Evidence map›Paper›PMID 18632615›Full record

ArticleCancer research2008

Cyclin D1b is aberrantly regulated in response to therapeutic challenge and promotes resistance to estrogen antagonists.

Ying Wang, Jeffry L Dean, Ewan K A Millar, Thai Hong Tran, Catriona M McNeil, Craig J Burd, Susan M Henshall, Fransiscus E Utama, Agnieszka Witkiewicz, Hallgeir Rui and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.0field-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

48 citing papers in PubMed, 65 citations in OpenAlex.

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  8. Article
  9. The role of alternative splicing in human cancer progression.American journal of cancer research · 2021
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  12. Review
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  16. Alternative Splicing as a Target for Cancer Treatment.International journal of molecular sciences · 2018
    Review
  17. Article
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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

13 authors at 7 institutions in 3 countries.

Ying WangDepartment of Cell and Cancer Biology, University of Cincinnati, Cincinnati, Ohio, USA.
Jeffry L Dean
Ewan K A Millar
Thai Hong Tran
Catriona M McNeil
Craig J Burd
Susan M Henshall
Fransiscus E Utama
Agnieszka Witkiewicz
Hallgeir Rui
Robert L Sutherland
Karen E Knudsen
Erik S Knudsen
Sidney Kimmel Cancer Center · USSt Vincent's Hospital Sydney · AUUniversity of Cincinnati · USGarvan Institute of Medical Research · AUNational Institute of Environmental Health Sciences · USSt. George Hospital · INThomas Jefferson University · US

Funding

X-Ray Crystallography and Macromolecular CharacterizationP30CA056036 · NCI · THOMAS JEFFERSON UNIVERSITY · PI DANIEL P SILVER · 1995 to 2026
$94.8M
Cyclin D1: repercussions of AR control and alternative splicing in prostate canceR01CA099996 · NCI · UNIVERSITY OF CINCINNATI · PI KNUDSEN, KAREN E · 2003 to 2013
$2.6M
BRG1/BRM: role in RB tumor suppressor signalingR01CA104213 · NCI · UNIVERSITY OF CINCINNATI · PI KNUDSEN, ERIK · 2004 to 2008
$1.2M
Stat5 as a gatekeeper in human breast cancer metastasisR01CA101841 · NCI · THOMAS JEFFERSON UNIVERSITY · PI RUI, HALLGEIR · 2004 to 2008
$1.2M
NCI NIH HHS CA099996NCI NIH HHS P30 CA056036NCI NIH HHS R01 CA099996NCI NIH HHS R01 CA101841NCI NIH HHS R01-CA101841NCI NIH HHS R01 CA104213NCI NIH HHS R01-CA104213
6 · The paper itself

Abstract

Cyclin D1 is a key mediator of cell cycle progression that is aberrantly regulated in multiple cancers, especially in breast cancers. A number of studies have indicated that a polymorphism in a splice donor site in the cyclin D1 gene is associated with alternative splicing and the production of the alternative cyclin D1b transcript. Furthermore, this polymorphism is selectively associated with disease outcomes. However, relatively little is known regarding the protein product of the alternatively spliced message, cyclin D1b. Using antibodies specific for cyclin D1b, it was found that this protein is readily detectable in a number of cancer cell lines and primary breast cancers. Whereas cyclin D1b interacts with cyclin-dependent kinase 4 (CDK4), it is relatively inefficient at mediating RB phosphorylation and cell cycle progression in model systems due to the lack of exon 5 of cyclin D1-encoded sequences. However, cyclin D1b protein levels are not significantly attenuated by DNA damage or antiestrogen treatment, indicating that the protein may have significant effect on the response to such therapeutic modalities. Whereas enforced expression of cyclin D1b was not sufficient to abrogate DNA damage checkpoint responses, it did efficiently overcome cell cycle arrest mediated by antiestrogen therapeutics. This action of cyclin D1b was not associated with effects on estrogen receptor activity, but was rather dependent on functional association with CDK4. Combined, these studies indicate that the cyclin D1b protein is aberrantly regulated and could contribute to therapeutic failure in the context of ER-positive breast cancer.

Indexed as

Drug Resistance, NeoplasmGene Expression Regulation, NeoplasticAntineoplastic AgentsBreast NeoplasmsCell Line, TumorCisplatinCyclin DCyclin-Dependent Kinase 4CyclinsEstrogen AntagonistsGene Expression ProfilingHeLa CellsHumansPhosphorylationPolymorphism, GeneticReceptors, EstrogenAntineoplastic AgentsCDK4 protein, humanCisplatinCyclin DCyclin-Dependent Kinase 4CyclinsEstrogen AntagonistsReceptors, Estrogen

Identifiers

PMID18632615
PMCPMC8220573
OpenAlexW2108143474

What OpenQuestion holds

Textmetadata
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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.