Evidence map›Paper›PMID 27657701›Full record

ReviewSmall GTPases2018

Filling GAPs in our knowledge: ARHGAP11A and RACGAP1 act as oncogenes in basal-like breast cancers.

Campbell D Lawson, Channing J Der

Open access · bronzeAbstract readReview
In one paragraph

Review in Small GTPases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 19% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. The hGIDLife science alliance · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Protooncogenic Role ofBioMed research international · 2023
    Article
  11. Article
  12. Fixing the GAP: The role of RhoGAPs in cancer.European journal of cell biology · 2022
    Review
  13. Article
  14. Comprehensive Analysis of Tripterine Anti-Ovarian Cancer Effects Using Weighted Gene Co-Expression Network Analysis and Molecular Docking.Medical science monitor : international medical journal of experimental and clinical research · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 2 institutions in 2 countries.

Campbell D Lawsona Randall Division of Cell and Molecular Biophysics, King's College London, New Hunt's House, Guy's Campus , London , UK.
Channing J Derb Department of Pharmacology and Lineberger Comprehensive Cancer Center , University of North Carolina at Chapel Hill , Chapel Hill , NC , USA.
King's College London · GBUniversity of North Carolina at Chapel Hill · US

Funding

BIOLOGICAL ACTIVITY OF RAS ONCOGENESR01CA042978 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 1986 to 2017
$5.9M
Mechanisms of PAK1 activation, signaling and tumor resistanceR01CA175747 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J., HAHN, KLAUS M. · 2014 to 2018
$1.8M
ERK inhibitor resistance and ERK isoform-dependent growth in pancreatic cancerR21CA179193 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 2014 to 2015
$407k
NCI NIH HHS R01 CA042978NCI NIH HHS R01 CA175747NCI NIH HHS R21 CA179193
6 · The paper itself

Abstract

Like RAS proteins, the aberrant function of RHO family small GTPases has been implicated in driving cancer development and growth. However, unlike the RAS family, where gain-of-function missense mutations are found in ∼25% of all human cancers, missense mutations are relatively rare in RHO proteins. Instead, altered RHO activity in cancer more commonly arises through the aberrant functions of RHO GTPase regulators. In many cancer types, altered expression and/or mutation of RHO-selective guanine nucleotide exchange factors (RHOGEFs) or GTPase-activating proteins (RHOGAPs), which activate or inactivate RHO GTPases, respectively, is observed. For example, deletion or loss of expression of the RHOA GAP DLC1 is well-established to drive cancer growth. Recently, we identified high expression of 2 RHOGAPs, ARHGAP11A and RACGAP1, in the basal-like breast cancer subtype. Unexpectedly, both of these RHOA GAPs exhibited properties of oncoproteins rather than tumor suppressors, in contrast to DLC1. In this commentary, we summarize our findings and speculate that different RHOA GAPs can play distinct roles in cancer depending on their spatial regulation and cancer type context. We also evaluate our results in light of recently-described cancer genome sequencing studies that have identified loss-of-function mutations of RHOA in specific cancer types.

Indexed as

OncogenesAnimalsBreast NeoplasmsGTPase-Activating ProteinsHumansGTPase-Activating ProteinsARHGAP11Abasal-like breast cancerMGCRACGAPMP-GAPRACGAP1RHOARHOGAP

Identifiers

PMID27657701
PMCPMC5997163
OpenAlexW2521981909

What OpenQuestion holds

Textmetadata
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.