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One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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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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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
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When DNA Repair Backfires - Trabectedin Induces DNA Breaks in Active Genes.

Vakil Takhaveev1, Kook Son2, Visesato Mor2

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Summary

Trabectedin is a potent anticancer drug that targets cancer cells with active DNA repair, specifically transcription-coupled nucleotide excision repair (TC-NER). This study visualizes TC-NER genome-wide, revealing how trabectedin induces DNA breaks in active genes.

Keywords:
DNA repairGenomicsPrecision oncologyTrabectedin

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Pharmacology

Background:

  • Anticancer drug efficacy is often limited by tumor DNA repair mechanisms.
  • Trabectedin, a marine natural product, exhibits enhanced lethality in cancer cells with active DNA repair, particularly transcription-coupled nucleotide excision repair (TC-NER).

Purpose of the Study:

  • To elucidate the mechanism by which trabectedin's toxicity depends on TC-NER.
  • To enable genome-wide visualization of TC-NER by mapping trabectedin-induced DNA damage.

Main Methods:

  • Mapping of 3'-hydroxyl groups of single-strand breaks (SSBs) resulting from the initial NER incision at trabectedin-DNA adducts.
  • Genome-wide visualization of TC-NER activity.

Main Results:

  • Incomplete TC-NER of trabectedin-DNA adducts leads to persistent SSBs.
  • Trabectedin-DNA adducts impede the second incision step in NER.
  • Trabectedin-induced SSBs are primarily located on transcribed strands of active genes, near transcription start sites.

Conclusions:

  • This study provides a method for genome-wide visualization of TC-NER.
  • Findings offer insights into trabectedin's mechanism of action and its potential in precision oncology.
  • The research contributes to understanding TC-NER and transcription regulation in cancer therapy.