Kinase fusion cell signaling pathways promote gene transcription, cell growth, proliferation, differentiation, and survival. These pathways also play a role in cellular metabolic regulation. Kinase fusions are abnormal genome alterations in tumor cells that result from the aberrant rearrangement of translocation of two genes, one of which encodes a protein kinase. 
Figure 1. Kinase fusions activate downstream cell signaling pathways such as MAP kinase signaling, JAK/STAT signaling, and PI3K/AKT1/MTOR signaling. Ultimately, the activation of downstream cell signaling pathways promotes gene transcription, cell growth, proliferation, differentiation, and survival.
BRAF, ABL1, BCR, ALK, and ROS1 are the most frequent biomarkers that serve as inclusion criteria in therapies targeting the kinase fusions pathway.
Biomarkers in the kinase fusions pathway serve as inclusion eligibility criteria in 537 clinical trials, of which 397 are open and 140 are closed. The genes ALK, BCR, BRAF, ROS1, and FGFR2 on this pathway most frequently harbor alterations that are inclusion eligibility criteria for clinical trials.
Of the trials that contain alteration(s) in the kinase fusions pathway as inclusion criteria, 6 are early phase 1 (5 open), 11 are n/a (10 open), 140 are phase 1 (84 open), 83 are phase 1/phase 2 (62 open), 236 are phase 2 (184 open), 8 are phase 2/phase 3 (7 open), 41 are phase 3 (34 open), and 9 are phase 4 (9 open) .