ReviewCancers2020
Roles of TrkC Signaling in the Regulation of Tumorigenicity and Metastasis of Cancer.
Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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
25 citing papers in PubMed, 44 citations in OpenAlex.
- Epigenetic Regulation of Trk Receptors and Neurotrophic Signalling in Neuroblastoma: Mechanisms, Plasticity, and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Integrated transcriptomic and immune-associated network analysis of breast cancer patient-derived organoids reveals candidate inflammatory biomarkers.Frontiers in bioengineering and biotechnology · 2026Article
- TrkA Expression as a Novel Prognostic Biomarker in Oral Squamous Cell Carcinoma.International journal of molecular sciences · 2025Article
- The Effects of Concurrent Training on Molecular, Functional, and Clinical Outcomes in Breast Cancer Survivors: A Pilot Study.Cancers · 2025Article
- 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
- TrkC protects against osteoarthritis progression by maintaining articular cartilage homeostasis.International journal of biological sciences · 2025Article
- Targeting PYK2, entrectinib allays anterior subcapsular cataracts in mice by regulating TGFβ2 signaling pathway.Molecular medicine (Cambridge, Mass.) · 2024Article
- The oncogenic fusion protein EML4-NTRK3 requires three salt bridges for stability and biological activity.Heliyon · 2024Article
- NTRK3 exhibits a pro-oncogenic function in upper tract urothelial carcinomas.The Kaohsiung journal of medical sciences · 2024Article
- Article
- The nerve cells in gastrointestinal cancers: from molecular mechanisms to clinical intervention.Oncogene · 2024Review
- Multimodal deep learning to predict prognosis in adult and pediatric brain tumors.Communications medicine · 2023Article
- Tropomyosin receptor kinase B (TrkB) signalling: targeted therapy in neurogenic tumours.The journal of pathology. Clinical research · 2023Review
- Review
- Optimizing Patient Pathways in Advanced Biliary Tract Cancers: Recent Advances and a French Perspective.Targeted oncology · 2023Review
- Downregulation of MMP1 functions in preventing perineural invasion of pancreatic cancer through blocking the NT-3/TrkC signaling pathway.Journal of clinical laboratory analysis · 2022Article
- Antibody-dependent cellular phagocytosis of tropomyosin receptor kinase C (TrkC) expressing cancer cells for targeted immunotherapy.Cancer immunology, immunotherapy : CII · 2022Article
- Whole-exome sequencing identified mutational profiles of urothelial carcinoma post kidney transplantation.Journal of translational medicine · 2022Article
- Novel Design of RNA Aptamers as Cancer Inhibitors and Diagnosis Targeting the Tyrosine Kinase Domain of the NT-3 Growth Factor Receptor Using a Computational Sequence-Based Approach.Molecules (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tropomyosin receptor kinase (Trk) C contributes to the clinicopathology of a variety of human cancers, and new chimeric oncoproteins containing the tyrosine kinase domain of TrkC occur after fusion to the partner genes. Overexpression of TrkC and TrkC fusion proteins was observed in patients with a variety of cancers, including mesenchymal, hematopoietic, and those of epithelial cell lineage. Both microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) were involved in the regulation of TrkC expression through transcriptional and posttranscriptional alteration. Aberrant activation of TrkC and TrkC fusion proteins markedly induces the epithelial-mesenchymal transition (EMT) program, growth rate, tumorigenic capacity via constitutive activation of Ras-MAP kinase (MAPK), PI3K-AKT, and the JAK2-STAT3 pathway. The clinical trial of TrkC or TrkC fusion-positive cancers with newly developed Trk inhibitors demonstrated that Trk inhibitors were highly effective in inducing tumor regression in patients who do not harbor mutations in the kinase domain. Recently, there has been a progressive accumulation of mutations in TrkC or the TrkC fusion protein detected in the clinic and its related cancer cell lines caused by high-throughput DNA sequencing. Despite given the high overall response rate against Trk or Trk fusion proteins-positive solid tumors, acquired drug resistance was observed in patients with various cancers caused by mutations in the Trk kinase domain. To overcome acquired resistance caused by kinase domain mutation, next-generation Trk inhibitors have been developed, and these inhibitors are currently under investigation in clinical trials.
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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.