  • To investigate the mechanisms underlying ecDNA dosage maintenance and regulation.
  • To understand the role of ecDNA in tumor adaptability and aggressiveness.

Main Methods:

  • Single-cell multiomics and multiplexed proteomics.
  • High-resolution imaging and live-cell time-course experiments.
  • Stochastic modeling and experimental manipulation of ecDNA dosage.

    • Main Results:

    • Higher ecDNA dosage correlates with proportional increases in transcript abundance, chromatin accessibility, protein levels, and proliferation.
    • Genes on ecDNA show distinct transcriptional scaling compared to chromosomal amplification.
    • Populations rapidly restore ecDNA dosage distribution after experimental disruption, indicating active regulation.

    Conclusions:

    • ecDNA-mediated gene expression provides tumors with rapid, population-level adaptability.
    • The continuous spectrum of ecDNA dosage is actively maintained, not passively inherited.
    • This mechanism contributes to the aggressive nature and treatment resistance of ecDNA-driven cancers.