Evidence map›Paper›PMID 23124507›Full record

ArticleInternational journal of cancer2013

Cancer cells preferentially lose small chromosomes.

Pascal H G Duijf, Nikolaus Schultz, Robert Benezra

Open access · greenAbstract read
In one paragraph

Article in International journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 178 citations in OpenAlex.

  1. Pooled it
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  5. Review
  6. Article
  7. Functional role of small extrachromosomal circular DNA in colorectal cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  8. Review
  9. Review
  10. Cancer in pregnancy: FIGO Best practice advice and narrative review.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2025
    Review
  11. Total whole-arm chromosome losses predict malignancy in human cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
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42 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

3 authors at 3 institutions in 2 countries.

Pascal H G DuijfDepartment of Cancer Biology and Genetics, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. duijf@uq.edu.au
Nikolaus Schultz
Robert Benezra
In-Q-Tel · USMemorial Sloan Kettering Cancer Center · USPrincess Alexandra Hospital · AU

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
MSKCC Center for Translational Cancer Genomic AnalysisU24CA143840 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI LADANYI, MARC, SANDER, CHRIS · 2009 to 2016
$11.5M
NCI NIH HHS P30 CA008748NCI NIH HHS U24 CA143840NCI NIH HHS U24CA143840
6 · The paper itself

Abstract

Genetic and genomic aberrations are the primary cause of cancer. Chromosome missegregation leads to aneuploidy and provides cancer cells with a mechanism to lose tumor suppressor loci and gain extra copies of oncogenes. Using cytogenetic and array-based comparative genomic hybridization data, we analyzed numerical chromosome aneuploidy in 43,205 human tumors and found that 68% of solid tumors are aneuploid. In solid tumors, almost all chromosomes are more frequently lost than gained with chromosomes 7, 12 and 20 being the only exceptions with more frequent gains. Strikingly, small chromosomes are lost more readily than large ones, but no such inverse size correlation is observed with chromosome gains. Because of increasing levels of proteotoxic stress, chromosome gains have been shown to slow cell proliferation in a manner proportional to the number of extra gene copies gained. However, we find that the extra chromosome in trisomic tumors does not preferentially have a low gene copy number, suggesting that a proteotoxicity-mediated proliferation barrier is not sustained during tumor progression. Paradoxically, despite a bias toward chromosome loss, gains of chromosomes are a poor prognostic marker in ovarian adenocarcinomas. In addition, we find that solid and non-solid cancers have markedly distinct whole-chromosome aneuploidy signatures, which may underlie their fundamentally different etiologies. Finally, preferential chromosome loss is observed in both early and late stages of astrocytoma. Our results open up new avenues of enquiry into the role and nature of whole-chromosome aneuploidy in human tumors and will redirect modeling and genetic targeting efforts in patients.

Indexed as

AneuploidyChromosome AberrationsAstrocytomaCentral Nervous System NeoplasmsComparative Genomic HybridizationCystadenocarcinoma, SerousFemaleGenomic InstabilityHumansKaryotypeMaleNeoplasmsNeoplasm StagingOvarian NeoplasmsPrognosis

Identifiers

PMID23124507
PMCPMC3587043
OpenAlexW1971165751

What OpenQuestion holds

Textmetadata
LicenceTDM
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.