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Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

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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...
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Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

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Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic...
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Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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

Cancer-Critical Genes I: Proto-oncogenes

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Overview of Transposition and Recombination02:13

Overview of Transposition and Recombination

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Transposons make up a significant part of genomes of various organisms. Therefore, it is believed that transposition played a major evolutionary role in speciation by changing genome sizes and modifying gene expression patterns. For example, in bacteria, transposition can lead to conferring antibiotic resistance. Movement of transposable elements within the genetic pool of pathogenic bacteria can aid in transfer of antibiotic-resistant genetic elements. In eukaryotes, transposons can carry out...
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DNA-only Transposons02:57

DNA-only Transposons

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DNA-only transposons are called autonomous transposons since they code for the enzyme transposase that is required for the transposition mechanism. Insertion of transposons can alter gene functions in multiple ways. They can mutate the gene, alter gene expression by introducing a novel promoter or insulator sequence, introduce new splice sites, and change the mRNA transcripts produced, or remodel chromatin structure.
The donor site from where the transposon is excised is either degraded or...
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Related Experiment Video

Updated: Apr 19, 2026

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma
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Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma

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Transposable Element Activation: A Hallmark of Cancer.

Katherine B Chiappinelli1, Kathleen H Burns2

  • 1George Washington University Washington, DC United States.

Cancer Discovery
|April 17, 2026
PubMed
Summary
This summary is machine-generated.

Transposable elements (TEs), mobile DNA sequences, are usually silenced but become active in cancer. Their expression contributes to tumor development and can be targeted for anti-cancer immune therapies, suggesting a new hallmark of cancer.

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Area of Science:

  • Genomics
  • Epigenetics
  • Cancer Biology

Background:

  • Transposable elements (TEs) comprise approximately half of the human genome.
  • In healthy cells, TEs are epigenetically silenced.
  • Oncogenic transformation leads to epigenetic dysregulation, activating TEs.

Purpose of the Study:

  • To elucidate the role of TEs in cancer development.
  • To explore the therapeutic potential of targeting TE activity.
  • To propose TE expression and activation as a new hallmark of cancer.

Main Methods:

  • Review of existing literature on TEs and cancer.
  • Analysis of epigenetic mechanisms regulating TE expression.
  • Investigation of TE-mediated insertional mutagenesis and inflammation.

Main Results:

  • TEs contribute to six established hallmarks of cancer.
  • Activated TEs drive transcriptional rewiring and genomic instability.
  • TEs trigger inflammatory responses that can be therapeutically exploited.

Conclusions:

  • Widespread TE expression and activation represent a significant factor in oncogenesis.
  • Targeting TE-induced inflammation offers a promising strategy for cancer immunotherapy.
  • The study proposes TE activity as a novel hallmark of cancer.