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Mismatch Repair01:20

Mismatch Repair

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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DNA Distortion and Damage
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Genome instability and crosstalk with the immune response.

Roman M Chabanon1,2, François-Xavier Danlos3,4, Kaissa Ouali3,5

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Harnessing cancer

Keywords:
AneuploidyAnti-tumour immune responseCytoplasmic nucleic acidDNA damage responseGenomic instabilityReplication stressTumour immunogenicity

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Area of Science:

  • Cancer Biology and Immunology
  • Genomic Instability and DNA Damage Response
  • Immuno-oncology Therapeutics

Background:

  • Cancer is characterized by genome instability, inflammation, and immune escape.
  • A complex network links genome instability, DNA damage response (DDR), and tumor immunogenicity.
  • Immune checkpoint blockers (ICB) have shown clinical success, driving interest in immuno-oncology.

Purpose of the Study:

  • To review the interplay between genome instability and tumor immunogenicity.
  • To explore mechanisms and consequences of this crosstalk, including chromosomal instability.
  • To discuss DDR-based biomarkers for ICB response and emerging therapeutic combinations.

Main Methods:

  • Literature review of scientific and clinical evidence.
  • Analysis of feedforward and feedback mechanisms in the DDR-immunity interplay.
  • Examination of clinical developments in DDR-based immuno-oncology strategies.

Main Results:

  • Genomic instability can impair cancer cell fitness and enhance anti-tumor immunity.
  • The DDR plays a crucial role in modulating tumor immunogenicity.
  • Emerging DDR-based biomarkers predict response to ICB therapies.

Conclusions:

  • Exploiting genomic instability offers a promising strategy for cancer immunotherapy.
  • DDR-based immunomodulatory therapies hold potential across various cancer types.
  • Therapeutic combinations targeting the DDR-immunity axis are advancing in clinical development.