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 698 clinical trials, of which 476 are open and 222 are closed. The genes ALK, BRAF, BCR, 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, 10 are early phase 1 (6 open), 11 are n/a (7 open), 171 are phase 1 (89 open), 109 are phase 1/phase 2 (81 open), 321 are phase 2 (234 open), 7 are phase 2/phase 3 (4 open), 55 are phase 3 (44 open), and 10 are phase 4 (9 open) .