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Related Concept Videos

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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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.
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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...
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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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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Genome-wide Purification of Extrachromosomal Circular DNA from Eukaryotic Cells
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Extrachromosomal DNA-relieving heredity constraints, accelerating tumour evolution.

C Bailey1, M J Shoura2, P S Mischel3

  • 1Cancer Evolution and Genome Instability Laboratory, The Francis Crick Institute, London, UK.

Annals of Oncology : Official Journal of the European Society for Medical Oncology
|April 11, 2020
PubMed
Summary
This summary is machine-generated.

Extrachromosomal DNA (ecDNA) allows cancer cells to rapidly adapt and evolve. These structures accelerate tumor heterogeneity and drug resistance, impacting cancer progression and survival.

Keywords:
double minutesextrachromosomal DNAextrachromosomal circular DNAtumour evolution

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Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Extrachromosomal DNA (ecDNA) facilitates rapid cancer cell adaptation.
  • ecDNA structures contain oncogenes and regulatory elements, lacking centromeres for unequal segregation.

Purpose of the Study:

  • To review recent discoveries on ecDNA's role in tumor evolution.
  • To highlight ecDNA's contribution to cancer aggressiveness and drug resistance.

Main Methods:

  • Literature review of recent studies on ecDNA in cancer.
  • Analysis of ecDNA's impact on tumor microenvironment and heterogeneity.

Main Results:

  • ecDNA drives tumor heterogeneity through non-Mendelian inheritance.
  • Favorable epigenetic modifications on ecDNA enhance positive selection.
  • ecDNA is linked to aggressive tumor behavior, poor survival, and drug resistance.

Conclusions:

  • ecDNA accelerates intratumoral heterogeneity and cellular fitness.
  • One in four solid tumors exhibit cells with ecDNA structures.
  • Understanding ecDNA is crucial for cancer evolution and treatment strategies.