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

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

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)520-530
Number of pages11
JournalLeukemia Research
Issue number5
Publication statusPublished - May 2013


  • Chronic myeloproliferative neoplasms
  • CMML
  • Molecular target
  • Proliferation
  • ROS1
  • Tyrosine kinase

ASJC Scopus subject areas

  • Cancer Research
  • Hematology
  • Oncology


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