ReviewDrugs2021
Detecting and Targeting NTRK Fusions in Cancer in the Era of Tumor Agnostic Oncology.
Review in Drugs, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Systematic review of NTRK 1/2/3 fusion prevalence pan-cancer and across solid tumours.Scientific reports · 2023Pooled it
- Translational and Implementation Barrier in the Management of Biliary Tract Cancer: Diagnostic, Molecular, Therapeutic, and Patient-Centered Challenges.Journal of gastroenterology and hepatology · 2026Review
- From fragments to full pictures: how long-read sequencing platforms are revolutionizing oncology research.Molecular biology reports · 2026Review
- Seven Shades of Triple Negativity: A Review Unveiling the Low-Grade Spectrum of Breast Cancer.Cancers · 2025Review
- The Evolving Interplay Between Targeted Therapy and Surgery for Resectable Lung Cancer.Cancers · 2025Review
- Preclinical Evaluation of the Oral Toxicity, Genotoxicity, and Safety Pharmacology of LPM4870108, a Novel Potent Tropomyosin Receptor Kinase Inhibitor.Pharmacology research & perspectives · 2025Article
- Role of NTRK Fusion Genes in the Tumor Immune Microenvironment of HPV (+/-) Cervical Cancer.Journal of medical virology · 2025Review
- The state of the art in secondary pharmacology and its impact on the safety of new medicines.Nature reviews. Drug discovery · 2024Review
- A Study of Alternative TrkA Splicing Identifies TrkAIII as a Novel Potentially Targetable Participant in PitNET Progression.Biology · 2024Article
- Perioperative and palliative systemic treatments for biliary tract cancer.Therapeutic advances in medical oncology · 2024Review
- The synergistic effects of anoikis-related genes and EMT-related genes in the prognostic prediction of Wilms tumor.Frontiers in molecular biosciences · 2024Article
- Recent advances in non-small cell lung cancer targeted therapy; an update review.Cancer cell international · 2023Review
- NTRK2 gene fusions are uncommon in pilocytic astrocytoma.Molecular biology reports · 2022Article
- Toward in vivo proof of binding ofEJNMMI research · 2022Article
- Cancer Therapy Guided by Mutation Tests: Current Status and Perspectives.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gene rearrangements involving the neurotrophic receptor kinase genes NTRK1, NTRK2, and NTRK3 (referred to as TRK, encoding TRKA, TRKB, and TRKC, respectively) result in highly oncogenic fusions. TRK fusions are rare, with a prevalence of < 1% in solid tumors. Detection of TRK fusions can be based on fluorescence in-situ hybridization (FISH), immunohistochemistry (IHC), and next-generation sequencing (NGS), where RNA sequencing is the most sensitive method. Inhibition of TRK fusions with highly selective small-molecule TRK inhibitors (TRKi) such as entrectinib and larotrectinib, results in profound responses in most cancer patients, regardless of cancer histology. Even response in CNS metastases is relatively common. Although responses are often durable, many patients develop resistance to TRKi due to mutations in one of the TRK genes, or due to genetic alterations conferring activation of alternative oncogenic signaling pathways. Second-generation TRKi have been developed, which can overcome some of the TRK resistance mutations. TRKi are well tolerated, with most common adverse events being related to on-target/off-tumor inhibition of TRKs.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.