Evidence map›Paper›PMID 21472139›Full record

ArticleNeoplasia (New York, N.Y.)2011

Characterization of aneuploid populations with trisomy 7 and 20 derived from diploid human colonic epithelial cells.

Peter Ly, Ugur Eskiocak, Sang B Kim, Andres I Roig, Suzie K Hight, Dypti R Lulla, Ying S Zou, Kimberly Batten, Woodring E Wright, Jerry W Shay

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Investigating the Consequences of Aneuploidy in Cancer and Normal Tissue.Advances in experimental medicine and biology · 2026
    Review
  3. The Hallmarks of Aneuploidy in Cancer and Congenital Syndromes.Annual review of genomics and human genetics · 2025
    Review
  4. KaryoTap Enables Aneuploidy Detection in Thousands of Single Human Cells.bioRxiv : the preprint server for biology · 2024
    Article
  5. Review
  6. Article
  7. The Antagonistic and Synergistic Role of FePharmaceuticals (Basel, Switzerland) · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Double-checking chromosome segregation.The Journal of cell biology · 2023
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Aneuploidy: Cancer strength or vulnerability?International journal of cancer · 2019
    Review
  18. Review
  19. Article
  20. Article
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

10 authors at 2 institutions in 1 country.

Peter LyDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Ugur Eskiocak
Sang B Kim
Andres I Roig
Suzie K Hight
Dypti R Lulla
Ying S Zou
Kimberly Batten
Woodring E Wright
Jerry W Shay
The University of Texas Southwestern Medical Center · USBoston University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromosomal instability leading to aneuploidy occurs in most sporadic colorectal cancers (CRCs) and is believed to be an early driving force in disease progression. Despite this observation, the cellular advantages conferred by these cytogenetic alterations are poorly understood. Here, we provide evidence that serum-free passage of originally diploid, immortalized human colonic epithelial cells (HCECs) gave rise to the acquisition of trisomy 7 (+7), an aneuploidy detected in more than 40% of colorectal adenomas. These cells remain diploid under long-term growth in 2% serum conditions. Analysis by GTG banding and fluorescent in situ hybridization detected no rare preexisting +7 cell in the original population, suggesting a conversion of diploid cells to an aneuploid state. The acquisition of +7 also precedes loss or truncation of the adenomatosis polyposis coli gene as both diploid and +7 cells express full-length, functional protein. Coculturing of fluorescent-labeled cells demonstrate that +7 HCECs have a growth advantage over diploid cells in serum-free conditions. Defects in cell migration and aberrant regulation of the epidermal growth factor receptor, located on chromosome 7p, are also detected in +7 HCECs. Interestingly, knockdown of TP53 and expression of K-Ras(V12) in +7 HCECs resulted in the emergence of trisomy 20, another nonrandom aneuploidy observed in ∼85% of CRC. In summary, we describe isogenic colonic epithelial cells that represent cytogenetic changes occurring frequently in sporadic CRC. The emergence and characterization of trisomy 7 and 20 demonstrate that these HCECs may serve as unique human cell-based models to examine the effects of chromosomal instability in CRC progression.

Indexed as

Chromosomes, Human, Pair 7DiploidyAneuploidyCarcinomaCell Culture TechniquesCells, CulturedCell SeparationChromosomal InstabilityChromosomes, Human, Pair 20ColonColorectal NeoplasmsCulture Media, Serum-FreeCytogenetic AnalysisEpithelial CellsGene DeletionGenes, APCCulture Media, Serum-Free

Identifiers

PMID21472139
PMCPMC3071083
OpenAlexW1577353247

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.