Evidence map›Paper›PMID 21893191›Full record

ReviewCellular signalling2012

Rac signaling in breast cancer: a tale of GEFs and GAPs.

Eva Wertheimer, Alvaro Gutierrez-Uzquiza, Cinthia Rosemblit, Cynthia Lopez-Haber, Maria Soledad Sosa, Marcelo G Kazanietz

Abstract readReview
In one paragraph

Review in Cellular signalling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed
7.3field-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

127 citing papers in PubMed, 219 citations in OpenAlex.

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  4. Molecular mechanisms of PI3K isoform dependence in embryonic growth.Journal of the Turkish German Gynecological Association · 2024
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  13. GenusMarine drugs · 2022
    Review
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  20. Article

67 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

6 authors at 1 institution in 1 country.

Eva WertheimerDepartment of Pharmacology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6160, USA.
Alvaro Gutierrez-UzquizaDepartment of Pharmacology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6160, USA.
Cinthia RosemblitDepartment of Pharmacology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6160, USA.
Cynthia Lopez-HaberDepartment of Pharmacology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6160, USA.
Maria Soledad SosaDepartment of Pharmacology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6160, USA.
Marcelo G KazanietzDepartment of Pharmacology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6160, USA. Electronic address: marcelog@upenn.edu.
University of Pennsylvania · US

Funding

Chimaerins:receptors for diacylglycerol &phorbol estersR01CA074197 · NCI · UNIVERSITY OF PENNSYLVANIA · PI KAZANIETZ, MARCELO G. · 1997 to 2012
$4.2M
ErbB receptor signaling via small G-proteins in breast cancerR01CA139120 · NCI · UNIVERSITY OF PENNSYLVANIA · PI KAZANIETZ, MARCELO G. · 2010 to 2014
$1.8M
Heregulin signaling via small GTPases in mitogenesis and tumorigenesisR01CA129133 · NCI · UNIVERSITY OF PENNSYLVANIA · PI KAZANIETZ, MARCELO G. · 2009 to 2010
$640k
NCI NIH HHS CA129133NCI NIH HHS CA139120NCI NIH HHS CA74197NCI NIH HHS R01 CA074197NCI NIH HHS R01 CA129133NCI NIH HHS R01 CA139120
6 · The paper itself

Abstract

Rac GTPases, small G-proteins widely implicated in tumorigenesis and metastasis, transduce signals from tyrosine-kinase, G-protein-coupled receptors (GPCRs), and integrins, and control a number of essential cellular functions including motility, adhesion, and proliferation. Deregulation of Rac signaling in cancer is generally a consequence of enhanced upstream inputs from tyrosine-kinase receptors, PI3K or Guanine nucleotide Exchange Factors (GEFs), or reduced Rac inactivation by GTPase Activating Proteins (GAPs). In breast cancer cells Rac1 is a downstream effector of ErbB receptors and mediates migratory responses by ErbB1/EGFR ligands such as EGF or TGFα and ErbB3 ligands such as heregulins. Recent advances in the field led to the identification of the Rac-GEF P-Rex1 as an essential mediator of Rac1 responses in breast cancer cells. P-Rex1 is activated by the PI3K product PIP3 and Gβγ subunits, and integrates signals from ErbB receptors and GPCRs. Most notably, P-Rex1 is highly overexpressed in human luminal breast tumors, particularly those expressing ErbB2 and estrogen receptor (ER). The P-Rex1/Rac signaling pathway may represent an attractive target for breast cancer therapy.

Indexed as

Signal TransductionAnimalsBreast NeoplasmsCell AdhesionCell CommunicationCell MovementCell ProliferationCell Transformation, NeoplasticEpidermal Growth FactorErbB ReceptorsFemaleGTPase-Activating ProteinsGuanine Nucleotide Exchange FactorsHumansMiceNeuregulinsEpidermal Growth FactorErbB ReceptorsGTPase-Activating ProteinsGuanine Nucleotide Exchange FactorsNeuregulinsPhosphatidylinositol 3-Kinasesrac GTP-Binding ProteinsReceptors, G-Protein-CoupledTransforming Growth Factor alpha

Identifiers

PMID21893191
PMCPMC3312797
OpenAlexW2042264070

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.