Evidence map›Paper›PMID 27597943›Full record

ReviewFrontiers in cell and developmental biology2016

The Under-Appreciated Promiscuity of the Epidermal Growth Factor Receptor Family.

Sean P Kennedy, Jordan F Hastings, Jeremy Z R Han, David R Croucher

Abstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
–field-weighted citation impact
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

43 citing papers in PubMed.

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  13. Oxidised IL-33 drives COPD epithelial pathogenesisThe European respiratory journal · 2023
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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

4 authors.

Sean P KennedySystems Biology Ireland, University College DublinDublin, Ireland; Kinghorn Cancer Centre, Garvan Institute of Medical ResearchSydney, NSW, Australia.
Jordan F HastingsKinghorn Cancer Centre, Garvan Institute of Medical Research Sydney, NSW, Australia.
Jeremy Z R HanKinghorn Cancer Centre, Garvan Institute of Medical Research Sydney, NSW, Australia.
David R CroucherKinghorn Cancer Centre, Garvan Institute of Medical ResearchSydney, NSW, Australia; School of Medicine, University College DublinDublin, Ireland; St Vincent's Hospital Clinical School, University of New South WalesSydney, NSW, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Each member of the epidermal growth factor receptor (EGFR) family plays a key role in normal development, homeostasis, and a variety of pathophysiological conditions, most notably in cancer. According to the prevailing dogma, these four receptor tyrosine kinases (RTKs; EGFR, ERBB2, ERBB3, and ERBB4) function exclusively through the formation of homodimers and heterodimers within the EGFR family. These combinatorial receptor interactions are known to generate increased interactome diversity and therefore influence signaling output, subcellular localization and function of the heterodimer. This molecular plasticity is also thought to play a role in the development of resistance toward targeted cancer therapies aimed at these known oncogenes. Interestingly, many studies now challenge this dogma and suggest that the potential for EGFR family receptors to interact with more distantly related RTKs is much greater than currently appreciated. Here we discuss how the promiscuity of these oncogenic receptors may lead to the formation of many unexpected receptor pairings and the significant implications for the efficiency of many targeted cancer therapies.

Indexed as

cancerEGFRERBB2ERBB3ERBB4heterodimerisationreceptor tyrosine kinasetherapeutic resistance

Identifiers

PMID27597943
PMCPMC4992703

What OpenQuestion holds

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Registered trials

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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.