PU.1 expression is restored upon treatment of chronic myeloid leukemia patients

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 seve...

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Veröffentlicht in:	Cancer letters 2008-11, Vol.270 (2), p.328-336
Hauptverfasser:	Albajar, Marta, Gutierrez, Pilar, Richard, Carlos, Rosa-Garrido, Manuel, Gómez-Casares, M. Teresa, Steegmann, Juan L, León, Javier, Delgado, M. Dolores
Format:	Artikel
Sprache:	eng
Schlagworte:	Adult Aged Aged, 80 and over Animals Antineoplastic Agents - therapeutic use Benzamides Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Bone marrow CML patients Disease Female Fusion Proteins, bcr-abl - genetics Fusion Proteins, bcr-abl - metabolism Gene expression Gene Expression Regulation, Leukemic - drug effects Hematology, Oncology and Palliative Medicine Humans Imatinib Imatinib Mesylate Interferon Interferon-alpha - therapeutic use Interferon-α K562 Cells Kinases Leukemia Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism Male Mice Middle Aged Mutation Myeloid Cells - metabolism Patients Piperazines - therapeutic use Plasmids Polycythemia Vera - genetics Polycythemia Vera - metabolism Protein Kinase Inhibitors - therapeutic use Proteins Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism PU.1 Pyrimidines - therapeutic use Recombinant Proteins RNA Interference RNA, Messenger - metabolism RNA, Small Interfering - metabolism Rodents Thrombocythemia, Essential - genetics Thrombocythemia, Essential - metabolism Trans-Activators - genetics Trans-Activators - metabolism Transcription factors Transfection Treatment Outcome
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Zusammenfassung:	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.
ISSN:	0304-3835 1872-7980
DOI:	10.1016/j.canlet.2008.05.024