Evidence map›Paper›PMID 31562956›Full record

ReviewSeminars in cancer biology2020

Rare epidermal growth factor receptor (EGFR) mutations in non-small cell lung cancer.

Peter T Harrison, Simon Vyse, Paul H Huang

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06520189 (Value of F-18 FDG PET/CT for the Prediction of EGFR Mutation in Lung Cancer Patients), which is not on this map. Cited by 353 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
353citing papers in PubMed, 1 pooled it
35.2field-weighted citation impact, top 1% 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.

NCT06520189 not yet recruitingnot on this mapstarted 2024, after this paper: background citation

Value of F-18 FDG PET/CT for the Prediction of EGFR Mutation in Lung Cancer Patients

TypeobservationalSponsorAssiut UniversityRan2024 to 2028Enrolled60ConditionsLung CancerArmsF-18 FDGPET/CT
3 · Its place in the literature

Who cites it

353 citing papers in PubMed, 1 synthesis or guideline pooled it, 595 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Article
  8. Article
  9. Article
  10. Lung cancer screening in Lithuania: a cost-effectiveness analysis.Journal of comparative effectiveness research · 2026
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Complete response in disseminatedTranslational lung cancer research · 2026
    Article
  17. Review
  18. Review
  19. Article
  20. JIN-A02, a Mutant-Selective Fourth-Generation EGFR Inhibitor, Overcomes C797S-Mediated Resistance and Demonstrates Intracranial Activity in NSCLC.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article

293 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Peter T HarrisonDivision of Molecular Pathology, The Institute of Cancer Research, London, SW3 6JB, UK.
Simon VyseDivision of Molecular Pathology, The Institute of Cancer Research, London, SW3 6JB, UK.
Paul H HuangDivision of Molecular Pathology, The Institute of Cancer Research, London, SW3 6JB, UK. Electronic address: paul.huang@icr.ac.uk.
Institute of Cancer Research · GB

Funding

Cancer Research UK 19281Cancer Research UK C36478/A19281
6 · The paper itself

Abstract

Epidermal growth factor receptor (EGFR) mutations are the second most common oncogenic driver event in non-small cell lung cancer (NSCLC). Classical activating mutations (exon 19 deletions and the L858R point mutation) comprise the vast majority of EGFR mutations and are well defined as strong predictors for good clinical response to EGFR tyrosine kinase inhibitors (EGFRi). However, low frequency mutations including point mutations, deletions, insertions and duplications occur within exons 18-25 of the EGFR gene in NSCLC and are associated with poorer responses to EGFRi. Despite an increased uptake of more sensitive detection methods to identify rare EGFR mutations in patients, our understanding of the biology of these rare EGFR mutations is poor compared to classical mutations. In particular, clinical data focused on these mutations is lacking due to their rarity and challenges in trial recruitment, resulting in an absence of effective treatment strategies for many low frequency EGFR mutations. In this review, we describe the structural and mechanistic features of rare EGFR mutations in NSCLC and discuss the preclinical and clinical evidence for EGFRi response for individual rare EGFR mutations. We also discuss EGFRi sensitivity for complex EGFR mutations, and conclude by offering a perspective on the outstanding questions and future steps required to make advances in the treatment of NSCLC patients that harbour rare EGFR mutations.

Indexed as

MutationAllelesAmino Acid SubstitutionCarcinoma, Non-Small-Cell LungErbB ReceptorsExonsGenetic Association StudiesGenetic Predisposition to DiseaseHumansLung NeoplasmsEGFR protein, humanErbB ReceptorsEGFRKinase inhibitorLung cancerSignal transductionTargeted therapy

Identifiers

PMID31562956
PMCPMC7083237
OpenAlexW2976516489

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.