PU.1 expression is restored upon treatment of chronic myeloid leukemia patients.
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-alpha 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-alpha 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.
Albajar
Marta
M
Departamento de Biología Molecular and Instituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Universidad de Cantabria-CSIC-IDICAN, Facultad de Medicina, 39011 Santander, Spain.
Gutierrez
Pilar
P
Richard
Carlos
C
Rosa-Garrido
Manuel
M
Gómez-Casares
M Teresa
MT
Steegmann
Juan L
JL
León
Javier
J
Delgado
M Dolores
MD
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D000970:Antineoplastic Agents; D001549:Benzamides; D014408:Biomarkers, Tumor; D016044:Fusion Proteins, bcr-abl; D000068877:Imatinib Mesylate; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D010879:Piperazines; D047428:Protein Kinase Inhibitors; D011518:Proto-Oncogene Proteins; D011743:Pyrimidines; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D011994:Recombinant Proteins; D015534:Trans-Activators; D000099232:Proto-Oncogene Protein Spi-1