Evidence map›Paper›PMID 16863592›Full record

ArticleCell division2006

The cyclin D1b splice variant: an old oncogene learns new tricks.

Karen E Knudsen

Open access · goldAbstract read
In one paragraph

Article in Cell division, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. G870A Polymorphic Variants ofDiagnostics (Basel, Switzerland) · 2022
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The double dealing of cyclin D1.Cell cycle (Georgetown, Tex.) · 2020
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Cyclin D1 G870A polymorphism and glioma risk in a Chinese population.International journal of clinical and experimental medicine · 2015
    Article
  17. Review
  18. Aberrant expression of cyclin D1 in cancer.Signal transduction insights · 2015
    Article
  19. Review
  20. Review
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

1 author at 1 institution in 1 country.

Karen E KnudsenDepartment of Cell Biology, Center for Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0521, USA. karen.knudsen@uc.edu
University of Cincinnati · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The function of cyclin D1 as a positive regulator of the cell cycle and proto-oncogene has been well established. Cyclin D1 elicits its pro-proliferative function early in G1 phase, through its ability to activate cyclin dependent kinase (CDK) 4 or 6. Active CDK4/6-cyclin D1 complexes phosphorylate substrates that are critical for modulating G1 to S phase progression, and in this manner promote cellular proliferation. Emerging data from a number of model systems revealed that cyclin D1 also holds multiple, kinase-independent cellular functions. First, cyclin D1 assists in sequestering CDK inhibitors (e.g. p27kip1), thus bolstering late G1 CDK activity. Second, cyclin D1 is known to bind and modulate the action of several transcription factors that hold significance in human cancers. Thus, cyclin D1 impinges on several distinct pathways that govern cancer cell proliferation. Although intragenic somatic mutation of cyclin D1 in human disease is rare, cyclin D1 gene translocation, amplification and/or overexpression are frequent events in selected tumor types. Additionally, a polymorphism in the cyclin D1 locus that may affect splicing has been implicated in increased cancer risk or poor outcome. Recent functional analyses of an established cyclin D1 splice variant, cyclin D1b, revealed that the cyclin D1b isoform harbors unique activities in cancer cells. Here, we review the literature implicating cyclin D1b as a mediator of aberrant cellular proliferation in cancer. The differential roles of cyclin D1 and the cyclin D1b splice variant in prostate cancer will be also be addressed, wherein divergent functions have been linked to altered proliferative control.

Identifiers

PMID16863592
PMCPMC1559605
OpenAlexW2168734424

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.