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Related Concept Videos

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,...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
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

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Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
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Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...

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Related Experiment Video

Updated: Jun 5, 2026

Transmitochondrial Cybrid Generation Using Cancer Cell Lines
07:49

Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

Mitochondrial capture by a transmissible cancer.

Clare A Rebbeck1, Armand M Leroi, Austin Burt

  • 1Department of Life Sciences, Imperial College London, Silwood Park, Ascot, Berkshire, SL5 7PY, UK.

Science (New York, N.Y.)
|January 22, 2011
PubMed
Summary

Canine transmissible venereal tumor (CTVT), a unique infectious cancer, periodically acquires host mitochondria. This occurs because the cancer

Area of Science:

  • Veterinary Oncology
  • Evolutionary Biology
  • Cell Biology

Background:

  • Canine transmissible venereal tumor (CTVT) is a clonal, naturally occurring cancer that is transmitted as a living cell between dogs.
  • CTVT is one of the oldest known cancer lineages, originating approximately 10,000 years ago.
  • The unique biology of CTVT provides insights into cancer evolution and host-pathogen interactions.

Purpose of the Study:

  • To investigate the evolutionary history and genetic mechanisms underlying CTVT.
  • To explore the role of mitochondrial dynamics in the adaptation and persistence of CTVT.
  • To understand how CTVT maintains its viability and infectivity over long periods.

Main Methods:

  • Phylogenetic analysis of mitochondrial DNA sequences.

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  • Comparative genomics of CTVT samples and host canids (dogs and wolves).
  • Mitochondrial function and degeneration assays.
  • Main Results:

    • Phylogenetic analyses revealed that CTVT has acquired host mitochondria on multiple occasions throughout its history.
    • CTVT's own mitochondria exhibit high mutation rates and relaxed selection, leading to degeneration.
    • Host-derived mitochondria appear to be more functionally fit, facilitating cancer cell survival.

    Conclusions:

    • CTVT's ability to acquire and utilize host mitochondria is a key adaptation for its long-term survival and transmission.
    • Mitochondrial degeneration in CTVT highlights the evolutionary pressures on cancer cell organelles.
    • Understanding these mechanisms could inform strategies against transmissible cancers.