Evidence map›Paper›PMID 23390492›Full record

ArticlePloS one2013

Constitutive CCND1/CDK2 activity substitutes for p53 loss, or MYC or oncogenic RAS expression in the transformation of human mammary epithelial cells.

Damian J Junk, Rocky Cipriano, Martha Stampfer, Mark W Jackson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Stabilization of cyclin D3 protein by CDKN1A (p21Cell communication and signaling : CCS · 2026
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  2. UHRF1 Controls the Timing of RAD51 Removal During DNA Damage Repair Through Suppressing RFWD3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

4 authors at 2 institutions in 1 country.

Damian J JunkDepartment of Pathology, Case Western Reserve University, Cleveland, Ohio, USA.
Rocky Cipriano
Martha Stampfer
Mark W Jackson
Case Western Reserve University · USLawrence Berkeley National Laboratory · US

Funding

RESEARCH ONCOLOGY TRAINING GRANTT32CA059366 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI JACKSON, MARK W. · 1993 to 2025
$5.5M
NCI NIH HHS T32 CA059366
6 · The paper itself

Abstract

Cancer develops following the accumulation of genetic and epigenetic alterations that inactivate tumor suppressor genes and activate proto-oncogenes. Dysregulated cyclin-dependent kinase (CDK) activity has oncogenic potential in breast cancer due to its ability to inactivate key tumor suppressor networks and drive aberrant proliferation. Accumulation or over-expression of cyclin D1 (CCND1) occurs in a majority of breast cancers and over-expression of CCND1 leads to accumulation of activated CCND1/CDK2 complexes in breast cancer cells. We describe here the role of constitutively active CCND1/CDK2 complexes in human mammary epithelial cell (HMEC) transformation. A genetically-defined, stepwise HMEC transformation model was generated by inhibiting p16 and p53 with shRNA, and expressing exogenous MYC and mutant RAS. By replacing components of this model, we demonstrate that constitutive CCND1/CDK2 activity effectively confers anchorage independent growth by inhibiting p53 or replacing MYC or oncogenic RAS expression. These findings are consistent with several clinical observations of luminal breast cancer sub-types that show elevated CCND1 typically occurs in specimens that retain wild-type p53, do not amplify MYC, and contain no RAS mutations. Taken together, these data suggest that targeted inhibition of constitutive CCND1/CDK2 activity may enhance the effectiveness of current treatments for luminal breast cancer.

Indexed as

Cell CycleCell LineCell Transformation, NeoplasticCyclin D1Cyclin-Dependent Kinase 2Epithelial CellsFemaleGene ExpressionHumansMammary Glands, HumanProto-Oncogene Proteins c-mycras ProteinsRNA, Small InterferingSignal TransductionTumor Suppressor Protein p53CCND1 protein, humanCDK2 protein, humanCyclin D1Cyclin-Dependent Kinase 2MYC protein, humanProto-Oncogene Proteins c-mycras ProteinsRNA, Small InterferingTumor Suppressor Protein p53

Identifiers

PMID23390492
PMCPMC3563539
OpenAlexW2046429728

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.