Evidence map›Paper›PMID 11830638›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

Centrosome amplification drives chromosomal instability in breast tumor development.

Wilma L Lingle, Susan L Barrett, Vivian C Negron, Antonino B D'Assoro, Kelly Boeneman, Wanguo Liu, Clark M Whitehead, Carol Reynolds, Jeffrey L Salisbury

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 253 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
253citing papers in PubMed, 1 pooled it
12.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

253 citing papers in PubMed, 1 synthesis or guideline pooled it, 566 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Oxidative stress and serum deprivation influence the evolution of newly formed tetraploid cells during tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  11. Investigating the Consequences of Aneuploidy in Cancer and Normal Tissue.Advances in experimental medicine and biology · 2026
    Review
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193 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Wilma L LingleDivision of Experimental Pathology, Tumor Biology Program, Mayo Clinic, Rochester, MN 55905, USA. lingle@mayo.edu
Susan L Barrett
Vivian C Negron
Antonino B D'Assoro
Kelly Boeneman
Wanguo Liu
Clark M Whitehead
Carol Reynolds
Jeffrey L Salisbury
Mayo Clinic · US

Funding

CENTROSOME HYPERTROPHY IN HUMAN BREAST TUMORSR01CA072836 · NCI · MAYO CLINIC ROCHESTER · PI SALISBURY, JEFFREY L · 1998 to 2006
$1.9M
NCI NIH HHS CA72836NCI NIH HHS R01 CA072836
6 · The paper itself

Abstract

Earlier studies of invasive breast tumors have shown that 60-80% are aneuploid and approximately 80% exhibit amplified centrosomes. In this study, we investigated the relationship of centrosome amplification with aneuploidy, chromosomal instability, p53 mutation, and loss of differentiation in human breast tumors. Twenty invasive breast tumors and seven normal breast tissues were analyzed by fluorescence in situ hybridization with centromeric probes to chromosomes 3, 7, and 17. We analyzed these tumors for both aneuploidy and unstable karyotypes as determined by chromosomal instability. The results were then tested for correlation with three measures of centrosome amplification: centrosome size, centrosome number, and centrosome microtubule nucleation capacity. Centrosome size and centrosome number both showed a positive, significant, linear correlation with aneuploidy and chromosomal instability. Microtubule nucleation capacity showed no such correlation, but did correlate significantly with loss of tissue differentiation. Centrosome amplification was detected in in situ ductal carcinomas, suggesting that centrosome amplification is an early event in these lesions. Centrosome amplification and chromosomal instability occurred independently of p53 mutation, whereas p53 mutation was associated with a significant increase in centrosome microtubule nucleation capacity. Together, these results demonstrate that independent aspects of centrosome amplification correlate with chromosomal instability and loss of tissue differentiation and may be involved in tumor development and progression. These results further suggest that aspects of centrosome amplification may have clinical diagnostic and/or prognostic value and that the centrosome may be a potential target for cancer therapy.

Indexed as

AneuploidyBreast NeoplasmsCell NucleusCentrosomeChromosome AberrationsChromosomesDNA Mutational AnalysisGenes, p53HumansIn Situ Hybridization, FluorescenceKaryotypingMicroscopy, FluorescenceMicrotubulesMutationPloidiesTumor Cells, Cultured

Identifiers

PMID11830638
PMCPMC122305
OpenAlexW1967149801

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.