ROS1 was first reported as a potential driver oncogene in NSCLC in 2012. Patients with ROS1 rearrangements comprise approximately 1% to 3% of all NSCLC (5). Chromosomal rearrangement with a variety of partners leads to constitutive activation of ROS1, and the hybrid kinase is able to drive proliferation of oncogene-dependent cells (5). In addition to NSCLCs, ROS1 rearrangements are reported in glioblastoma, cholangiocarcinoma, gastric adenocarcinoma, ovarian serous tumors, inflammatory myofibroblastic tumors, and chronic myelomonocytic leukemia (7).
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