Evidence map›Paper›PMID 23644662›Full record

ReviewOncogene2014

Signaling through cyclin D-dependent kinases.

Y J Choi, L Anders

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed, 2 pooled it
10.8field-weighted citation impact, top 1% 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

143 citing papers in PubMed, 2 syntheses or guidelines pooled it, 280 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Stabilization of cyclin D3 protein by CDKN1A (p21Cell communication and signaling : CCS · 2026
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83 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 2 institutions in 1 country.

Y J Choi1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, USA [2] Department of Genetics, Harvard Medical School, Boston, MA, USA.
L AndersDepartment of Biology, Massachusetts Institute of Technology, Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA, USA.
Dana-Farber Cancer Institute · USWhitehead Institute for Biomedical Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Research over the past quarter century has identified cyclin D-dependent kinases, CDK4 and CDK6, as the major oncogenic drivers among members of the CDK superfamily. CDK4/6 are rendered hyperactive in the majority of human cancers through a multitude of genomic alterations. Sustained activation of these protein kinases provides cancer cells with the power to enter the cell cycle continuously by triggering G1-S-phase transitions and dramatically shortening the duration of the G1 phase. It has also become clear, however, that CDK4/6 effectively counter cancer cell-intrinsic tumor suppression mechanisms, senescence and apoptosis, which must be overcome during cell transformation and kept at bay throughout all stages of tumorigenesis. As a central 'node' in cellular signaling networks, cyclin D-dependent kinases sense a plethora of mitogenic signals to orchestrate specific transcriptional programs. As the complexity of the cellular signaling network regulated by these oncogenic kinases unfolds, much remains to be learned about its architecture, its dynamics and the consequences of its perturbation.

Indexed as

AnimalsCell CycleCell Transformation, NeoplasticCyclin DCyclin-Dependent KinasesHumansProtein UnfoldingSignal TransductionCyclin DCyclin-Dependent Kinases

Identifiers

PMID23644662
OpenAlexW1998040747

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.