Evidence map›Paper›PMID 29871878›Full record

ReviewBiochemical Society transactions2018

RHO GTPases in cancer: known facts, open questions, and therapeutic challenges.

Xosé R Bustelo

Open access · greenAbstract readReview
In one paragraph

Review in Biochemical Society transactions, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

57 citing papers in PubMed, 83 citations in OpenAlex.

  1. A RAC1 SUMOylation switch governs breast cancer metastasis.Signal transduction and targeted therapy · 2026
    Article
  2. Article
  3. How Functional Variants Reconfigure the Rac2 Conformational Landscape.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Tumor-derived RAC1Science advances · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Structural Dynamics of Rho GTPases.Journal of molecular biology · 2025
    Review
  11. Article
  12. RAC1 signaling in prostate cancer: VAV GEFs take center stage.Frontiers in cell and developmental biology · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. RHOAScience signaling · 2023
    Article
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

1 author at 1 institution in 1 country.

Xosé R BusteloCentro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, and Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, 37007 Salamanca, Spain xbustelo@usal.es.
Centro de Investigación Biomédica en Red de Cáncer · ES

Funding

Worldwide Cancer Research 14-1248
6 · The paper itself

Abstract

RHO GTPases have been traditionally associated with protumorigenic functions. While this paradigm is still valid in many cases, recent data have unexpectedly revealed that RHO proteins can also play tumor suppressor roles. RHO signaling elements can also promote both pro- and antitumorigenic effects using GTPase-independent mechanisms, thus giving an extra layer of complexity to the role of these proteins in cancer. Consistent with these variegated roles, both gain- and loss-of-function mutations in RHO pathway genes have been found in cancer patients. Collectively, these observations challenge long-held functional archetypes for RHO proteins in both normal and cancer cells. In this review, I will summarize these data and discuss new questions arising from them such as the functional and clinical relevance of the mutations found in patients, the mechanistic orchestration of those antagonistic functions in tumors, and the pros and cons that these results represent for the development of RHO-based anticancer drugs.

Indexed as

AnimalsHumansMutationNeoplasmsrho GTP-Binding Proteinsrho GTP-Binding ProteinsCDC42GTPaseRACRHORHO GAPRHO GEF

Identifiers

PMID29871878
PMCPMC7615761
OpenAlexW2807373400

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.