Ocean with island above the surface and octopus submerged below, suggesting that there’s more to some cancers than meets the eye
THERE’S MORE TO SOME CANCERS THAN MEETS THE EYE

What's Driving The Tumor?

Actionable alterations may be present in many tumors1,2

30% to 49%
of patients who undergo tumor genomic profiling may have an actionable alteration1,2

TRK* fusion proteins are often a primary oncogenic driver
across multiple tumor types3,4

NTRK gene fusions are oncogenic drivers caused by genomic rearrangement
NTRK gene fusions are oncogenic drivers caused by genomic rearrangement
NTRK gene fusions are oncogenic drivers caused by genomic rearrangement
Image for illustrative purposes only.
  • In TRK fusion cancer, the NTRK a gene fuses with an unrelated gene, causing overexpression of the TRK fusion protein3,5-7
  • Research has identified NTRK gene fusions in more than 2 dozen types of common and rare solid tumors3-5,7
  • TRK fusion proteins may be mutually exclusive of other oncogenic drivers8

Specific tests can uncover
TRK fusion cancer

Next-generation SequencingNext-generation sequencing (NGS)3,6,9,10
ImmunohistochemistryPan-TRK immunohistochemistry assays (IHC)11
DNA fluorescence in situ hybridizationDNA fluorescence in situ hybridization (FISH)9,10,12
Reverse transcription polymerase chain reactionReverse transcription polymerase chain reaction (RT-PCR)9,13
ADD NTRK  GENE FUSION TO YOUR TESTING PROTOCOL

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*TRK, tropomyosin receptor kinase.
aNTRK, neurotrophic receptor tyrosine kinase.

References: 1. Massard C, Michiels S, Ferte C, et al. High-throughput genomics and clinical outcome in hard-to-treat advanced cancers: results of the MOSCATO 01 trial. Cancer Discov. 2017;7(6):586-595. 2. Boland GM, Piha-Paul SA, Subbiah V, et al. Clinical next generation sequencing to identify actionable aberrations in a phase I program. Oncotarget. 2015;6(24):20099-20110. 3. Vaishnavi A, Le AT, Doebele RC. Cancer Discov. 2015;5(1):25-34. 4. Okimoto RA, Bivona TG. Tracking down response and resistance to TRK inhibitors. Cancer Discov. 2016;6(1):14-16. 5. Amatu A, Sartore-Bianchi A, Siena S. ESMO Open. 2016;1(2):e000023. 6. Kumar-Sinha C, Kalyana-Sundaram S, Chinnaiyan AM. Landscape of gene fusions in epithelial cancers: seq and ye shall find. Genome Med. 2015;7:129. doi:10.1186/s13073-015-0252-1. 7. Lange AM, Lo H-W. Inhibiting TRK proteins in clinical cancer therapy. Cancers. 2018;10(4):E105. doi:10.3390/cancers10040105. 8. Stransky N, Cerami E, Schalm S, Lim JL, Lengauer C. The landscape of kinase fusions in cancer. Nat Commun. 2014;5:4846. doi:10.1038/ncomms5846. 9. Abel HJ, Al-Kateb H, Cottrell CE, et al. Detection of gene rearrangements in targeted clinical next-generation sequencing. J Mol Diagn. 2014;16(4):405-417. 10. Rogers T-M, Arnau GM, Ryland GL, et al. Multiplexed transcriptome analysis to detect ALK, ROS1 and RET rearrangements in lung cancer. Sci Rep. 2017;7:42259. doi:10.1038/srep42259. 11. Hechtman JF, Benayed R, Hyman DM, 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. 12. Yan L, Zhang W. Precision medicine becomes reality—tumor type-agnostic therapy. Cancer Commun. 2018;38(1):6. doi:10.1186/s40880-018-0274-3. 13. Vendrell JA, Taviaux S, Béganton B, et al. Detection of known and novel ALK fusion transcripts in lung cancer patients using next-generation sequencing approaches. Sci Rep. 2017;7(1):12510. doi:10.1038/s41598-017-12679-8.