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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...
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...
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,...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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...
Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
Epigenetic Regulation01:37

Epigenetic Regulation

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...

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Related Experiment Video

Updated: Jun 26, 2026

Robust Detection of Gene Amplification in Formalin-Fixed Paraffin-Embedded Samples by Fluorescence In Situ Hybridization
03:55

Robust Detection of Gene Amplification in Formalin-Fixed Paraffin-Embedded Samples by Fluorescence In Situ Hybridization

Published on: July 12, 2024

Extrachromosomal DNA Amplification as a Prognostic Factor for Cancer.

Filip Gajewski1, Joanna Pec1, Jakub Kleinrok2

  • 1Student Scientific Association, The Department of Pneumonology, Oncology and Allergology, Medical University of Lublin, Doktora Kazimierza Jaczewskiego 8, 20-090 Lublin, Poland.

Journal of Personalized Medicine
|June 25, 2026
PubMed
Summary

Extrachromosomal DNA (ecDNA) amplification drives cancer evolution and resistance. Detecting ecDNA offers a new way to predict patient outcomes and develop targeted therapies.

Keywords:
biomarkercancer prognosisdrug resistanceextrachromosomal DNA (ecDNA)genomic instabilityoncogene amplificationtargeted therapytumour heterogeneity

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Last Updated: Jun 26, 2026

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10:27

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

Published on: July 25, 2020

Area of Science:

  • Oncology
  • Genomics
  • Cancer Biology

Background:

  • Extrachromosomal DNA (ecDNA) amplification is a key driver of genomic instability and aggressive cancer progression.
  • ecDNA's role in tumor evolution and its potential as a prognostic marker and therapeutic target are increasingly recognized.

Purpose of the Study:

  • To review the mechanisms by which ecDNA drives tumor evolution.
  • To assess the potential of ecDNA as a prognostic marker and therapeutic target in cancer.

Main Methods:

  • Integration of findings from diverse detection platforms including FISH, whole-genome sequencing, and specialized reconstruction algorithms.
  • Analysis of data across a wide range of cancer types.

Main Results:

  • ecDNA elements carry high-copy oncogene amplifications and segregate unevenly during cell division, promoting intratumoral heterogeneity and therapeutic resistance.
  • Pan-cancer surveys show ecDNA in a significant tumor subset, notably liposarcoma, glioblastoma, and HER2-positive breast cancer, correlating with adverse clinical outcomes.

Conclusions:

  • ecDNA amplification is a credible adverse prognostic indicator, promising for risk stratification and treatment guidance.
  • Clinical adoption of ecDNA detection is limited by the lack of standardized, scalable, and reproducible methods.