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The authors found a significant association between the localization of RET mutations and the expression of three genes: NNAT (suggested to be a tumour suppressor gene), CDC14B (involved in cell cycle control) and NTRK3 (tyrosine receptor kinase that undergoes rearrangement in papillary thyroid cancer) in patients with medullary thyroid cancer.
High TrkC mRNA expression appears to be frequent in the sonic hedgehog subgroup and seems not to have a major effect on therapy responsiveness in medulloblastoma patients.
Data show that neurotrophin 3 receptor TrkC acts as an activator in tumorigenicity and metastasis of colorectal cancer, and was frequently overexpressed in colorectal cancer (CRC) cells, patients' tumor samples.
LINC00052 could regulate NTRK3 expression by forming complementary base pairing with miR-128 and miR-485-3p to reduce the luciferase activity of NTRK3 3'UTR.
Case Reports: mammary analog secretory carcinoma of the thyroid gland with ETV6 rearrangement and ETV6-NTRK3 gene fusion.
The prevalence of ETV6-NTRK3 kinase fusions were determined in papillary thyroid cancer of adult population
We report the case of a patient with an initial diagnosis of salivary acinic cell carcinoma later reclassified as Mammary analogue secretory carcinoma after next-generation sequencing revealed an ETV6-NTRK3 fusion.
Data suggest that kinase domains of neurotrophin receptor isoforms, TRKA, TRKB, and TRKC, exhibit a bulky phenylalanine gatekeeper, leading to a small and unattractive back pocket/binding site for antineoplastic kinase inhibitors. [REVIEW]
Pan-Trk immunohistochemistry is a time-efficient and tissue-efficient screen for NTRK fusions, particularly in driver-negative advanced malignancies and potential cases of secretory carcinoma and congenital fibrosarcoma.
5 gastrointestinal stromal tumors cases lacking alterations in the KIT/PDGFRA/SDHx/RAS pathways, including two additional cases with FGFR1-TACC1 and ETV6-NTRK3 fusions, are reported.
NTRK fusions occur in a subset of young patients with mesenchymal or sarcoma-like tumors at a low frequency
High expression of TrkC is associated with glioblastoma.
Study found that copy number variations of NTRK3 were associated with platinum-sensitive and platinum-resistant recurrences. Amplification of NTRK3 perfectly predicted platinum-sensitive relapse of ovarian cancer.
we demonstrate the expression of the ETV6-NTRK3 fusion oncogene in a small subset of inflammatory myofibroblastic tumors
ETV6-NTRK3 translocated papillary thyroid carcinomas are locoregionally aggressive and can metastasize distantly.
We report 6 cases of secretory carcinomas of the skin harboring the ETV6-NTRK3 gene fusion
ETV6-NTRK3, MYO5A-NTRK3 and MYH9-NTRK3 fusions are identified in Spitz tumours and demonstrated that NTRK3 fusions constitutively activate the mitogen-activated protein kinase, phosphoinositide 3-kinase and phospholipase Cgamma1 pathways in melanocytes.
A subset of ALK-negative inflammatory myofibroblastic tumour (IMT) have rearrangement of ROS1, ETV6 or NTRK3 as a possible oncogenic mechanism.
TrkC-miR2 as a novel regulator of Wnt signaling, which might be a candidate oncogenic colorectal cancer biomarker.
High expression of TrkA, TrkB, or TrkC was significantly associated with histopathology
TrkC signals to the podocyte actin cytoskeleton to induce migration by phosphorylating WAVE2 Erk dependently. This signaling mechanism may be important for TrkC-mediated cytoskeletal dynamics in podocyte disease.
In a retinitis pigmentosa mouse model, TrkC activity generates phosphorylated Erk, which upregulates glial TNF-alpha, causing selective neuronal death.
our data suggest that Runx3 may play a crucial role in the development of DRGs by regulating the expression of Ntrk3 variants
adult homozygous TrkAC knock-in mice displayed severe deficits in acute and tissue injury-induced pain, representing the first viable adult Trk mouse mutant with a pain phenotype
TrkC expression in E13.5 VCG neurons requires NeuroD and that TrkC expression may be necessary for the normal migration and innervations of those neurons.
The dependence receptor TrkC interacts with Cobra1.TrkC killer fragment shuttles with Cobra1 to the mitochondria to engage apoptosis.
ETV6-SAM domain interface mutations block ETV6-NTRK3-induced cellular transformation
This study demonistrated that NTRK3 plays a role in panic disorder by regulating hippocampus-dependent fear memories.
Despite elimination of TrkC mRNA, no differences in development of kindling were detected between TrkC conditional null and wild type control mice.
find that both IRS1 and kinase active IGF1R are required for ETV6-NTRK3 transformation, that tyrosine phosphorylated IRS1 is present in high molecular weight complexes with EN and IGF1R, and that EN colocalizes with IGF1R at the plasma membrane
Data describe the distribution and changes of TrkB and TrkC in the dopamine neurons of the substantia nigra by comparison of control and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) Parkinson disease mouse model.
Data suggest that postsynaptic TrkC trans interaction with presynaptic PTPsigma generates bidirectional adhesion and recruitment essential for excitatory synapse development and positions these signaling molecules at the center of synaptic pathways.
Dok6 selectively binds to the NPQY motif of TrkC through its phosphotyrosine-binding (PTB) domain in a kinase activity-dependent manner.
TrkA and TrkC instruct developing neurons to die, both in vitro and in vivo. By contrast, TrkB, a closely related receptor primarily expressed in the central nervous system, does not.
Transgenic mice overexpressing TrkC present susceptibility in their response to stress characterized by subtle changes in the HPA axis, marked changes in acute stress-induced brain activation and altered coping strategies.
Data suggest that Runx3 is required for the specification of TrkC-expressing trigeminal ganglion neurons, conveying mechanoreceptive signals from the Merkel cells of the whisker vibrissae to the spinal trigeminal nucleus pars interpolaris.
TrkC is expressed in the mouse cochlear nucleus by around post-natal day 8 and peaks around d30. TrkC immunostain was cytoplasmic.
both trkA and trkC neurotropin receptors influence germ cell numbers during testis development and events such as seminiferous cord formation
role of both full-length and truncated isoforms of trkC in Merkel innervation
trkC detected in lung homogenate, on the surface of interstitial macrophages, but not in alveolar macrophages; a previously unknown trafficking signal occurs through neurotrophins in peripheral lung
This gene encodes a member of the neurotrophic tyrosine receptor kinase (NTRK) family. This kinase is a membrane-bound receptor that, upon neurotrophin binding, phosphorylates itself and members of the MAPK pathway. Signalling through this kinase leads to cell differentiation and may play a role in the development of proprioceptive neurons that sense body position. Mutations in this gene have been associated with medulloblastomas, secretory breast carcinomas and other cancers. Several transcript variants encoding different isoforms have been found for this gene.
ETS related protein-neurotrophic receptor tyrosine kinase fusion protein
, ETV6-NTRK3 fusion
, NT-3 growth factor receptor
, tyrosine kinase receptor C
, neural receptor protein-tyrosine kinase (trkC)
, trkC tyrosine kinase
, neurotrophic tyrosine kinase receptor type 3
, tyrosine kinase C receptor, TrkC receptor, high-affinity neurotrophin receptor
, neurotrophic tyrosine kinase, receptor, type 3
, NT-3 growth factor receptor-like