Evidence map›Paper›PMID 28830985›Full record

ArticleMolecular cancer therapeutics2017

Characterization of

Kristina B Emdal, Antje Dittmann, Raven J Reddy, Rebecca S Lescarbeau, Sheri L Moores, Sylvie Laquerre, Forest M White

Open access · greenAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Tyrosine phosphoproteome profiling identifies cell-intrinsic signals limiting the efficacy of tyrosine kinase inhibitor therapies.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

7 authors at 2 institutions in 1 country.

Kristina B EmdalDepartment of Biological Engineering and David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts.
Antje DittmannDepartment of Biological Engineering and David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts.
Raven J ReddyDepartment of Biological Engineering and David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts.
Rebecca S LescarbeauDepartment of Biological Engineering and David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts.
Sheri L MooresOncology, Janssen Research and Development, LLC, Spring House, Pennsylvania.
Sylvie LaquerreOncology, Janssen Research and Development, LLC, Spring House, Pennsylvania.
Forest M WhiteDepartment of Biological Engineering and David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts. fwhite@mit.edu.
Massachusetts Institute of Technology · USSpringhouse · US

Funding

Interdepartmental Biotechnology Training ProgramT32GM008334 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI WITTRUP, KARL DANE · 1989 to 2018
$15.2M
Trans Network ProjectU54CA210180 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI WHITE, FOREST M · 2016 to 2020
$10.2M
Engineered Antibody EGFR Antagonist Cancer TherapeuticsR01CA096504 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI WITTRUP, KARL DANE · 2002 to 2017
$9.7M
NCI NIH HHS R01 CA096504NCI NIH HHS U54 CA210180NIGMS NIH HHS T32 GM008334
6 · The paper itself

Abstract

Approximately 10% of non-small cell lung cancer (NSCLC) patients in the United States and 40% of NSCLC patients in Asia have activating epidermal growth factor receptor (EGFR) mutations and are eligible to receive targeted anti-EGFR therapy. Despite an extension of life expectancy associated with this treatment, resistance to EGFR tyrosine kinase inhibitors and anti-EGFR antibodies is almost inevitable. To identify additional signaling routes that can be cotargeted to overcome resistance, we quantified tumor-specific molecular changes that govern resistant cancer cell growth and survival. Mass spectrometry-based quantitative proteomics was used to profile

Indexed as

AcrylamidesAdaptor Proteins, Signal TransducingAniline CompoundsAnimalsAntibodies, BispecificBenzodioxolesCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationDrug Resistance, NeoplasmErbB ReceptorsHumansIndolesMiceMutationPiperazinesAcrylamidesAdaptor Proteins, Signal TransducingamivantamabAniline CompoundsAntibodies, BispecificBenzodioxolesEGFR protein, humanErbB ReceptorsGAB1 protein, humanIndolesMET protein, humanosimertinibPiperazinesProtein Kinase InhibitorsProto-Oncogene Proteins c-metPyrimidinesQuinazolinessaracatinibSHC1 protein, humansrc-Family KinasesSrc Homology 2 Domain-Containing, Transforming Protein 1

Identifiers

PMID28830985
PMCPMC5669802
OpenAlexW2747268799

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.