Daniela CilloniSonia CarturanEnrico BraccoValentina CampiaValentina RossoDavide TortiChiara CalabreseValentina GaidanoPimjai NiparuckAlessandra FavoleElisabetta SignorinoIlaria IacobucciAnnalisa MoranoLuciana De LucaPellegrino MustoFrancesco FrassoniGiuseppe SaglioUniversita degli Studi di TorinoMahidol UniversityAlma Mater Studiorum Universita di BolognaIRCCS-CROB, Referral Cancer Center of BasilicataIRCCS Istituto Giannina Gaslini - Ospedale Pediatrico2018-10-192018-10-192013-05-01Leukemia Research. Vol.37, No.5 (2013), 520-53018735835014521262-s2.0-84875889772https://repository.li.mahidol.ac.th/handle/20.500.14594/31321Chronic 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.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyMedicineArticleSCOPUS10.1016/j.leukres.2013.01.014