Cancer Types

TRK Fusion Cancer

Some cancers are caused by specific changes in genes. Genes carry instructions for proteins in cells and an abnormal change to the genes can lead to an alteration of the proteins, which can cause uncontrolled cell growth and formation of a  cancerous tumor.

One type of genetically-driven cancer is called tropomyosin receptor kinase (TRK) fusion cancer.

Neurotrophic tyrosine receptor kinase (NTRK) genes provide instructions for TRK proteins. When an NTRK gene joins or “fuses” with an unrelated gene, it starts to produce an altered TRK fusion protein. This TRK fusion protein becomes active and causes a cancerous tumor to grow.


What makes this cancer unique?

TRK fusion cancer is a very unique and rare disease and is defined by this specific gene alteration. The cancer is not related to a certain type of tissue or the age of the patient; it can occur anywhere in the body, in both children and in adults.


How can TRK fusion cancer be diagnosed?

Only specific genomic tests can detect NTRK gene fusions, the underlying cause of TRK fusion cancer. By testing patients and finding out what is driving their cancer, doctors could target the root of the disease. It is important that high-quality genomic testing that looks for actionable targets becomes part of routine clinical practice so patients have the chance to benefit from therapies that selectively inhibit the oncogenic driver that causes their cancer.


download (4)


With emerging research on TRK fusion cancer, we are one step closer to precision medicine, where tumor genetics, rather than where the tumor is in the body, help doctors select specific treatment approaches that could more likely benefit their patients.



1 Vaishnavi A, et al. TRKing down an old oncogene in a new era of targeted therapy. Cancer Discov. 2015;5(1):25-34.

2  Amatu A, et al.  ESMO Open. 2016;1(2):e000023.

3  Kumar-Sinha C, et al. Landscape of gene fusions in epithelial cancers: seq and ye shall find. Genome Med. 2015;7:129. doi:10.1186/s13073-015- 0252-1.

4 Okimoto RA, Bivona TG. Tracking Down Response and Resistance to TRK Inhibitors. Cancer Discov. 2016;6(1):14-16.

5 Bishop JA, et al. Mammary Analog Secretory Carcinoma of Salivary Glands. Hum Pathol. 2013;44:1982-1988.

6 Krings G, et al. Genomic profiling of breast secretory carcinomas reveals distinct genetics from other breast cancers and similarity to mammary analog secretory carcinomas. Mod Pathol. 2017;30:1086–99.

7 Yoshihara K, et al. The landscape and therapeutic relevance of cancer-associated transcript fusions. Oncogene. 2015; 34(37):4845-4854.

8 Ross JS, et al. New routes to targeted therapy of intrahepatic cholangiocarcinomas revealed by next-generation sequencing. Oncologist. 2014;19:235-242.

Vaishnavi A, et al. Oncogenic and drug sensitive NTRK1 rearrangements in lung cancer. Nat Med.2013;19(11):1469-1472.

10 Shi E, et al. FGFR1 and NTRK3 actionable alterations in “Wild-Type” gastrointestinal stromal tumors. J Transl Med. 2016 Dec 14;14(1):339.

11 Gatalica Z, et al. Molecular characterization of cancers with NTRK gene fusions. Mod Pathol. 2019;32(1):147-153.

12 Okamura, et al. Analysis of NTRK Alterations in Pan-Cancer Adult and Pediatric Malignancies: Implications for NTRK-Targeted Therapeutics. JCO Precision Oncology. 2018 :2, 1-20.

13 Bourgeois JM, et al. Molecular detection of the ETV6-NTRK3 gene fusion differentiates congenital fibrosarcoma from other childhood spindle cell tumors. Am J Surg Pathol. 2000;24(7):937-946.

14 Rubin BP, et al. Congenital Mesoblastic Nephroma t(12;15) Is Associated with ETV6-NTRK3 Gene Fusion. Am J Pathol. 1998;153:1451-1458.

15 Tognon C, et al. Expression of the ETV6-NTRK3 gene fusion as a primary event in human secretory breast carcinoma. Cancer Cell. 2002;2:367-376.

16 Argani P, et al. Detection of the ETV6-NTRK3 Chimeric RNA of Infantile Fibrosarcoma/Cellular Congenital Mesoblastic Nephroma in Paraffin-Embedded Tissue: Application to Challenging Pediatric Renal Stromal Tumors. Mod Pathol. 2000;13:29-36.

17 Wu G, et al. The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma. Nat Genet. 2014;46:444-450.

18 Abel HJ, et al. Detection of gene rearrangements in targeted clinical next-generation sequencing. J Mol Diagn. 2014;16(4):405-417.

19 Rogers T-M, et al. Sci Rep. 2017;7:42259. doi:10.1038/srep42259.

20 Hechtman JF, et al. Pan-trk immunohistochemistry is an efficient and reliable screen for the detection of NTRK fusions. Am J Surg Pathol. 2017;41(11):1547-1551.

21 Weier HU, et al. Rapid physical mapping of the human trk protooncogene (NTRK1) to human chromosome 1q21-q

22 by P1 clone selection, fluorescence in situ hybridization (FISH), and computer-assisted microscopy. Genomics 1995;26:390–3. doi:10.1016/0888-7543(95)80226-C.