Evidence map›Paper›PMID 21515363›Full record

ReviewCellular signalling2011

Cdc42 in oncogenic transformation, invasion, and tumorigenesis.

Kristy Stengel, Yi Zheng

Abstract readReview
In one paragraph

Review in Cellular signalling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 2% 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

136 citing papers in PubMed, 1 synthesis or guideline pooled it, 230 citations in OpenAlex.

  1. Pooled it
  2. A Novel Pharmacologic Activity of Ketorolac for Therapeutic Benefit in Ovarian Cancer Patients.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015
    Trial
  3. Article
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  5. Article
  6. Article
  7. Subtype-Specific mInternational journal of molecular sciences · 2026
    Article
  8. Review
  9. Materials today. Bio · 2025
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Himalayan flora: targeting various molecular pathways in lung cancer.Medical oncology (Northwood, London, England) · 2023
    Review

76 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 1 institution in 1 country.

Kristy StengelDivision of Experimental Hematology and Cancer Biology, Children's Research Foundation, 3333 Burnet Avenue, Cincinnati, OH 45229, USA.
Yi Zheng
University of Cincinnati · US

Funding

Cincinnati Center for Excellence in Molecular HematologyP30DK090971 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2010 to 2015
$4.0M
Targeting Cdc42 in leukemia stem cellsR01CA150547 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI MULLOY, JAMES C, ZHENG, YI · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA150547NIDDK NIH HHS P30 DK090971
6 · The paper itself

Abstract

The Rho family of GTPases represents a class of Ras-related signaling molecules often deregulated in cancer. Rho GTPases switch from a GDP-bound, inactive state to a GTP-bound, active state in response to extracellular stimuli such as mitogens and extracellular matrix. In addition, Rho GTPase signaling can be altered in response to cell intrinsic factors such as changes in oncogenic or tumor suppressor signaling. In their active form, these proteins bind to a number of effector molecules, activating signaling cascades which regulate a variety of cellular processes including cytoskeletal reorganization, cell cycle progression, cell polarity and transcription. Here, we focus on one Rho family member, Cdc42, which is overexpressed in a number of human cancers. Consistent with a role in the promotion of tumorigenesis, activating mutations in Cdc42 and guanine nucleotide exchange factors are transforming, while inhibition of Cdc42 activity can impinge on cellular transformation following the activation of oncoproteins or loss of tumor suppressor function. Furthermore, Cdc42 activity has been implicated in the invasive phenotype which characterizes tumor metastasis, further suggesting that Cdc42 may be a useful target for therapeutic intervention. However, several recent studies in mice have unveiled a putative tumor suppressor function of Cdc42 in several tissue types which may involve cell polarity maintenance, suggesting that the role of Cdc42 in cancer development is complex and may be cell type specific.

Indexed as

Genes, Tumor SuppressorNeoplasm Invasivenesscdc42 GTP-Binding ProteinCell DivisionCell PolarityCell Transformation, NeoplasticErbB ReceptorsGene Expression Regulation, NeoplasticHumansMutationNeoplasm MetastasisOncogene ProteinsPhenotypeSignal Transductioncdc42 GTP-Binding ProteinErbB ReceptorsOncogene Proteins

Identifiers

PMID21515363
PMCPMC3115433
OpenAlexW2080264636

What OpenQuestion holds

Textmetadata
LicenceTDM
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.