Evidence map›Paper›PMID 40751567›Full record

ArticleThoracic cancer2025

Lung Adenocarcinoma Expressing an EML4-ALK Fusion Transcript With Premature Stop Codons and Response to Alectinib: A Case Report.

Mami Ozaki, Hiroaki Ikushima, Masaki Suzuki, Akira Yokoyama, Kensuke Fukuda, Kousuke Watanabe, Aya Shinozaki-Ushiku, Motohiro Kato, Tetsuo Ushiku, Hiroyuki Aburatani and 2 more

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

Article in Thoracic cancer, 2025. 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

12 authors.

Mami OzakiDepartment of Respiratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hiroaki IkushimaDepartment of Respiratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0002-7053-2841
Masaki SuzukiDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Akira YokoyamaDepartment of Respiratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kensuke FukudaDepartment of Respiratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kousuke WatanabeNext-Generation Precision Medicine Development Laboratory, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Aya Shinozaki-UshikuDivision of Integrative Genomics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Motohiro KatoDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0001-5145-1774
Tetsuo UshikuDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hiroyuki AburataniResearch Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.
Katsutoshi OdaDivision of Integrative Genomics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hidenori KageDepartment of Respiratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0003-3658-4442

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ALK fusions are well-established oncogenic drivers in lung cancer, typically resulting in ALK activation through dimerization mediated by partner proteins. However, alternative mechanisms of ALK activation have also been reported. We herein report an 80-year-old man with metastatic lung adenocarcinoma, who initially tested negative for ALK rearrangement using a polymerase chain reaction-based assay. RNA-based hybrid capture targeted sequencing later identified an EML4-ALK fusion transcript in which EML4 exon 15 and ALK intron 19 were fused. This resulted in a stop codon being retained in the unspliced ALK intron 19, preventing fusion protein translation. However, immunohistochemistry revealed overexpression of ALK, suggesting the existence of alternative translation initiation sites in exon 20 or downstream. The patient showed a marked response to alectinib therapy. This case underscores the importance of using multiple methods to detect actionable gene fusions and to ensure appropriate targeted therapy selection.

Indexed as

Adenocarcinoma of LungCarbazolesCodon, NonsenseLung NeoplasmsOncogene Proteins, FusionPiperidinesAged, 80 and overHumansMalealectinibCarbazolesCodon, NonsenseEML4-ALK fusion protein, humanOncogene Proteins, FusionPiperidinesALKcase reportcomprehensive genomic profilinglung cancerRNA‐sequencing

Identifiers

PMID40751567
PMCPMC12317366

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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.