Evidence map›Paper›PMID 26755435›Full record

ReviewCellular and molecular life sciences : CMLS2016

Molecular mechanisms that underpin EML4-ALK driven cancers and their response to targeted drugs.

Richard Bayliss, Jene Choi, Dean A Fennell, Andrew M Fry, Mark W Richards

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
9.2field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 109 citations in OpenAlex.

  1. Article
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  14. Clinical difference on the variants and co-mutation in a Chinese cohort with ALK-positive advanced non-small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Potential Therapeutic Strategy forJTO clinical and research reports · 2022
    Article
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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

5 authors at 3 institutions in 2 countries.

Richard BaylissDepartment of Molecular and Cell Biology, University of Leicester, Lancaster Road, Leicester, LE2 9HN, UK. r.w.bayliss@leeds.ac.uk.
Jene ChoiDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43 gil, Seoul, Korea.
Dean A FennellCancer Research UK Centre, University of Leicester, Lancaster Road, Leicester, LE3 9SQ, UK.
Andrew M FryDepartment of Molecular and Cell Biology, University of Leicester, Lancaster Road, Leicester, LE2 9HN, UK.
Mark W RichardsDepartment of Molecular and Cell Biology, University of Leicester, Lancaster Road, Leicester, LE2 9HN, UK.
University of Leicester · GBCancer Research UK · GBUlsan College · KR

Funding

Cancer Research UK 12772Cancer Research UK C24461/A12772Worldwide Cancer Research 13-0042Worldwide Cancer Research 16-0119
6 · The paper itself

Abstract

A fusion between the EML4 (echinoderm microtubule-associated protein-like) and ALK (anaplastic lymphoma kinase) genes was identified in non-small cell lung cancer (NSCLC) in 2007 and there has been rapid progress in applying this knowledge to the benefit of patients. However, we have a poor understanding of EML4 and ALK biology and there are many challenges to devising the optimal strategy for treating EML4-ALK NSCLC patients. In this review, we describe the biology of EML4 and ALK, explain the main features of EML4-ALK fusion proteins and outline the therapies that target EML4-ALK. In particular, we highlight the recent advances in our understanding of the structures of EML proteins, describe the molecular mechanisms of resistance to ALK inhibitors and assess current thinking about combinations of ALK drugs with inhibitors that target other kinases or Hsp90.

Indexed as

Anaplastic Lymphoma KinaseAnimalsCarcinoma, Non-Small-Cell LungCell Cycle ProteinsHSP90 Heat-Shock ProteinsHumansLungLung NeoplasmsMicrotubule-Associated ProteinsModels, MolecularMolecular Targeted TherapyOncogene Proteins, FusionProtein ConformationProtein Kinase InhibitorsReceptor Protein-Tyrosine KinasesSerine EndopeptidasesALK protein, humanAnaplastic Lymphoma KinaseCell Cycle ProteinsEML4-ALK fusion protein, humanEML4 protein, humanHSP90 Heat-Shock ProteinsMicrotubule-Associated ProteinsOncogene Proteins, FusionProtein Kinase InhibitorsReceptor Protein-Tyrosine KinasesSerine EndopeptidasesFusionKinaseLung cancerOncogeneStructural biology

Identifiers

PMID26755435
PMCPMC4761370
OpenAlexW2236017705

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.