Evidence map›Paper›PMID 29858187›Full record

ReviewCancer research2018

Targeting Rac and Cdc42 GTPases in Cancer.

María Del Mar Maldonado, Suranganie Dharmawardhane

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06075810 (A Phase 1 Open-Label, First-in-Human Trial of Oral MBQ-167 as Single Agent in Participants With Advanced Breast Cancer), which is not on this map. Cited by 175 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
175citing papers in PubMed, 1 pooled it
11.7field-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.

NCT06075810 phase1recruitingnot on this mapstarted 2023, after this paper: background citation

A Phase 1 Open-Label, First-in-Human Trial of Oral MBQ-167 as Single Agent in Participants With Advanced Breast Cancer

TypeinterventionalSponsorMBQ PharmaRan2023 to 2025Enrolled48ConditionsBreast Cancer, Breast Neoplasm, Breast Cancer Stage IVArmsMBQ-167
3 · Its place in the literature

Who cites it

175 citing papers in PubMed, 1 synthesis or guideline pooled it, 242 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. How Functional Variants Reconfigure the Rac2 Conformational Landscape.bioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Decoding Rho GTPase signalling networks in directed cell migration.Frontiers in cell and developmental biology · 2026
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

115 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.

María Del Mar MaldonadoDepartment of Biochemistry, School of Medicine, University of Puerto Rico, Medical Sciences Campus, San Juan, Puerto Rico.
Suranganie DharmawardhaneDepartment of Biochemistry, School of Medicine, University of Puerto Rico, Medical Sciences Campus, San Juan, Puerto Rico. su.d@upr.edu.
University of Puerto Rico, Medical Sciences Campus · PR

Funding

SCIENCE AND TECHNOLOGY COMPETENCY & EDUCATION CORE (STCE)P20GM103475 · NIGMS · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI Jose R. Rodriguez-Medina · 2012 to 2026
$52.9M
UPR/MDACC Partnership for Excellence in Cancer Research(Parent Grant U54 CA096297)U54CA096297 · NCI · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI SHARON Hermes GIORDANO, REYNOLD Eugenio LOPEZ-ENRIQUEZ · 2002 to 2026
$36.9M
RISE Option III: MBRS RISE at the UPR Medical Sciences CampusR25GM061838 · NIGMS · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI CADILLA, CARMEN LYDIA · 2000 to 2021
$25.5M
Targeting breast cancer progressionSC3GM084824 · NIGMS · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI DHARMAWARDHANE, SURANGANIE · 2008 to 2021
$1.6M
NCI NIH HHS U54 CA096297NIGMS NIH HHS P20 GM103475NIGMS NIH HHS R25 GM061838NIGMS NIH HHS SC3 GM084824
6 · The paper itself

Abstract

Rac and Cdc42 are small GTPases that have been linked to multiple human cancers and are implicated in epithelial to mesenchymal transition, cell-cycle progression, migration/invasion, tumor growth, angiogenesis, and oncogenic transformation. With the exception of the P29S driver mutation in melanoma, Rac and Cdc42 are not generally mutated in cancer, but are overexpressed (gene amplification and mRNA upregulation) or hyperactivated. Rac and Cdc42 are hyperactivated via signaling through oncogenic cell surface receptors, such as growth factor receptors, which converge on the guanine nucleotide exchange factors that regulate their GDP/GTP exchange. Hence, targeting Rac and Cdc42 represents a promising strategy for precise cancer therapy, as well as for inhibition of bypass signaling that promotes resistance to cell surface receptor-targeted therapies. Therefore, an understanding of the regulatory mechanisms of these pivotal signaling intermediates is key for the development of effective inhibitors. In this review, we focus on the role of Rac and Cdc42 in cancer and summarize the regulatory mechanisms, inhibitory efficacy, and the anticancer potential of Rac- and Cdc42-targeting agents.

Indexed as

Antineoplastic Agentscdc42 GTP-Binding ProteinGene Expression Regulation, NeoplasticHumansNeoplasmsProtein Bindingrac GTP-Binding ProteinsSignal TransductionUp-RegulationAntineoplastic Agentscdc42 GTP-Binding Proteinrac GTP-Binding Proteins

Identifiers

PMID29858187
PMCPMC6004249
OpenAlexW2807492413

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.