Myeloid-epithelial-reproductive tyrosine kinase, MERTK, is a receptor tyrosine kinase of the TAM (Tyro3, Axl and MERTK) family, expressed in numerous cancers¹.

The extracellular N-terminal domain contains two immunoglobulin-like and two fibronectin 3 domains, followed by a hydrophobic single pass transmembrane domain, and a cytoplasmic C-terminal tail containing a tyrosine kinase domain^1,2.

Auto-phosphorylation induced by ligand binding influences a range of downstream signaling pathways and cellular functions². The physiological roles of MERTK include regulation of tissue homeostasis and repair, innate immune control, and platelet aggregation. However, aberrant expression of this protein promotes neoplasia, cell cycle progression, proliferation and tumor growth, resistance to apoptosis, and promotion of tumor metastases.

MERTK is involved in the activation of several canonic oncogenic signaling pathways in various types of cancers including: leukemia, non-small cell lung cancer, glioblastoma, melanoma, prostate cancer, breast cancer, colon cancer and gastric cancer^1,3,4.

Due to its pivotal role in cancer development and metastasis, multiple therapeutic approaches are currently in development to inhibit MERTK, including ligand "traps" and small-molecule tyrosine kinase inhibitors⁴.