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Related Concept Videos

Homologous Recombination02:31

Homologous Recombination

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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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Nucleotide Excision Repair01:38

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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...
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Long-patch Base Excision Repair01:02

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Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
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Overview of DNA Repair02:25

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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Mismatch Repair01:36

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Overview
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Fixing Double-strand Breaks02:04

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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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Related Experiment Video

Updated: Aug 9, 2025

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging
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Patient Assessment and Therapy Planning Based on Homologous Recombination Repair Deficiency.

Wenbin Li1, Lin Gao2, Xin Yi3

  • 1Department of Pathology, National Cancer Center / National Clinical Research Center for Cancer / Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.

Genomics, Proteomics & Bioinformatics
|February 15, 2023
PubMed
Summary

Homologous recombination repair deficiency (HRD) is a biomarker for cancer therapies, but its assessment is complex. This review clarifies HRD biology and clinical evidence to standardize its use in cancer care.

Keywords:
BiomarkerDNA damage responseHarmonizationHomologous recombination repair deficiencyPoly(ADP-ribose) polymerase inhibitor

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Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Homologous recombination repair deficiency (HRD) arises from defects in DNA damage response genes.
  • HRD is present in certain cancer types and is relevant for cancer prevention and treatment strategies.
  • HRD is recognized as a biomarker for predicting patient response to PARP inhibitors and platinum-based chemotherapy.

Purpose of the Study:

  • To review the biological basis and clinical evidence supporting HRD as a cancer biomarker.
  • To address the complexities and controversies surrounding HRD assessment and its clinical application.
  • To propose a framework for standardizing HRD evaluation methods.

Main Methods:

  • Literature review of biological mechanisms of HRD.
  • Analysis of clinical studies investigating HRD biomarkers.
  • Evaluation of different HRD assessment methodologies (gene-level, genomic scars, mutational signatures).

Main Results:

  • HRD is a complex biomarker with significant implications for targeted cancer therapies.
  • Current HRD assessment methods show inconsistencies, leading to controversial interpretations.
  • Standardization is needed to accurately evaluate HRD's contribution and clinical utility.

Conclusions:

  • HRD is a clinically relevant biomarker for specific cancer therapies.
  • Harmonization of HRD assessment assays is crucial for reliable clinical application.
  • Further research and standardization efforts will enhance the utility of HRD in precision oncology.