Evidence map›Paper›PMID 40274716›Full record

ArticleTargeted oncology2025

Impact of EGFR Mutation Subtypes on Response to Chemoimmunotherapy and Chemotherapy in Non-Small-Cell Lung Cancer After EGFR-TKI Failure.

Kenji Morimoto, Tadaaki Yamada, Naoki Furuya, Hisashi Tanaka, Akihiro Yoshimura, Tomohiro Oba, Makoto Hibino, Takahito Fukuda, Yasuhiro Goto, Akira Nakao and 13 more

Abstract read
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In one paragraph

Article in Targeted oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. 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

23 authors.

Kenji MorimotoDepartment of Pulmonary Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465, Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.
Tadaaki YamadaDepartment of Pulmonary Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465, Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan. tayamada@koto.kpu-m.ac.jp.ORCID http://orcid.org/0000-0002-6945-281X
Naoki FuruyaDivision of Respiratory Medicine, Department of Internal Medicine, St. Marianna University School of Medicine, Kanagawa, Japan.
Hisashi TanakaDepartment of Respiratory Medicine, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Akihiro YoshimuraDepartment of Respiratory Medicine, Japanese Red Cross Kyoto Daini Hospital, Kyoto, Japan.
Tomohiro ObaDepartment of Respiratory Medicine, Saitama Red Cross Hospital, Saitama, Japan.
Makoto HibinoDepartment of Respiratory Medicine, Shonan Fujisawa Tokushukai Hospital, Kanagawa, Japan.
Takahito FukudaDepartment of Respiratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Yasuhiro GotoDepartment of Respiratory Medicine, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Akira NakaoDepartment of Respiratory Medicine, Fukuoka University Hospital, Fukuoka, Japan.
Shinsuke OgusuDivision of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga, Japan.
Yuta OkazakiDepartment of Thoracic Oncology, Kansai Medical University, Osaka, Japan.
Taishi HaradaDepartment of Medical Oncology, Fukuchiyama City Hospital, Fukuchiyama, Kyoto, Japan.
Takayo OtaDepartment of Breast Medical Oncology, Izumi City General Hospital, Izumi, Japan.
Ken MasubuchiDivision of Respiratory Medicine, Gunma Prefectural Cancer Center, Ota, Gunma, Japan.
Koji MikamiDepartment of Respiratory Medicine and Hematology, School of Medicine, Hyogo Medical University, Nishinomiya, Hyogo, Japan.
Tae HataDepartment of Pulmonary Medicine, Rakuwakai Otowa Hospital, Kyoto, Japan.
Shoki MatsumotoDepartment of Respiratory Medicine, Japanese Red Cross Kyoto Daiichi Hospital, Kyoto, Japan.
Ryoichi HondaDepartment of Respiratory Medicine, Kokuho Asahi Chuo Hospital, Asahi, Japan.
Koji DateDepartment of Pulmonary Medicine, Kyoto Chubu Medical Center, Nantan, Kyoto, Japan.
Yusuke ChiharaDepartment of Respiratory Medicine, Uji-Tokushukai Medical Center, Uji, Kyoto, Japan.
Hayato KawachiDepartment of Pulmonary Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465, Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.
Koichi TakayamaDepartment of Pulmonary Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465, Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe efficacy of immune checkpoint inhibitor (ICI) monotherapy on non-small-cell lung cancer (NSCLC) varies by epidermal growth factor receptor (EGFR) mutation subtypes. However, the impact of these subtypes on the clinical outcomes of chemoimmunotherapy (Chemo+ICI) or platinum-based chemotherapy (Chemo) in real-world practice remains unclear.

objectiveThis study evaluated the impact of EGFR mutation subtypes on NSCLC treatment outcomes of Chemo and Chemo+ICI. PATIENTS AND

methodsWe retrospectively analyzed patients with advanced or recurrent EGFR-mutant NSCLC from 20 institutions between January 2017 and July 2022. Patients received Chemo with or without ICI after failure of EGFR-tyrosine kinase inhibitors. Common EGFR mutations were categorized as exon 19 deletions and exon 21 L858R mutations.

resultsAmong the 403 patients, 205 (50.9%) had exon 19 deletions, and 198 (49.1%) had L858R mutations. For patients with L858R mutations, Chemo+ICI significantly improved progression-free survival (PFS) compared with Chemo (7.0 vs 5.3 months; p = 0.04). However, no significant difference in PFS was observed between treatments for patients with exon 19 deletions (6.7 vs 6.0 months; p = 0.96). Multivariate analysis identified Chemo+ICI as an independent predictor of PFS in patients with L858R mutations (hazard ratio 0.63; 95% confidence interval 0.43-0.92; p = 0.02).

conclusionsAmong patients with common EGFR mutation subtypes, those with L858R mutations demonstrated significantly improved PFS with Chemo+ICI than with Chemo. These findings suggest that Chemo+ICI may offer a more effective treatment option for patients with L858R-mutant NSCLC, warranting further investigation in prospective studies.

Indexed as

Carcinoma, Non-Small-Cell LungImmunotherapyLung NeoplasmsProtein Kinase InhibitorsAdultAgedAged, 80 and overErbB ReceptorsFemaleHumansMaleMiddle AgedMutationRetrospective StudiesEGFR protein, humanErbB ReceptorsProtein Kinase Inhibitors

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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.