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Related Concept Videos

Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

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...
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

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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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...
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¹³C NMR: Distortionless Enhancement by Polarization Transfer (DEPT)

When proton-coupled carbon-13 spectra are simplified by a broadband proton decoupling technique, structural information about the coupled protons is lost. Distortionless enhancement by polarization transfer (DEPT) is a technique that provides information on the number of hydrogens attached to each carbon in a molecule. While the DEPT experiment utilizes complex pulse sequences, the pulse delay and flip angle are specifically manipulated. The resulting signals have different phases depending on...
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Tracheostomy decannulation is a significant milestone in the liberation of mechanically ventilated patients. Despite its importance, there is no universally accepted protocol for this procedure. This demands an evidence-based, individualized approach.
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Decatenation: fixing your knots.

Duncan J Clarke1

  • 1University of Minnesota.

Blood
|August 29, 2009
PubMed
Summary
This summary is machine-generated.

Acute leukemia cells develop drug resistance by activating a topoisomerase II stimulator. This mechanism allows cancer cells to proliferate even when this essential enzyme is inhibited by drugs.

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Last Updated: Jun 20, 2026

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Area of Science:

  • Oncology
  • Molecular Biology
  • Hematology

Background:

  • Understanding drug resistance in cancer is crucial for improving treatment efficacy.
  • Acute leukemia poses significant therapeutic challenges due to acquired resistance mechanisms.

Discussion:

  • Wray and colleagues elucidate a novel resistance pathway in acute leukemia.
  • This pathway involves the activation of a stimulator of topoisomerase II.
  • This activation enables leukemia cell proliferation despite topoisomerase II inhibition.

Key Insights:

  • Identified a specific mechanism of drug resistance in acute leukemia.
  • Highlighted the role of topoisomerase II activity regulation in resistance.
  • Demonstrated how leukemia cells bypass drug-induced enzyme inhibition.

Outlook:

  • Findings offer potential new targets for overcoming drug resistance in leukemia.
  • Further research could lead to the development of novel therapeutic strategies.
  • This study advances the understanding of molecular mechanisms underlying cancer therapy failure.