Evidence map›Paper›PMID 39156250›Full record

ArticleCureus2024

Investigation of the Efficacy of Epidermal Growth Factor Receptor (EGFR)-Tyrosine Kinase Inhibitor in Patients With EGFR Exon 21 L858R Point Mutation-Positive Non-small Cell Lung Cancer.

Yutaka Takahara, Ryudai Abe, Sumito Nagae, Takuya Tanaka, Yoko Ishige, Ikuyo Shionoya, Kouichi Yamamura, Masafumi Nojiri, Masaharu Iguchi

Abstract read
In one paragraph

Article in Cureus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

9 authors.

Yutaka TakaharaRespiratory Medicine, Kanazawa Medical University, Uchinada, JPN.
Ryudai AbeRespiratory Medicine, Kanazawa Medical University, Uchinada, JPN.
Sumito NagaeRespiratory Medicine, Kanazawa Medical University, Uchinada, JPN.
Takuya TanakaRespiratory Medicine, Kanazawa Medical University, Uchinada, JPN.
Yoko IshigeRespiratory Medicine, Kanazawa Medical University, Uchinada, JPN.
Ikuyo ShionoyaRespiratory Medicine, Kanazawa Medical University, Uchinada, JPN.
Kouichi YamamuraRespiratory Medicine, Kanazawa Medical University, Uchinada, JPN.
Masafumi NojiriRespiratory Medicine, Kanazawa Medical University, Uchinada, JPN.
Masaharu IguchiRespiratory Medicine, Kanazawa Medical University, Uchinada, JPN.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTreatment of advanced non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) has a higher response rate than with conventional chemotherapy in patients positive for EGFR mutations. However, the efficacy of EGFR-TKI therapy may be reduced in patients positive for the EGFR exon 21 L858R point mutation.

objectiveTo determine the clinical characteristics of patients with EGFR exon 21 L858R point mutation-positive NSCLC who are non-responders to EGFR-TKI therapy and the factors that predict response to EGFR-TKI therapy.

methodsPatients with NSCLC treated with EGFR-TKIs were evaluated for response after treatment, and those who responded were compared with those who did not respond.

resultsOf 31 patients, 21 (67.7%) responded to EGFR-TKI therapy (the response group). There were significantly more programmed death ligand 1 (PDL1)-negative patients in the response group than in the non-response group. A significantly higher number of patients in the PDL1-positive group developed interstitial lung disease (ILD) after EGFR-TKI therapy than those in the PDL1-negative group.

conclusionEGFR-TKI therapy is likely to be non-responsive in PDL1-positive patients with EGFR exon 21 L858R point mutation-positive NSCLC. The PDL1-positive group is at a high risk of developing ILD.

Indexed as

egfr exon 21 l858r point mutationegfr gene mutationegfr-tkiinterstitial lung diseasensclcpdl1 expression

Identifiers

PMID39156250
PMCPMC11330089

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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.