Evidence map›Paper›PMID 22004085›Full record

ReviewFuture medicinal chemistry2011

Inhibition of Ras for cancer treatment: the search continues.

Antonio T Baines, Dapeng Xu, Channing J Der

Abstract readReview
In one paragraph

Review in Future medicinal chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
197citing papers in PubMed, 1 pooled it
12.5field-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

197 citing papers in PubMed, 1 synthesis or guideline pooled it, 378 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. RAS GTPases and Interleaflet Coupling in the Plasma Membrane.Cold Spring Harbor perspectives in biology · 2023
    Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

137 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

3 authors at 2 institutions in 1 country.

Antonio T BainesDepartment of Biology and the Cancer Research Program, JLC-Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, NC 27707, USA.
Dapeng Xu
Channing J Der
North Carolina Central University · USUniversity of North Carolina at Chapel Hill · US

Funding

TISSUE PROCUREMENT &ANALYSISP50CA106991 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TEPPER, JOEL E · 2004 to 2009
$12.1M
VALIDATION OF INHIBITORS OF RHO GTPASES FOR CANCER TREATMENTU19CA067771 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI SEBTI, SAID M · 1995 to 2009
$8.9M
BIOLOGICAL ACTIVITY OF RAS ONCOGENESR01CA042978 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 1986 to 2017
$5.9M
NCCU-BBRI/UNC-LINEBERGER PARTNERSHIP IN CANCER RESEARCHU56CA092077 · NCI · NORTH CAROLINA CENTRAL UNIVERSITY · PI RICHARDSON, MICHELER RICARDO · 2001 to 2008
$2.5M
Mechanism and role of DLC-1 tumor suppressor loss in lung cancerR01CA129610 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 2008 to 2012
$1.5M
Role of RGS proteins in Ras- and B-Raf--mediated transformationR01CA127152 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 2007 to 2011
$1.1M
Genetic dissection and inhibitor targeting of Rac signaling in pancreatic cancer.R21CA161494 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 2011 to 2012
$354k
The Role of Pim Kinases as a Novel Molecular Target in Pancreatic CancerSC2CA137845 · NCI · NORTH CAROLINA CENTRAL UNIVERSITY · PI BAINES, ANTONIO THOMAS · 2008 to 2010
$280k
NCI NIH HHS CA042978NCI NIH HHS CA106991NCI NIH HHS CA127152NCI NIH HHS CA129610NCI NIH HHS CA137845NCI NIH HHS CA67771NCI NIH HHS CA92077NCI NIH HHS P50 CA106991NCI NIH HHS R01 CA042978NCI NIH HHS R01 CA127152NCI NIH HHS R01 CA129610NCI NIH HHS R21 CA161494NCI NIH HHS SC2 CA137845NCI NIH HHS U19 CA067771NCI NIH HHS U56 CA092077
6 · The paper itself

Abstract

The RAS oncogenes (HRAS, NRAS and KRAS) comprise the most frequently mutated class of oncogenes in human cancers (33%), thus stimulating intensive effort in developing anti-Ras inhibitors for cancer treatment. Despite intensive effort, to date, no effective anti-Ras strategies have successfully made it to the clinic. We present an overview of past and ongoing strategies to inhibit oncogenic Ras in cancer. Since approaches to directly target mutant Ras have not been successful, most efforts have focused on indirect approaches to block Ras membrane association or downstream effector signaling. While inhibitors of effector signaling are currently under clinical evaluation, genome-wide unbiased genetic screens have identified novel directions for future anti-Ras drug discovery.

Indexed as

Antineoplastic AgentsGenes, rasGenome-Wide Association StudyHumansMutationNeoplasmsOncogene Protein p21(ras)Signal TransductionAntineoplastic AgentsOncogene Protein p21(ras)

Identifiers

PMID22004085
PMCPMC3347641
OpenAlexW2128826373

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.