Evidence map›Paper›PMID 42002533›Full record

ArticleCancer reports (Hoboken, N.J.)2026

Pleomorphic Carcinoma With EGFR and Concomitant Mutations Transformed From Lung Adenocarcinoma: A Case Report.

Yuki Akazawa, Takashi Sato, Yuri Yagami, Yurika Kesen, Tomohiro Furo, Atsuko Watanabe, Jumpei Endo, Maito Nakano, Hiroto Kurata, Hiromi Matsuo and 3 more

Abstract readCase Reports
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer reports (Hoboken, N.J.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Yuki AkazawaDepartment of Respiratory Medicine, Kitasato University School of Medicine, Sagamihara, Japan.ORCID 0009-0006-0380-2713
Takashi SatoDepartment of Respiratory Medicine, Kitasato University School of Medicine, Sagamihara, Japan.ORCID 0000-0002-2338-1665
Yuri YagamiDepartment of Respiratory Medicine, Kitasato University School of Medicine, Sagamihara, Japan.
Yurika KesenDepartment of Pathology, Kitasato University School of Medicine, Sagamihara, Japan.
Tomohiro FuroDepartment of Respiratory Medicine, Kitasato University School of Medicine, Sagamihara, Japan.
Atsuko WatanabeDepartment of Respiratory Medicine, Kitasato University School of Medicine, Sagamihara, Japan.
Jumpei EndoDepartment of Respiratory Medicine, Kitasato University School of Medicine, Sagamihara, Japan.
Maito NakanoDepartment of Respiratory Medicine, Kitasato University School of Medicine, Sagamihara, Japan.
Hiroto KurataDepartment of Respiratory Medicine, Kitasato University School of Medicine, Sagamihara, Japan.
Hiromi MatsuoDepartment of Respiratory Medicine, Kitasato University School of Medicine, Sagamihara, Japan.
Yoshiro NakaharaDepartment of Respiratory Medicine, Kitasato University School of Medicine, Sagamihara, Japan.
Jiichiro SasakiResearch and Development Center for New Medical Frontiers, Kitasato University School of Medicine, Sagamihara, Japan.ORCID 0000-0002-4353-4382
Katsuhiko NaokiDepartment of Respiratory Medicine, Kitasato University School of Medicine, Sagamihara, Japan.ORCID 0000-0002-9637-1388

Funding

Japan Society for the Promotion of Science 23K07609
6 · The paper itself

Abstract

backgroundTransformation to small cell carcinoma, squamous cell carcinoma, and rarely, pleomorphic carcinoma (PC) has been reported to be found in EGFR-mutated lung cancer with acquired resistance to EGFR tyrosine kinase inhibitors (TKIs). However, evidence for underlying factors including genomic profiles associated with PC transformation has been lacking. CASE: We report a case of EGFR-mutated lung adenocarcinoma that transformed to PC confirmed by an autopsy after stereotactic radiotherapy and treatment with EGFR-TKIs. Comprehensive genomic profiling of the autopsy tissue revealed BRAF G466A, KRAS L19F, and NF1 Q2324* mutations in addition to EGFR E746_A750del. Anti-cancer treatments with radiation and EGFR-TKIs accompanying these gene alterations might induce the histological transformation and resistance to EGFR-TKIs.

conclusionThis report adds an insight into the involvement of genetic events in histological transformation in EGFR-mutated lung cancer.

Indexed as

Adenocarcinoma of LungCell Transformation, NeoplasticLung NeoplasmsDrug Resistance, NeoplasmErbB ReceptorsHumansMaleMutationNeurofibromin 1Protein Kinase InhibitorsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)BRAF protein, humanEGFR protein, humanErbB ReceptorsKRAS protein, humanNeurofibromin 1NF1 protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)drug resistanceEGFR mutationgenomic profilinghistological transformationlung cancerpleomorphic carcinoma

Identifiers

PMID42002533
PMCPMC13092422

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.