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Related Concept Videos

Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

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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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Cancers Originate from Somatic Mutations in a Single Cell02:21

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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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Separation of Sister Chromatids02:17

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At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
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Related Experiment Video

Updated: Jan 8, 2026

Capturing Common Fragile Site Breaks by Native γH2A.X ChIP
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Capturing Common Fragile Site Breaks by Native γH2A.X ChIP

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Chromosome shattering in cancer.

Stanley Clarke1, Marcin Imieliński1

  • 1Perlmutter Cancer Center, NYU Langone Health, New York, NY, USA.

Science (New York, N.Y.)
|December 11, 2025
PubMed
Summary

A protein that cuts double-stranded DNA was found to cause chromosome scrambling in human cancer cells. This DNA-cutting protein activity is linked to genomic instability in cancer.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • Genomic instability is a hallmark of cancer.
  • Chromosome abnormalities contribute to cancer development and progression.
  • Understanding the mechanisms driving genomic instability is crucial for cancer therapy.

Purpose of the Study:

  • To investigate the role of DNA-cutting proteins in chromosome scrambling.
  • To identify specific proteins involved in generating structural variations in cancer genomes.
  • To explore potential therapeutic targets related to DNA repair and genome maintenance.

Main Methods:

  • Analysis of human cancer cell lines.
  • Protein activity assays.
  • Chromosome spread analysis.

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  • Genomic sequencing techniques.

    • Main Results:

    • A specific protein capable of cutting double-stranded DNA was identified.
    • This protein's activity was directly correlated with increased chromosome scrambling.
    • The mechanism involves aberrant DNA cleavage leading to genomic rearrangements.

    Conclusions:

    • A DNA-cutting protein is a key driver of chromosome scrambling in human cancers.
    • Targeting this protein's activity may offer a novel strategy for cancer treatment.
    • Further research is needed to elucidate the full implications of this finding for cancer biology.