Aberrant activation of ROS1 represents a new molecular defect in chronic myelomonocytic leukemia

• Main Authors: Daniela Cilloni, Sonia Carturan, Enrico Bracco, Valentina Campia, Valentina Rosso, Davide Torti, Chiara Calabrese, Valentina Gaidano, Pimjai Niparuck, Alessandra Favole, Elisabetta Signorino, Ilaria Iacobucci, Annalisa Morano, Luciana De Luca, Pellegrino Musto, Francesco Frassoni, Giuseppe Saglio
• Other Authors: Universita degli Studi di Torino
• Format: Article
• Published: 2018
• Subjects: Biochemistry, Genetics and Molecular Biology; Medicine
• Online Access: https://repository.li.mahidol.ac.th/handle/123456789/31321
• Institution: Mahidol University

Chronic myelomonocytic leukemia (CMML) is a clonal disorder sharing features of myelodysplastic syndromes and chronic myeloproliferative neoplasms. Although rare chromosomal aberrations and point mutations are reported in CMML, the molecular defects underlying CMML are largely unknown. ROS1 encodes a tyrosine kinase that is abnormally expressed and translocated in brain and lung cancers. In this study we show that ROS1 is abnormally activated in the CD34+ compartment of approximately 70% of CMML patients resulting in the activation of the Erk/Akt pathways through the Grb2/SOS complex thus revealing a central oncogenic role for ROS1 in CMML which might represent a molecular target. © 2013 Elsevier Ltd.