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Related Concept Videos

Nucleotide Excision Repair

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 Repair

Nucleotide Excision Repair

Nucleotide Excision Repair

Nucleotide Excision Repair

Overview of DNA Repair

Overview of DNA Repair

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.
Chemically...

Overview of DNA Repair

Overview of DNA Repair

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.
Chemically...

Mutations

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...

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Related Experiment Video

Updated: Jun 24, 2026

Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes

Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes

Published on: May 23, 2025

Enhancing radiosensitivity: targeting the DNA repair pathways.

Timothy J Jorgensen¹

¹Department of Radiation Medicine, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC 20057, USA. tjorge01@georgetown.edu

Cancer Biology & Therapy

|March 17, 2009

Summary

Targeting cancer cell DNA repair pathways can overcome radioresistance and improve radiotherapy. Exploiting molecular differences between tumor and normal cells offers new strategies for radiosensitization.

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Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes

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Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells

Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells

Published on: June 9, 2020

Area of Science:

Oncology
Molecular Biology
Radiotherapy

Background:

Radiotherapy is effective for local tumor control but limited by intrinsic radioresistance.
DNA repair pathways protect cells from radiation-induced DNA damage, presenting a therapeutic target.
Exploiting differential DNA repair between tumor and normal cells is crucial for radiosensitization.

Purpose of the Study:

To review novel strategies for targeting DNA repair to enhance radiotherapy efficacy.
To explore molecular differentials for tumor-specific targeting of DNA repair.
To discuss challenges and future directions in radiosensitization.

Main Methods:

Review of recent advances in DNA repair mechanisms and tumor biology.
Discussion of synthetic lethal, replicative stress, cell cycle, and hypoxia-based approaches.
Case study on PARP1 inhibitors in BRCA1/2 mutated breast cancer.

Main Results:

Advances in understanding DNA repair and tumor biology reveal molecular differentials for targeted therapy.
New strategies like synthetic lethality and targeting replicative stress show promise for radiosensitization.
PARP1 inhibitors demonstrate efficacy in specific genetic contexts (e.g., BRCA mutations).

Conclusions:

Targeting DNA repair pathways offers a promising avenue to overcome radioresistance in cancer.
Identifying tumor-specific vulnerabilities in DNA repair is key to developing effective radiosensitizing strategies.
Further research into novel approaches and overcoming challenges is essential for clinical translation.