title: 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-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.
authors.affiliation: Departamento de Biología Molecular and Instituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Universidad de Cantabria-CSIC-IDICAN, Facultad de Medicina, 39011 Santander, Spain.
authors.forename: Marta
authors.initials: M
authors.lastname: Albajar
authors.forename: Pilar
authors.initials: P
authors.lastname: Gutierrez
authors.forename: Carlos
authors.initials: C
authors.lastname: Richard
authors.forename: Manuel
authors.initials: M
authors.lastname: Rosa-Garrido
authors.forename: M Teresa
authors.initials: MT
authors.lastname: Gómez-Casares
authors.forename: Juan L
authors.initials: JL
authors.lastname: Steegmann
authors.forename: Javier
authors.initials: J
authors.lastname: León
authors.forename: M Dolores
authors.initials: MD
authors.lastname: Delgado
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001549:Benzamides; D014408:Biomarkers, Tumor / Q000235:genetics / Q000378:metabolism*; D005260:Female; D016044:Fusion Proteins, bcr-abl / Q000235:genetics / Q000378:metabolism; D015973:Gene Expression Regulation, Leukemic / Q000187:drug effects; D006801:Humans; D000068877:Imatinib Mesylate; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D020014:K562 Cells; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008875:Middle Aged; D022423:Myeloid Cells / Q000378:metabolism; D010879:Piperazines / Q000627:therapeutic use*; D011087:Polycythemia Vera / Q000235:genetics / Q000378:metabolism; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism*; D011743:Pyrimidines / Q000627:therapeutic use*; D034622:RNA Interference; D012333:RNA, Messenger / Q000378:metabolism; D034741:RNA, Small Interfering / Q000378:metabolism; D011994:Recombinant Proteins; D013920:Thrombocythemia, Essential / Q000235:genetics / Q000378:metabolism; D015534:Trans-Activators / Q000235:genetics / Q000378:metabolism*; D014162:Transfection; D016896:Treatment Outcome; D000099232:Proto-Oncogene Protein Spi-1
chemical_list: 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