Evidence map›Paper›PMID 22588876›Full record

ArticleCancer discovery2012

Occupy EGFR.

Jin H Park, Mark A Lemmon

Open access · greenAbstract readComment
In one paragraph

Article in Cancer discovery, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Jin H ParkDepartment of Biochemistry and Biophysics and Graduate Group in Biochemistry and Molecular Biophysics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19194-6059, USA.
Mark A Lemmon
University of Pennsylvania · US

Funding

ERBB RECEPTOR HOMO- AND HETERO- DIMERIZATIONR01CA079992 · NCI · UNIVERSITY OF PENNSYLVANIA · PI LEMMON, MARK A · 1999 to 2013
$3.7M
Signaling by growth factor receptors with intracellular pseudokinase domainsR01GM099891 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI LEMMON, MARK A · 2012 to 2015
$1.6M
NCI NIH HHS R01 CA079992NIGMS NIH HHS R01 GM099891
6 · The paper itself

Abstract

Erlotinib and gefitinib inhibit the growth of non-small cell lung cancer tumors that harbor activating epidermal growth factor receptor (EGFR) mutations but are ineffective against EGFR variants found in glioblastoma. New studies by Barkovich and colleagues and Vivanco and colleagues show that these drugs only occupy the active sites of glioblastoma-derived EGFR mutants to a limited extent and fail to inhibit the activated receptor. Other EGFR inhibitors that target distinct receptor conformations are more effective in the treatment of glioblastoma. These studies reveal distinct drug selectivities for different EGFR mutations and show that an analysis of binding-site occupancy should be considered as a biomarker for inhibitor efficacy in targeting EGFR.

Indexed as

AnimalsBrain NeoplasmsErbB ReceptorsErlotinib HydrochlorideGliomaHumansLung NeoplasmsProtein Kinase InhibitorsQuinazolinesErbB ReceptorsErlotinib HydrochlorideProtein Kinase InhibitorsQuinazolines

Identifiers

PMID22588876
PMCPMC3354646
OpenAlexW2569400214

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.