Author/Authors :
Albajar، نويسنده , , Marta and Gutiérrez، نويسنده , , Pilar and Richard، نويسنده , , Carlos and Rosa-Garrido، نويسنده , , Manuel and Gَmez-Casares، نويسنده , , M. Teresa and Steegmann، نويسنده , , Juan L. and Leَn، نويسنده , , Javier and Delgado، نويسنده , , M. Dolores، نويسنده ,
Abstract :
The PU.1 transcription factor is a crucial regulator of hematopoiesis which expression is altered in various leukemic processes. Our previous work in chronic myeloid leukemia (CML) cells demonstrated that interferon-α upregulated PU.1 expression. Here we show that expression of PU.1 is severely impaired in patients with CML at diagnosis. However, the PU.1 suppression is abrogated in patients in remission, after interferon-α or imatinib treatment. These effects are not found in patients with other myeloproliferative diseases such as polycythemia vera or essential thrombocythemia. PU.1 could, therefore, be used as an additional marker of the response to the treatment of the CML.
Keywords :
PU.1 , CML patients , interferon-? , Imatinib
