Evidence map›Paper›PMID 25225063›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2014

Molecular pathways: targeting RAC-p21-activated serine-threonine kinase signaling in RAS-driven cancers.

Nicole M Baker, Hoi Yee Chow, Jonathan Chernoff, Channing J Der

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. RHOAScience signaling · 2023
    Article
  7. Review
  8. Article
  9. The Essential Role of Rac1 Glucosylation inFrontiers in microbiology · 2022
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Resistance to KRASFrontiers in oncology · 2021
    Review
  17. Article
  18. Review
  19. Review
  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

4 authors at 2 institutions in 1 country.

Nicole M BakerDepartment of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina. Lineberger Comprehensive Cancer Center, Chapel Hill, North Carolina.
Hoi Yee ChowCancer Biology Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania.
Jonathan ChernoffCancer Biology Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania.
Channing J DerDepartment of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina. Lineberger Comprehensive Cancer Center, Chapel Hill, North Carolina. cjder@med.unc.edu.
Fox Chase Cancer Center · USUniversity 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
The Role of p21-Activated Kinases in Malignant MesotheliomaR01CA148805 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI CHERNOFF, JONATHAN, TESTA, JOSEPH R. · 2011 to 2020
$4.0M
Targeting the Kinome in Neurofibromatosis type 1R01CA142928 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI CHERNOFF, JONATHAN · 2010 to 2019
$3.9M
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
Defining the Role and Mechanism of Pak1 in Supporting Pancreatic CancerF31CA180628 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BAKER, NICOLE MARIE · 2014 to 2016
$71k
NCI NIH HHS 1F31CA180628NCI NIH HHS CA042978NCI NIH HHS CA142928NCI NIH HHS CA148805NCI NIH HHS CA175747NCI NIH HHS CA179193NCI NIH HHS F31 CA180628NCI NIH HHS R01 CA042978NCI NIH HHS R01 CA175747NCI NIH HHS R21 CA179193
6 · The paper itself

Abstract

Cancers driven by oncogenic Ras proteins encompass some of the most deadly human cancer types, and there is a pressing need to develop therapies for these diseases. Although recent studies suggest that mutant Ras proteins may yet be druggable, the most promising and advanced efforts involve inhibitors of Ras effector signaling. Most efforts to target Ras signaling have been aimed at the ERK mitogen-activated protein kinase and the phosphoinositide 3-kinase signaling networks. However, to date, no inhibitors of these Ras effector pathways have been effective against RAS-mutant cancers. This ineffectiveness is due, in part, to the involvement of additional effectors in Ras-dependent cancer growth, such as the Rac small GTPase and the p21-activated serine-threonine kinases (PAK). PAK proteins are involved in many survival, cell motility, and proliferative pathways in the cell and may present a viable new target in Ras-driven cancers. In this review, we address the role and therapeutic potential of Rac and group I PAK proteins in driving mutant Ras cancers.

Indexed as

AnimalsHumansNeoplasmsp21-Activated KinasesProto-Oncogene Proteins c-aktSignal Transductionp21-Activated KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID25225063
PMCPMC4166583
OpenAlexW2131228597

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.