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Related Concept Videos

Base Excision Repair01:54

Base Excision Repair

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.
The first step of...
Base Excision Repair01:54

Base Excision Repair

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.
The first step of...
Long-patch Base Excision Repair01:02

Long-patch Base Excision Repair

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:
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
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

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Related Experiment Video

Updated: Jul 5, 2026

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
09:19

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo

Published on: February 6, 2015

Targeting base excision repair for chemosensitization.

Sanjay Adhikari1, Sujata Choudhury, Partha S Mitra

  • 1Lombardi Comprehensive Cancer Center, 3800 Reservoir Road NW, Georgetown University Medical Center, Washington, DC 20057, USA.

Anti-Cancer Agents in Medicinal Chemistry
|May 14, 2008
PubMed
Summary
This summary is machine-generated.

Targeting DNA repair pathways, specifically base excision repair (BER), can enhance cancer chemotherapy. Inhibiting BER proteins like N-Methylpurine DNA glycosylase (MPG) or AP-endonuclease (APE) increases cancer cell sensitivity to chemotherapy drugs.

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Quantitative, Real-time Analysis of Base Excision Repair Activity in Cell Lysates Utilizing Lesion-specific Molecular Beacons
15:01

Quantitative, Real-time Analysis of Base Excision Repair Activity in Cell Lysates Utilizing Lesion-specific Molecular Beacons

Published on: August 6, 2012

Related Experiment Videos

Last Updated: Jul 5, 2026

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
09:19

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo

Published on: February 6, 2015

Quantitative, Real-time Analysis of Base Excision Repair Activity in Cell Lysates Utilizing Lesion-specific Molecular Beacons
15:01

Quantitative, Real-time Analysis of Base Excision Repair Activity in Cell Lysates Utilizing Lesion-specific Molecular Beacons

Published on: August 6, 2012

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Base excision repair (BER) is a critical endogenous pathway for repairing DNA damage.
  • Chemotherapy and radiation therapy induce DNA damage but can lead to therapeutic resistance via DNA repair.
  • BER proteins can repair chemotherapy-induced DNA damage, contributing to treatment resistance and adverse side effects.

Purpose of the Study:

  • To investigate the potential of inhibiting BER proteins to enhance chemosensitivity in cancer treatment.
  • To explore pharmacological inhibition of DNA repair pathways as a strategy to overcome therapeutic resistance.

Main Methods:

  • Preclinical studies involving inhibition of specific BER proteins, including N-Methylpurine DNA glycosylase (MPG) and AP-endonuclease (APE).
  • Utilizing genetic modifications like MPG knockout (MPG(-/-)) and MPG knockdown via siRNA.
  • Employing small molecule inhibitors against APE.

Main Results:

  • Elimination or knockdown of MPG rendered cancer cells hypersensitive to alkylating chemotherapeutics.
  • Inhibition of APE using small molecule inhibitors sensitized cancer cells to alkylating chemotherapeutics.
  • These findings suggest BER proteins are key mediators of therapeutic resistance.

Conclusions:

  • Pharmacological inhibition of BER proteins, such as MPG and APE, represents a promising strategy to enhance the efficacy of current chemotherapy regimens.
  • Targeting BER proteins can minimize therapeutic resistance and reduce the likelihood of adverse side effects associated with cancer treatments.
  • MPG and other BER proteins are potential therapeutic targets for chemosensitization in cancer therapy.