Absence of FGFR3–TACC3 rearrangement in hematological malignancies with numerical chromosomal alteration

Hematology/Oncology and Stem Cell Therapy

E. Fabiani¹  M. Ginevrino²  M. Divona²  P. Curzi³  P. Panetta³  G. Falconi⁴  C. Banella⁴  G. Catalano⁵  N.I. Noguera⁶  M.T. Voso⁶ 

[1] Deparment of Molecular Medicine, University of Pavia, Pavia, Italy;Department of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy;Department of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy;Neuro-oncohematology Unit, IRCCS Santa Lucia Foundation, Rome, Italy;Neurogenetics Unit, IRCCS Santa Lucia Foundation, Rome, Italy;Policlinico Tor Vergata, Rome, Italy;

关键词: Acute myeloid leukemia;    Aneuploidy;    FGFR3–TACC3;    Glioblastoma;    Myelodysplastic syndromes;   

DOI  :  

来源: DOAJ

【 摘 要 】

FGFR–TACC, found in different tumor types, is characterized by the fusion of a member of fibroblast grown factor receptor (FGFR) tyrosine kinase (TK) family to a member of the transforming acidic coiled-coil (TACC) proteins. Because chromosome numerical alterations, hallmarks of FGFR–TACC fusions are present in many hematological disorders and there are no data on the prevalence, we studied a series of patients with acute myeloid leukemia and myelodysplastic syndrome who presented numerical alterations using cytogenetic traditional analysis. None of the analyzed samples showed FGFR3–TACC3 gene fusion, so screening for this mutation at diagnosis is not recommended.

【 授权许可】

Unknown