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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...
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
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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.
There are several types of targeted therapies against specific...

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Related Experiment Video

Updated: Jun 6, 2026

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging
06:44

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging

Published on: April 28, 2021

Targeting DNA repair pathways in AML.

Alan D D'Andrea1

  • 1Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA. alan_dandrea@dfci.harvard.edu

Best Practice & Research. Clinical Haematology
|December 7, 2010
PubMed
Summary
This summary is machine-generated.

Cancer DNA repair deficiencies can be targeted with new inhibitors to resensitize cancers to therapy. Biomarkers in the Fanconi anemia pathway may predict which acute myeloid leukemia patients benefit from these drugs.

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Related Experiment Videos

Last Updated: Jun 6, 2026

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging
06:44

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Published on: April 28, 2021

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
10:59

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Published on: August 21, 2021

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay
13:10

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay

Published on: June 9, 2017

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Cancer cells frequently exhibit DNA repair pathway deficiencies, influencing treatment sensitivity and resistance.
  • Restoration of DNA repair pathways can lead to therapeutic resistance.
  • DNA repair pathway inhibitors offer a strategy to resensitize cancers to conventional treatments like chemotherapy and radiation.

Purpose of the Study:

  • To explore the potential of DNA repair pathway inhibitors in cancer therapy.
  • To identify specific cancer types and patient subsets that may benefit from these inhibitors.
  • To investigate the role of biomarkers in predicting sensitivity to DNA repair inhibitors.

Main Methods:

  • Review of major DNA repair pathways and their druggable targets.
  • Analysis of the application of DNA repair inhibitors, specifically poly-ADP-ribose polymerase (PARP) inhibitors.
  • Examination of potential biomarkers for identifying patient sensitivity.

Main Results:

  • There are six major DNA repair pathways, each with identified targets and biomarkers.
  • Poly-ADP-ribose polymerase (PARP) inhibitors show potential utility in a subset of acute myeloid leukemia (AML) patients.
  • Patients with complex karyotypes or secondary AML may represent a sensitive group.
  • Fanconi anemia repair pathway biomarkers could predict sensitivity to novel drugs.

Conclusions:

  • Targeting DNA repair pathways with inhibitors can overcome treatment resistance.
  • Poly-ADP-ribose polymerase (PARP) inhibitors represent a promising therapeutic strategy for specific acute myeloid leukemia (AML) patient populations.
  • Fanconi anemia pathway biomarkers are crucial for identifying patients likely to respond to DNA repair inhibitor therapy.