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Related Concept Videos

DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

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...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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...
The DNA Replication Fork01:02

The DNA Replication Fork

An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication forks, one in...
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
Homologous Recombination02:31

Homologous Recombination

The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...

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Related Experiment Video

Updated: May 26, 2026

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
06:25

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

Published on: February 10, 2023

Comprehensive Analysis Reveals Adaptive DNA Repair and Replication Stress Networks in Genomically Unstable Breast

Farah Ramadan, Sara Zahraeifard, Ujwal Subedi

    Biorxiv : the Preprint Server for Biology
    |May 25, 2026
    PubMed
    Summary

    Breast cancer tumors with genomic instability tolerate DNA damage through rewiring of DNA damage response (DDR) and replication stress tolerance (RST) pathways. These adaptive mechanisms promote tumor resilience and offer potential therapeutic targets.

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    Area of Science:

    • Oncology
    • Genetics
    • Molecular Biology

    Background:

    • Genomic instability is a key feature of breast cancer.
    • Mechanisms of DNA damage tolerance in tumors are not well understood.

    Purpose of the Study:

    • To analyze how DNA damage response (DDR) and replication stress tolerance (RST) networks are altered in genomically unstable breast tumors.
    • To identify potential therapeutic vulnerabilities.

    Main Methods:

    • Comprehensive analysis of multi-cohort breast cancer datasets.
    • Utilized fraction of genome altered (FGA) as a metric for chromosomal instability.
    • Mapped genetic interactions among drivers and DDR genes.

    Main Results:

    • BRCA-mutant tumors show high genomic instability with increased expression of multiple DNA repair pathways.
    • Heightened pathway activity correlates with increased genome alteration, suggesting damage tolerance.
    • RST programs contribute to tumor fitness under replication stress.
    • Adaptive states are common in aggressive subtypes and intensify with progression.

    Conclusions:

    • Compensatory genome-maintenance programs drive tumor resilience in breast cancer.
    • Pathway-specific vulnerabilities can be exploited for targeted therapies.
    • Understanding DDR and RST rewiring is crucial for developing novel treatment strategies.