Evidence map›Paper›PMID 28951536›Full record

ArticleScience signaling2017

Evaluation of the selectivity and sensitivity of isoform- and mutation-specific RAS antibodies.

Andrew M Waters, Irem Ozkan-Dagliyan, Angelina V Vaseva, Nicole Fer, Leslie A Strathern, G Aaron Hobbs, Basile Tessier-Cloutier, William K Gillette, Rachel Bagni, Gordon R Whiteley and 7 more

Open access · greenAbstract read
In one paragraph

Article in Science signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. In Situ RAS:RAF Binding Correlates with Response to KRASG12C Inhibitors in KRASG12C-Mutant Non-Small Cell Lung Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  7. bioRxiv : the preprint server for biology · 2025
    Article
  8. Article
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  10. Article
  11. Review
  12. Article
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  15. Exploiting the intrinsic misfolding propensity of the KRAS oncoprotein.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Article
  17. Article
  18. The role of KRAS splice variants in cancer biology.Frontiers in cell and developmental biology · 2022
    Review
  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

17 authors at 5 institutions in 2 countries.

Andrew M WatersLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.ORCID http://orcid.org/0000-0002-6058-5878
Irem Ozkan-DagliyanDepartment of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Angelina V VasevaLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Nicole FerNational Cancer Institute RAS Initiative, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc., Frederick, MD 21702, USA.ORCID http://orcid.org/0000-0002-7138-1360
Leslie A StrathernNational Cancer Institute RAS Initiative, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc., Frederick, MD 21702, USA.
G Aaron HobbsLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.ORCID http://orcid.org/0000-0002-4751-9681
Basile Tessier-CloutierDepartment of Molecular Oncology, BC Cancer Research Centre, Vancouver, British Columbia V5Z 1L3, Canada.ORCID http://orcid.org/0000-0001-8739-3879
William K GilletteNational Cancer Institute RAS Initiative, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc., Frederick, MD 21702, USA.ORCID http://orcid.org/0000-0002-8592-3642
Rachel BagniNational Cancer Institute RAS Initiative, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc., Frederick, MD 21702, USA.ORCID http://orcid.org/0000-0003-3940-2886
Gordon R WhiteleyNational Cancer Institute RAS Initiative, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc., Frederick, MD 21702, USA.ORCID http://orcid.org/0000-0001-7898-6269
James L HartleyNational Cancer Institute RAS Initiative, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc., Frederick, MD 21702, USA.
Frank McCormickNational Cancer Institute RAS Initiative, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc., Frederick, MD 21702, USA.
Adrienne D CoxLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Peter J HoughtonGreehey Children's Cancer Research Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
David G HuntsmanDepartment of Molecular Oncology, BC Cancer Research Centre, Vancouver, British Columbia V5Z 1L3, Canada.
Mark R PhilipsPerlmutter Cancer Institute, New York University School of Medicine, New York, NY 10016, USA.ORCID http://orcid.org/0000-0002-1179-8156
Channing J DerLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. cjder@med.unc.edu.ORCID http://orcid.org/0000-0002-7751-2747
Leidos (United States) · USUniversity of North Carolina at Chapel Hill · USBC Cancer Agency · CANew York University · USThe University of Texas Health Science Center at San Antonio · US

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Deborah F. Tate · 1985 to 2026
$201.5M
Integrated Training in Cancer Model SystemsT32CA009156 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 1985 to 2020
$19.7M
XENOGRAFT AND CELL LINE COREP01CA165995 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LONDON, CHERYL A · 2013 to 2017
$7.9M
Project 4: The role of codon bias in RAS tumorigenesisP01CA203657 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COUNTER, CHRISTOPHER M · 2016 to 2020
$7.9M
New Ways of Targeting K-RasR35CA197709 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MCCORMICK, FRANK PATRICK · 2016 to 2022
$6.7M
BIOLOGICAL ACTIVITY OF RAS ONCOGENESR01CA042978 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 1986 to 2017
$5.9M
Identification of synthetic lethal interactors in pancreatic cancerU01CA199235 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COX, ADRIENNE D, DER, CHANNING J. · 2015 to 2019
$2.5M
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
K-Ras mutant-specific vulnerabilities for novel pancreatic cancer therapiesF32CA200313 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI HOBBS, GUY AARON · 2015 to 2018
$141k
CCR NIH HHS HHSN261200800001CNCI NIH HHS F32 CA200313NCI NIH HHS HHSN261200800001ENCI NIH HHS P01 CA165995NCI NIH HHS P01 CA203657NCI NIH HHS P30 CA016086NCI NIH HHS R01 CA042978NCI NIH HHS R01 CA175747NCI NIH HHS R21 CA179193NCI NIH HHS R35 CA197709NCI NIH HHS T32 CA009156NCI NIH HHS U01 CA199235
6 · The paper itself

Abstract

There is intense interest in developing therapeutic strategies for RAS proteins, the most frequently mutated oncoprotein family in cancer. Development of effective anti-RAS therapies will be aided by the greater appreciation of RAS isoform-specific differences in signaling events that support neoplastic cell growth. However, critical issues that require resolution to facilitate the success of these efforts remain. In particular, the use of well-validated anti-RAS antibodies is essential for accurate interpretation of experimental data. We evaluated 22 commercially available anti-RAS antibodies with a set of distinct reagents and cell lines for their specificity and selectivity in recognizing the intended RAS isoforms and mutants. Reliability varied substantially. For example, we found that some pan- or isoform-selective anti-RAS antibodies did not adequately recognize their intended target or showed greater selectivity for another; some were valid for detecting G12D and G12V mutant RAS proteins in Western blotting, but none were valid for immunofluorescence or immunohistochemical analyses; and some antibodies recognized nonspecific bands in lysates from "Rasless" cells expressing the oncoprotein BRAF

Indexed as

MutationAnimalsAntineoplastic Agents, ImmunologicalCell Line, TumorFibroblastsHumansHybridomasMiceOncogene ProteinsProtein IsoformsProto-Oncogene Proteins B-rafras ProteinsRNA, Small InterferingAntineoplastic Agents, ImmunologicalBRAF protein, humanOncogene ProteinsProtein IsoformsProto-Oncogene Proteins B-rafras ProteinsRNA, Small Interfering

Identifiers

PMID28951536
PMCPMC5812265
OpenAlexW2760451174

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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.