Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Previous Page Next Page

Oncogenic gene fusions involving the neurotrophic tyrosine receptor kinase (NTRKoccur in numerous adult and paediatric tumour types [1-4], and have thus emerged as a promising therapeutic target across several tumour histologies [1]. The estimated frequency of NTRK gene fusions varies between tumour types ranging from a prevalence of >90% in some rare cancers (secretory carcinoma of the breast and salivary glands and infantile fibrosarcoma) to <1% in more common cancer types (click here to learn more about the epidemiology of NTRK gene fusions) [1-3]. The protein product of NTRK gene fusions (referred to as a tropomyosin receptor kinase [TRK] fusion protein) is constitutively active and results in cell growth, proliferation and survival pathway activation [1, 3, 4].


  1. Amatu A, Sartore-Bianchi A, Siena S. NTRK gene fusions as novel targets of cancer therapy across multiple tumour types. ESMO Open 2016; 1: e000023.
  2. Stransky N, Cerami E, Schalm S et al. The landscape of kinase fusions in cancer. Nat Commun 2014; 5: 4846.
  3. Cocco E, Scaltriti M, Drilon A. NTRK fusion-positive cancers and TRK inhibitor therapy. Nat Rev Clin Oncol 2018; 15: 731-747.
  4. Vaishnavi A, Le AT, Doebele RC. TRKing down an old oncogene in a new era of targeted therapy. Cancer Discov 2015; 5: 25-34.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings