The hypereosinophilic syndrome: fluorescence in situ hybridization detects the del(4)(q12)-FIP1L1/PDGFRA but not genomic rearrangements of other tyrosine kinases.

@article{Starza2005TheHS,
  title={The hypereosinophilic syndrome: fluorescence in situ hybridization detects the del(4)(q12)-FIP1L1/PDGFRA but not genomic rearrangements of other tyrosine kinases.},
  author={Roberta La Starza and Giorgina Specchia and Antonio Cuneo and Donatella Beacci and Chiara Nozzoli and Luigiana Luciano and Anna M Avent{\'i}n and Constantina Sambani and Nicoletta Testoni and Marco Foppoli and Rosangela Invernizzi and Peter Marynen and Massimo Fabrizio Martelli and Cristina Mecucci},
  journal={Haematologica},
  year={2005},
  volume={90 5},
  pages={
          596-601
        }
}
BACKGROUND AND OBJECTIVES According to WHO criteria, the idiopathic hypereosinophilic syndrome (HES) is defined as persistent eosinophilia (>1.5x10(9)/L) without underlying causes, which is associated with signs or symptoms of organ involvement. Increased bone marrow blasts (>5%) or cytogenetic/genetic markers indicate chronic eosinophilic leukemia (CEL). A cryptic deletion of 4q12, i.e. del(4)(q12), producing the FIP1L1/PDGFRA fusion gene, identifies a distinct CEL subgroup (4q-/CEL). Our aims… CONTINUE READING

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