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6 patients with mesenchymal tumors composed of infiltrative fibroblastic/myofibroblastic tumor cells were studied. Using next-generation DNA sequencing, TMP3-NTRK1 fusions were identified in 4 cases, an LMNA-NTRK1 fusion in one case, and a variant EML4-NTRK3 fusion in one case.
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High expression of NTRK1 is closely associated with favorable risk factors and outcomes of patients with neuroblastoma (NB). The transcription of variants 1/2 is regulated by the NTRK1 P1 promoter region which is epigenetically regulated by EZH2- related histone modifications. Also, NTRK1 contributes to EZH2-regulated NB cell differentiation.
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recurrent gene fusions in RAF1, BRAF, and NTRK1/2 kinases suggest a distinct molecular tumor subtype with consistent S100 and CD34 immunoreactivity
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NTRK1 gene Rearrangement is associated with Metastatic Colorectal Cancer.
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NTRK1 might be associated with the development of nonsyndromic cleft lip with or without cleft palate.
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Two novel compound heterozygous variants of NTRK1 (c.632T > A and c.1253_1254delTC) were identified in a pair of Chinese identical twins with Congenital Insensitivity to Pain and Anhidrosis.
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The above results suggest that rutin preconditioning ameliorates cerebral I/R injury in OVX rats through ER-mediated BDNF-TrkB and NGF-TrkA signaling.
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The TrkA peptide is competitive for metal binding with analogous peptides due to the N-terminal domain of NGF. These data provide cues for future exploration of the effect of metal ions on the activity of the NGF and its specific cellular receptor.
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The LMNA-NTRK1 fusion was likely the molecular driver of tumorigenesis and metastasis in this patient, and the observed effectiveness of crizotinib treatment provides clinical validation of this molecular target.
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that lipofibromatosis-like tumour represents a novel entity of NTRK1-associated neoplasms
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System xC(-)-mediated TrkA activation therefore presents a promising target for therapeutic intervention in cancer pain treatment.
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Results identified two known splice-site mutations, one known nonsense mutation and one novel missense mutation in three congenital insensitivity to pain with anhidrosis (CIPA) pedigrees. These findings expanded the spectrum of the NTRK1 mutations associated with CIPA patients, provided additional clues for the phenotype-genotype relationship beneath CIPA.
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27 mutations in NTRK1 from Congenital insensitivity to pain with anhidrosis cohort, including 15 novel mutations, are reported.
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NTRK1 was upregulated in 80% of head and neck squamous carcinoma tissue.
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TRKA expression can be found in 1.6% of solid tumours and can be paralleled by NTRK1 gene rearrangements or mostly copy number gain
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Cleaved intracellular domain of CD271 controls proliferation, while the interaction of CD271 with the neurotrophin receptor Trk-A modulates cell adhesiveness through dynamic regulation of a set of cholesterol synthesis genes relevant for patient survival.
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These results suggest that polymorphisms in NTRK1 play an important role in pain sensitivity in young Han Chinese women
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We developed a comprehensive model of acquired resistance to NTRK inhibitors in cancer with NTRK1 rearrangement and identified cabozantinib as a therapeutic strategy to overcome the resistance
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TrkA plays an important role in the pathogenesis of NPM-ALK(+) T-cell lymphoma.
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Results show frequent BRCA2, EGFR, and NTRK1/2/3 mutations in mismatch repair-deficient colorectal cancers , sugggesting personalized medicine strategies to treat the patients with advanced disease who may have no remaining treatment options
