Evidence map›Paper›PMID 25103305›Full record

Trial reportCancer2014

Monitoring of epidermal growth factor receptor tyrosine kinase inhibitor-sensitizing and resistance mutations in the plasma DNA of patients with advanced non-small cell lung cancer during treatment with erlotinib.

Boe S Sorensen, Lin Wu, Wen Wei, Julie Tsai, Britta Weber, Ebba Nexo, Peter Meldgaard

Registry-linked trialOpen access · hybridAbstract readClinical Trial
In one paragraph

Trial report in Cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02973204 (Circulating Tumor Cells and Tumor DNA in HCC and NET - Patient-specific Biomarkers for Clinical Decision Support and Tailored Relapse Diagnostics), which is not on this map. Cited by 119 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 1 pooled it
18.3field-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.

NCT02973204 completednot on this mapstarted 2016, after this paper: background citation

Circulating Tumor Cells and Tumor DNA in HCC and NET - Patient-specific Biomarkers for Clinical Decision Support and Tailored Relapse Diagnostics

Typeobservational_patient_registrySponsorUniversity of AarhusRan2016 to 2020Enrolled167ConditionsCarcinoma, Hepatocellular, Neuroendocrine TumorsArmsSorafenib, Radiofrequency ablation (RFA) or surgery, Everolimus, Lanreotide
3 · Its place in the literature

Who cites it

119 citing papers in PubMed, 1 synthesis or guideline pooled it, 192 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Detection of T790M, the Acquired Resistance EGFR Mutation, by Tumor Biopsy versus Noninvasive Blood-Based Analyses.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Trial
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Clinical Utility of ctDNA Analysis in Lung Cancer-A Review.Advances in respiratory medicine · 2025
    Review
  10. Review
  11. The APPLE trial in the evolving landscape of ctDNA monitoring.Translational lung cancer research · 2024
    Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Boe S SorensenDepartment of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark.
Lin Wu
Wen Wei
Julie Tsai
Britta Weber
Ebba Nexo
Peter Meldgaard
Aarhus University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe feasibility of monitoring epidermal growth factor receptor (EGFR) mutations in plasma DNA from patients with advanced non-small cell lung cancer (NSCLC) during treatment with erlotinib and its relation to disease progression was investigated.

methodsThe amount of EGFR-mutant DNA was tested in plasma DNA from patients with advanced NSCLC with allele-specific polymerase chain reaction assays. Blood samples from 23 patients with adenocarcinoma of NSCLC that carried tyrosine kinase inhibitor-sensitizing EGFR mutations were taken immediately before treatment with erlotinib. Additional blood samples were taken at timed intervals until erlotinib treatment was withdrawn.

resultsThe amount of plasma DNA with sensitizing EGFR mutations was found to be reduced after the first cycle of erlotinib treatment in 22 of 23 patients (96%). No patients presented with the resistant T790M mutation in the pretreatment sample, but at the time of disease progression the mutation was detected in plasma from 9 patients (39%). The quantitative data from the current study demonstrated that when a T790M mutation emerged in the blood it was accompanied by an increase in the original sensitizing EGFR mutation. When T790M was detected, it was found to be present in all subsequent blood samples from that patient. Most interestingly, the results of the current study demonstrated that monitoring the EGFR mutations in the blood allows for the detection of the T790M mutation up to 344 days before disease progression is clinically evident (range, 15-344 days).

conclusionsThe results of the current study demonstrated that serial monitoring of EGFR mutations in plasma DNA is feasible and may allow for the early detection of resistance mutations. These results warrant further studies to explore the clinical usefulness of such analysis.

Indexed as

AgedAged, 80 and overAntineoplastic AgentsCarcinoma, Non-Small-Cell LungCohort StudiesDisease ProgressionDNA Mutational AnalysisDNA, NeoplasmDrug Resistance, NeoplasmErbB ReceptorsErlotinib HydrochlorideFemaleHumansLung NeoplasmsMaleMiddle AgedAntineoplastic AgentsDNA, NeoplasmErbB ReceptorsErlotinib HydrochlorideProtein Kinase InhibitorsQuinazolinesepidermal growth factor receptor (EGFR) mutationserlotiniblung cancerplasma DNAresistance

Identifiers

PMID25103305
PMCPMC4303984
OpenAlexW1727679707

What OpenQuestion holds

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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.