Evidence map›Paper›PMID 38925616›Full record

ArticleCancer medicine2024

Prevalence of neurotrophic tropomyosin receptor kinase (NTRK) fusion gene positivity in patients with solid tumors in Japan.

Eiji Nakata, Tatsunori Osone, Toru Ogawa, Tomoyuki Taguchi, Kana Hattori, Shinji Kohsaka

Abstract read
In one paragraph

Article in Cancer medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

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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

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

  1. Future oncology (London, England) · 2025
    Pooled it
  2. Tumor-Agnostic Landscape withCurrent oncology (Toronto, Ont.) · 2026
    Observational
  3. Review
  4. Frontiers in medicine · 2026
    Article
  5. Article
  6. Review
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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

6 authors.

Eiji NakataDepartment of Orthopedic Surgery, Okayama University, Okayama, Japan.ORCID 0000-0002-5971-4142
Tatsunori OsoneFaculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Toru OgawaMedical Affairs & Pharmacovigilance, Bayer Yakuhin, Ltd, Osaka, Japan.
Tomoyuki TaguchiMedical Affairs & Pharmacovigilance, Bayer Yakuhin, Ltd, Osaka, Japan.
Kana HattoriMedical Affairs & Pharmacovigilance, Bayer Yakuhin, Ltd, Osaka, Japan.
Shinji KohsakaNational Cancer Center Research Institute, Tokyo, Japan.

Funding

Bayer Yakuhin, Ltd.
6 · The paper itself

Abstract

backgroundMembers of the neurotrophic tropomyosin receptor kinase (NTRK) gene family, NTRK1, NTRK2, and NTRK3 encode TRK receptor tyrosine kinases. Intra- or inter-chromosomal gene rearrangements produce NTRK gene fusions encoding fusion proteins which are oncogenic drivers in various solid tumors.

methodsThis study investigated the prevalence of NTRK fusion genes and identified fusion partners in Japanese patients with solid tumors recorded in the Center for Cancer Genomics and Advanced Therapeutics database of comprehensive genomic profiling test.

resultsIn the analysis population (n = 46,621), NTRK fusion genes were detected in 91 patients (0.20%). The rate was higher in pediatric cases (<18 years; 1.69%) than in adults (0.16%). NTRK gene fusions were identified in 21 different solid tumor types involving 38 different partner genes including 22 (57.9%) previously unreported NTRK gene fusions. The highest frequency of NTRK gene fusions was head and neck cancer (1.31%) and thyroid cancer (1.31%), followed by soft tissue sarcoma (STS; 0.91%). A total of 97 NTRK fusion gene partners were analyzed involving mainly NTRK1 (49.5%) or NTRK3 (44.2%) gene fusions. The only fusion gene detected in head and neck cancer was ETV6::NTRK3 (n = 22); in STS, ETV6::NTRK3 (n = 7) and LMNA::NTRK1 (n = 5) were common. Statistically significant mutual exclusivity of NTRK fusions with alterations was confirmed in TP53, KRAS, and APC. NTRK gene fusion was detected from 11 STS cases: seven unclassified sarcoma, three sarcoma NOS, and one Ewing sarcoma.

conclusionsNTRK gene fusion identification in solid tumors enables accurate diagnosis and potential TRK inhibitor therapy.

Indexed as

NeoplasmsOncogene Proteins, FusionReceptor, trkAAdolescentAdultAgedChildChild, PreschoolFemaleHumansJapanMaleMembrane GlycoproteinsMiddle AgedPrevalenceReceptor, trkBMembrane GlycoproteinsNTRK1 protein, humanNTRK3 protein, humanOncogene Proteins, FusionReceptor, trkAReceptor, trkBReceptor, trkCtropomyosin-related kinase-B, humancomprehensive genomic profilingneurotrophic tropomyosin receptor kinase (NTRK) gene fusionnext‐generation sequencingsolid tumors

Identifiers

PMID38925616
PMCPMC11199329

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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.