ArticleCancer letters2016
Entrectinib is a potent inhibitor of Trk-driven neuroblastomas in a xenograft mouse model.
Article in Cancer letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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.
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Who cites it
46 citing papers in PubMed, 86 citations in OpenAlex.
- Brain-derived neurotrophic factor in solid tumor angiogenesis and neurovascular-immune interactions (Review).Oncology letters · 2026Review
- Entrectinib attenuates LPS-induced neuroinflammation by inhibiting JNK, p38, and AKT pathways and ameliorates cognitive impairment.Archives of pharmacal research · 2026Article
- Multi-tyrosine kinase inhibitors: exploring immunomodulatory effects on various immune cell types in cancer.Cancer cell international · 2026Review
- High-throughput transcriptomic screening reveals entrectinib as a repositioning opportunity in 19q12 autism spectrum disorder.Scientific reports · 2025Article
- Optimal Control in Combination Therapy for Heterogeneous Cell Populations with Drug Synergies.Bulletin of mathematical biology · 2025Article
- diaPASEF-Powered Chemoproteomics Enables Deep Kinome Interaction Profiling.Journal of proteome research · 2025Article
- Advancements in neuroblastoma treatment: FDA-approved drugs and role of phytochemicals.Molecular biology reports · 2025Review
- A novel TRKB-activating internal tandem duplication characterizes a new mechanism of receptor tyrosine kinase activation.NPJ precision oncology · 2025Article
- Molecular crosstalk between GPCR and receptor tyrosine-protein kinase in neuroblastoma: molecular mechanism and therapeutic implications.Medical oncology (Northwood, London, England) · 2025Review
- Emerging clinical and research approaches in targeted therapies for high-risk neuroblastoma.Frontiers in oncology · 2025Review
- Targeting NTRK1 Enhances Immune Checkpoint Inhibitor Efficacy in NTRK1 Wild-Type Non-Small Cell Lung Cancer.Cancer research · 2024Article
- Review
- Narrative review: precision medicine applications in neuroblastoma-current status and future prospects.Translational pediatrics · 2024Review
- ALK inhibitors increase ALK expression and sensitize neuroblastoma cells to ALK.CAR-T cells.Cancer cell · 2023Article
- Targeted Therapies in Advanced Cholangiocarcinoma.Life (Basel, Switzerland) · 2023Review
- Review
- Tropomyosin receptor kinase B (TrkB) signalling: targeted therapy in neurogenic tumours.The journal of pathology. Clinical research · 2023Review
- Drugging Hijacked Kinase Pathways in Pediatric Oncology: Opportunities and Current Scenario.Pharmaceutics · 2023Review
- Article
- Research Progress on Small Molecules Inhibitors Targeting TRK Kinases.Current medicinal chemistry · 2023Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Neuroblastoma (NB) is one of the most common and deadly childhood solid tumors. These tumors are characterized by clinical heterogeneity, from spontaneous regression to relentless progression, and the Trk family of neurotrophin receptors plays an important role in this heterogeneous behavior. We wanted to determine if entrectinib (RXDX-101, Ignyta, Inc.), an oral Pan-Trk, Alk and Ros1 inhibitor, was effective in our NB model. In vitro effects of entrectinib, either as a single agent or in combination with the chemotherapeutic agents Irinotecan (Irino) and Temozolomide (TMZ), were studied on an SH-SY5Y cell line stably transfected with TrkB. In vivo growth inhibition activity was studied in NB xenografts, again as a single agent or in combination with Irino-TMZ. Entrectinib significantly inhibited the growth of TrkB-expressing NB cells in vitro, and it significantly enhanced the growth inhibition of Irino-TMZ when used in combination. Single agent therapy resulted in significant tumor growth inhibition in animals treated with entrectinib compared to control animals [p < 0.0001 for event-free survival (EFS)]. Addition of entrectinib to Irino-TMZ also significantly improved the EFS of animals compared to vehicle or Irino-TMZ treated animals [p < 0.0001 for combination vs. control, p = 0.0012 for combination vs. Irino-TMZ]. We show that entrectinib inhibits growth of TrkB expressing NB cells in vitro and in vivo, and that it enhances the efficacy of conventional chemotherapy in in vivo models. Our data suggest that entrectinib is a potent Trk inhibitor and should be tested in clinical trials for NBs and other Trk-expressing tumors.
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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.