Evidence map›Paper›PMID 42616271›Full record

ArticleHuman cell2026

Establishment and functional characterization of an EGFR-amplified tumoroid from squamous cell carcinoma of unknown primary.

Miki Iwai, Etsuko Yokota, Takuro Yukawa, Kizuki Matsumoto, Takashi Urano, Kazutaka Nakashima, Hiroyoshi Doihara, Nagio Takigawa, Hideyo Fujiwara, Takashi Akiyama and 4 more

Abstract read
In one paragraph

Article in Human cell, 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

14 authors.

Miki IwaiKawasaki Medical School, Central Research Institute, Okayama, Japan.
Etsuko YokotaDepartment of General Surgery, Kawasaki Medical School, Okayama, 700-8505, Japan.
Takuro YukawaDepartment of General Surgery, Kawasaki Medical School, Okayama, 700-8505, Japan.
Kizuki MatsumotoDepartment of General Surgery, Kawasaki Medical School, Okayama, 700-8505, Japan.
Takashi UranoDepartment of General Surgery, Kawasaki Medical School, Okayama, 700-8505, Japan.
Kazutaka NakashimaDepartment of General Surgery, Kawasaki Medical School, Okayama, 700-8505, Japan.
Hiroyoshi DoiharaDepartment of General Surgery, Kawasaki Medical School, Okayama, 700-8505, Japan.
Nagio TakigawaKawasaki Medical School, Central Research Institute, Okayama, Japan.
Hideyo FujiwaraDepartment of Pathology, Kawasaki Medical School, Okayama, Japan.
Takashi AkiyamaDepartment of Pathology, Kawasaki Medical School, Okayama, Japan.
Minoru HaisaKawasaki Medical School General Medical Center, Okayama, Japan.
Yoshio NaomotoDepartment of General Surgery, Kawasaki Medical School, Okayama, 700-8505, Japan.
Takuya FukazawaKawasaki Medical School, Central Research Institute, Okayama, Japan. fukazawat@med.kawasaki-m.ac.jp.ORCID http://orcid.org/0000-0003-2890-0599
Tomoki YamatsujiDepartment of General Surgery, Kawasaki Medical School, Okayama, 700-8505, Japan.

Funding

Japan Society for the Promotion of Science 22H03164Japan Society for the Promotion of Science 23K08142
6 · The paper itself

Abstract

Carcinoma of unknown primary (CUP) remains a clinically challenging malignancy with limited treatment options and poor prognosis. Although genomic profiling has identified potentially actionable alterations, optimal therapeutic strategies are often unclear. Here, we report the establishment and characterization of a patient-derived tumoroid from an EGFR-amplified CUP and evaluate its utility as a functional model for therapeutic assessment. The patient-derived tumoroid (PDT-CUP#1) was successfully established from resected tumor tissue and maintained in long-term culture. Whole-exome sequencing demonstrated genomic concordance between the PDT-CUP#1 and the original tumor. Quantitative PCR and fluorescence in situ hybridization confirmed EGFR amplification. Xenograft tumors derived from PDT-CUP#1 recapitulated the histopathological features of the original lesion. Functional drug testing demonstrated differential sensitivity among EGFR-targeted agents. Whereas EGFR tyrosine kinase inhibition resulted in modest growth suppression, anti-EGFR monoclonal antibodies exhibited moderate antitumor effects, and an EGFR-targeted antibody-drug conjugate showed the most pronounced growth inhibition. Notably, the therapeutic sensitivity observed in the tumoroids was generally consistent with the patient's clinical response to platinum-based chemotherapy combined with necitumumab. These findings demonstrate that a CUP-derived tumoroid can be successfully established while preserving the key molecular and pathological features of the original tumor. This model provides a platform for functional evaluation of therapeutic vulnerabilities and offers proof-of-concept for integrating patient-derived tumoroids into therapeutic decision-making in CUP.

Indexed as

Carcinoma, Squamous CellErbB ReceptorsGene AmplificationNeoplasms, Unknown PrimaryAnimalsAntibodies, MonoclonalHumansMolecular Targeted TherapyAntibodies, MonoclonalEGFR protein, humanErbB ReceptorsCarcinoma of unknown primaryEGFR amplificationFunctional precision oncologySensitivity testTumoroid

Identifiers

PMID42616271
PMCPMC13490018

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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.