ReviewCancers2018
Inhibiting TRK Proteins in Clinical Cancer Therapy.
Review in Cancers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 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
80 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.
- Pooled it
- Dual inhibitors of CDK2 and TRKA kinases: design, synthesis, antiproliferative activity and molecular modeling of novel pyrazolopyrimidine derivatives.RSC advances · 2026Article
- Pan-TRK expression and NTRK gene aberrations in meningiomas: association with tumor grade and proliferative activity.The journal of pathology. Clinical research · 2026Article
- Atlas-Guided Nanocarrier Strategies Targeting Spatial NTRK2/MAPK Signaling in EGFR-TKI-Resistant Niches of Esophageal Squamous Cell Carcinoma.Pharmaceutics · 2026Review
- Dissociation Between Tumor Response and PTTM Progression During Entrectinib Therapy in NTRK Fusion-Positive Colon Cancer.Current oncology (Toronto, Ont.) · 2025Article
- Review
- 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
- Role of TRKC and NT-3 proteins in the progression and prognosis of colorectal cancer.Translational cancer research · 2025Article
- A comprehensive bioinformatic evaluation of the NTRK family's potential as prognostic biomarkers in breast cancer.Bioinformatics advances · 2025Article
- Design, Synthesis and Molecular Modeling of Pyrazolo[1,5-Pharmaceuticals (Basel, Switzerland) · 2024Article
- NTRK fusion promotes tumor migration and invasion through epithelial-mesenchymal transition and closely interacts with ECM1 and NOVA1.BMC cancer · 2024Article
- Tumor immune microenvironment of colorectal cancer identifies novel prognostic signature and potential therapeutic drugs.Cancer biomarkers : section A of Disease markers · 2024Article
- Dual inhibition of the TrkA and JAK2 pathways using entrectinib and pacritinib suppresses the growth and metastasis of HER2-positive and triple-negative breast cancers.Cancer letters · 2024Article
- Pyrazolo[1,5-Molecules (Basel, Switzerland) · 2024Review
- Clinical characteristics and treatment patterns of patients withJournal of managed care & specialty pharmacy · 2024Article
- Prevalence of neurotrophic tropomyosin receptor kinase (NTRK) fusion gene positivity in patients with solid tumors in Japan.Cancer medicine · 2024Article
- Secretory Carcinoma of the Breast with Apocrine Differentiation-A Peculiar Entity.Medicina (Kaunas, Lithuania) · 2024Article
- Review
- The contribution of the nervous system in the cancer progression.BMB reports · 2024Review
20 more citing papers are in PubMed but not listed here.
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gene rearrangements resulting in the aberrant activity of tyrosine kinases have been identified as drivers of oncogenesis in a variety of cancers. The tropomyosin receptor kinase (TRK) family of tyrosine receptor kinases is emerging as an important target for cancer therapeutics. The TRK family contains three members, TRKA, TRKB, and TRKC, and these proteins are encoded by the genes NTRK1, NTRK2, and NTRK3, respectively. To activate TRK receptors, neurotrophins bind to the extracellular region stimulating dimerization, phosphorylation, and activation of downstream signaling pathways. Major known downstream pathways include RAS/MAPK/ERK, PLCγ, and PI3K/Akt. While being rare in most cancers, TRK fusions with other proteins have been well-established as oncogenic events in specific malignancies, including glioblastoma, papillary thyroid carcinoma, and secretory breast carcinomas. TRK protein amplification as well as alternative splicing events have also been described as contributors to cancer pathogenesis. For patients harboring alterations in TRK expression or activity, TRK inhibition emerges as an important therapeutic target. To date, multiple trials testing TRK-inhibiting compounds in various cancers are underway. In this review, we will summarize the current therapeutic trials for neoplasms involving NTKR gene alterations, as well as the promises and setbacks that are associated with targeting gene fusions.
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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.