Cancer-driving mutations are found across a wide range of tumor types yet are often only present in a subset of tumor cells, making early detection and subsequent treatment difficult. Many cancer types are driven by the signaling pathways downstream of tyrosine kinase receptors such as Akt, Ras, and Stat. Previously developed therapeutics targeting specific kinases have been highly profitable, yet resistance often occurs due to alternative methods of activating tumor dependent downstream pathways. Inhibitors of the Tropomyosin Kinase Receptors (TRK) family encoded by NTRK genes, are currently used for treating tumors with Trk gene fusions but have limitations due to tumor resistance. Hutch investigators have discovered a novel splice variant of the tyrosine receptor kinase B (TrkB) protein, TrkB.T1, that is highly expressed across nearly all human cancers when compared to normal. Using a highly specific novel antibody they developed against this isoform, their in vitro and in-vivo data demonstrate that this TrkB isoform has a causal role in the development of many types of cancers, and that its forced expression drives multiple tumor types in mice. Therefore, TrkB.T1 provides a useful validated target for cancer therapeutics, as well as represents a biomarker for the detection and observation of a variety of cancers.
Use of their novel antibody as a rapid cancer diagnostic from blood or urine
Discovery of small molecule binders for diagnostics and therapeutics Development of cell therapies against these targets
Quicker and less invasive diagnostics for a variety of cancers
Improved efficacy over commercial TRK receptor targeted therapies
The market for cancer therapeutics is expected to reach 181 billion USD by 2026, and the global market for cancer diagnostics is expected to reach 249 billion by 2026.
Eric Holland, M.D., Ph.D; Senior VP and Director; Human Biology Division