Evidence map›Paper›PMID 30101911›Full record

ArticleInternal medicine (Tokyo, Japan)2018

An EGFR-mutated Lung Adenocarcinoma Undergoing Squamous Cell Carcinoma Transformation Exhibited a Durable Response to Afatinib.

Mitsuo Sato, Akira Matsui, Yoshie Shimoyama, Norihito Omote, Masahiro Morise, Tetsunari Hase, Ichidai Tanaka, Kojiro Suzuki, Yoshinori Hasegawa

Open access · diamondAbstract readCase Reports
In one paragraph

Article in Internal medicine (Tokyo, Japan), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Mitsuo SatoDepartment of Respiratory Medicine, Nagoya University Graduate School of Medicine, Japan.
Akira MatsuiDepartment of Respiratory Medicine, Nagoya University Graduate School of Medicine, Japan.
Yoshie ShimoyamaDepartment of Pathology, Nagoya University Graduate School of Medicine, Japan.
Norihito OmoteDepartment of Respiratory Medicine, Nagoya University Graduate School of Medicine, Japan.
Masahiro MoriseDepartment of Respiratory Medicine, Nagoya University Graduate School of Medicine, Japan.
Tetsunari HaseDepartment of Respiratory Medicine, Nagoya University Graduate School of Medicine, Japan.
Ichidai TanakaDepartment of Respiratory Medicine, Nagoya University Graduate School of Medicine, Japan.
Kojiro SuzukiDepartment of Radiology, Nagoya University Graduate School of Medicine, Japan.
Yoshinori HasegawaDepartment of Respiratory Medicine, Nagoya University Graduate School of Medicine, Japan.
Nagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Squamous cell carcinoma (SCC) transformation has been identified as a mechanism of resistance to first-generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), gefitinib or erlotinib, in EGFR-mutated lung cancer. However, whether second- or third-generation TKIs can overcome resistance due to SCC transformation remains unclear. We herein report an EGFR-mutated lung adenocarcinoma undergoing transformation into SCC that exhibited a durable response to afatinib, which is a second-generation irreversible EGFR-TKI. We suggest that afatinib can be considered as a treatment option for EGFR-mutated tumor undergoing SCC transformation, particularly in the absence of a T790M mutation.

Indexed as

Adenocarcinoma of LungAfatinibCarcinoma, Squamous CellDrug Resistance, NeoplasmErbB ReceptorsErlotinib HydrochlorideFemaleGefitinibHumansLung NeoplasmsMiddle AgedMutationProtein Kinase InhibitorsProtein-Tyrosine KinasesAfatinibEGFR protein, humanErbB ReceptorsErlotinib HydrochlorideGefitinibProtein Kinase InhibitorsProtein-Tyrosine KinasesafatinibEGFR mutationerlotinibsquamous cell carcinoma transformation

Identifiers

PMID30101911
PMCPMC6306534
OpenAlexW2887132960

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.