Evidence map›Paper›PMID 28807941›Full record

ReviewCancer research2017

The Rac GTPase in Cancer: From Old Concepts to New Paradigms.

Marcelo G Kazanietz, Maria J Caloca

Abstract readReview
In one paragraph

Review in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
9.5field-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

111 citing papers in PubMed, 212 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Diallyl disulfide in oncotherapy: molecular mechanisms and therapeutic potentials.Apoptosis : an international journal on programmed cell death · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Cancers · 2025
    Article
  13. RAC1 signaling in prostate cancer: VAV GEFs take center stage.Frontiers in cell and developmental biology · 2025
    Article
  14. Article
  15. NAR genomics and bioinformatics · 2024
    Article
  16. Article
  17. Apoptosis and eryptosis: similarities and differences.Apoptosis : an international journal on programmed cell death · 2024
    Review
  18. Article
  19. Review
  20. Article

51 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 2 countries.

Marcelo G KazanietzDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. marcelog@upenn.edu mj.caloca@csic.es.
Maria J CalocaInstituto de Biología y Genética Molecular, Consejo Superior de Investigaciones Científicas, Universidad de Valladolid, Valladolid, Spain. marcelog@upenn.edu mj.caloca@csic.es.
Instituto de Biomedicina y Genética Molecular de Valladolid · ESTranslational Therapeutics (United States) · US

Funding

Protein kinase C and lung carcinogenesisR01ES026023 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI KAZANIETZ, MARCELO G. · 2015 to 2019
$2.3M
Effectors of protein kinase C-mediated tumor progressionR01CA196232 · NCI · UNIVERSITY OF PENNSYLVANIA · PI KAZANIETZ, MARCELO G. · 2016 to 2022
$2.0M
CXCL13: a mediator of prostate cancer progressionR01CA189765 · NCI · UNIVERSITY OF PENNSYLVANIA · PI KAZANIETZ, MARCELO G. · 2015 to 2019
$1.8M
NCI NIH HHS R01 CA189765NCI NIH HHS R01 CA196232NIEHS NIH HHS R01 ES026023
6 · The paper itself

Abstract

Rho family GTPases are critical regulators of cellular functions that play important roles in cancer progression. Aberrant activity of Rho small G-proteins, particularly Rac1 and their regulators, is a hallmark of cancer and contributes to the tumorigenic and metastatic phenotypes of cancer cells. This review examines the multiple mechanisms leading to Rac1 hyperactivation, particularly focusing on emerging paradigms that involve gain-of-function mutations in Rac and guanine nucleotide exchange factors, defects in Rac1 degradation, and mislocalization of Rac signaling components. The unexpected pro-oncogenic functions of Rac GTPase-activating proteins also challenged the dogma that these negative Rac regulators solely act as tumor suppressors. The potential contribution of Rac hyperactivation to resistance to anticancer agents, including targeted therapies, as well as to the suppression of antitumor immune response, highlights the critical need to develop therapeutic strategies to target the Rac pathway in a clinical setting.

Indexed as

AnimalsHumansNeoplasmsrho GTP-Binding ProteinsSignal Transductionrho GTP-Binding Proteins

Identifiers

PMID28807941
PMCPMC5645227
OpenAlexW2747641745

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.