Evidence map›Paper›PMID 35701073›Full record

ArticleGenome research2022

Extensive protein dosage compensation in aneuploid human cancers.

Klaske M Schukken, Jason M Sheltzer

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
–field-weighted citation impact
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

63 citing papers in PubMed, 84 citations in OpenAlex.

  1. Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026
    Review
  2. Article
  3. Pretreatment Chromosomal Instability Correlates With Radiation Sensitivity in Squamous Cell Cancers.International journal of radiation oncology, biology, physics · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Investigating the Consequences of Aneuploidy in Cancer and Normal Tissue.Advances in experimental medicine and biology · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. The Hallmarks of Aneuploidy in Cancer and Congenital Syndromes.Annual review of genomics and human genetics · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Generation of Monosomy 21q Human iPS Cells by CRISPR/Cas9-Mediated Interstitial Megabase Deletion.Genes to cells : devoted to molecular & cellular mechanisms · 2025
    Article

3 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

2 authors at 1 institution in 1 country.

Klaske M SchukkenYale School of Medicine, New Haven, Connecticut 06511, USA.
Jason M SheltzerYale School of Medicine, New Haven, Connecticut 06511, USA.
Yale University · US

Funding

Identification and characterization of genomic features affecting survival duration in cancerDP5OD021385 · OD · COLD SPRING HARBOR LABORATORY · PI SHELTZER, JASON · 2015 to 2020
$2.8M
Discovering the mechanisms-of-action of mistargeted anti-cancer agentsR01CA237652 · NCI · YALE UNIVERSITY · PI SHELTZER, JASON · 2020 to 2024
$1.6M
NCI NIH HHS R01 CA237652NIH HHS DP5 OD021385
6 · The paper itself

Abstract

Aneuploidy is a hallmark of human cancers, but the effects of aneuploidy on protein expression remain poorly understood. To uncover how chromosome copy number changes influence the cancer proteome, we conducted an analysis of hundreds of human cancer cell lines and tumors with matched copy number, RNA expression, and protein expression data. We found that a majority of proteins show dosage compensation and fail to change by the degree expected based on chromosome copy number alone. We uncovered a variety of gene groups that were recurrently buffered upon both chromosome gain and loss, including protein complex subunits and cell cycle genes. Several genetic and biophysical factors were predictive of protein buffering, highlighting complex post-translational regulatory mechanisms that maintain appropriate gene product dosage. Finally, we established that chromosomal aneuploidy has a moderate effect on the expression of oncogenes and tumor suppressors, showing that these key cancer drivers can be subject to dosage compensation as well. In total, our comprehensive analysis of aneuploidy and dosage compensation across cancers will help identify the key driver genes encoded on altered chromosomes and will shed light on the overall consequences of aneuploidy during tumor development.

Indexed as

AneuploidyNeoplasmsChromosomesDosage Compensation, GeneticGene DosageHumans

Identifiers

PMID35701073
PMCPMC9341510
OpenAlexW4282826843

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.