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NTRK1, NTRK2, and NTRK3 code for the receptors TRKA, TRKB, and TRKC respectively. Each of the TRK receptors is activated by a different binding factor, which triggers phosphorylation of the proteins’ intracellular kinase domain, setting off various signaling pathways that ultimately lead to central and peripheral nervous system development1.

NTRK genes almost always become oncogenic through the same mechanism: the gene’s 3’ region fuses with the 5’ sequence of a partner gene, creating a chimeric fusion protein with a constitutively activated NTRK kinase domain. This leads to deregulated neural development – neuron growth, differentiation, proliferation, and apoptosis all fall into disarray, and important synaptic pathways are compromised1.

So far, NTRK fusions have been found to occur with around 90% frequency in a collection of relatively rare cancers (secretory breast carcinoma, mammary analogue secretory carcinoma, cellular or mixed congenital mesoblastic nephroma and infantile fibrosarcoma), and lower frequency in a variety of other malignancies (non-small cell lung cancer, colorectal carcinoma, and acute myeloid leukemia, to name a few). NTRK aberrations have also been implicated in certain neuronal disorders, including anhidrosis, epilepsy and depression1.

TRK proteins are receptor tyrosine kinases, like the clinically significant ALK gene, which allow them to be targeted by the same medications that are used in patients with ALK aberrations2. In 2017, the tyrosine kinase inhibitors entrectinib and larotrectinib were granted FDA breakthrough designation for the treatment of NTRK fusion-positive solid tumors3.

  1. Amatu, Alessio, Andrea Sartore-Bianchi, and Salvatore Siena. "NTRK gene fusions as novel targets of cancer therapy across multiple tumour types." ESMO open 1.2 (2016): e000023.
  2. Raez, Luis E., and Christian Rolfo. "Neurotrophic tyrosine kinase gene fusions: another opportunity for targeting in lung cancer." (2016): 1-4.
  3. Cocco, E., Scaltriti, M., & Drilon, A. (2018). NTRK fusion-positive cancers and TRK inhibitor therapy. Nature Reviews Clinical Oncology, 1.

NTRK1 Break Apart FISH Probe 1p23.1

Fusion partners for NTRK1 can include TPM3 and LMNA, both of which are associated with increased responsiveness to entrectinib.

  • Targeting NTRK fusion in non-small cell lung cancer: rationale and clinical evidence
    Ricciuti, B., Brambilla, M., Metro, G. et al. Med Oncol (2017) 34: 105 ,
  • Neurotrophic tyrosine kinase gene fusions: another opportunity for targeting in lung cancer
    Raez, L., Rolfo, C., Future Medicine (2016) 5: 1 ,
  • Sensitivity to Entrectinib Associated With a Novel LMNA-NTRK1 Gene Fusion in Metastatic Colorectal Cancer
    Sartore-Bianchi A., Ardini E., Bosotti R., et al.; Journal of the National Cancer Institute, (2016) Volume 108, Issue 1, 1, djv306 ,
NTRK2 Break Apart FISH Probe 9q21.33

NTRK2 fusions have been identified in brain tumors, low- grade glioma, and other cancers. Clinical implications are similar to those of NTRK1 and NTRK3

NTRK3 Break Apart FISH Probe 15q25.3

Empire Genomics’ NTRK3 break apart probe was used to study NTRK3 fusions in childhood melanocytic neoplasms

  • Identification of NTRK3 Fusions in Childhood Melanocytic Neoplasms
    Wang, L., Busam, K., Benayed, R., et al. The Journal of Molecular Diagnostics (2017) vol. 19: issue 3, pg 387-396 ,

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