title: Expression of c-fos correlates with IFN-alpha responsiveness in Philadelphia chromosome positive chronic myelogenous leukemia.
abstract: This study evaluates (i) constitutive levels of oncogene and p53 transcripts in chronic phase CML patients and (ii) their modulations subsequent to in vivo therapy with rIFN-alpha 2c. Peripheral blood mononuclear cells (pbmc) and bone marrow cells of 26 patients were examined for c-fos, c-myc, p53 and the hybrid bcr/abl mRNA levels. Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive mRNA levels of the hybrid bcr/abl, c-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of c-fos and downregulation of c-myc mRNA levels in responder patients.
authors.affiliation: Department of Internal Medicine, University Hospital Innsbruck, Austria.
authors.forename: B
authors.initials: B
authors.lastname: Eibl
authors.forename: E
authors.initials: E
authors.lastname: Greiter
authors.forename: K
authors.initials: K
authors.lastname: Grünewald
authors.forename: G
authors.initials: G
authors.lastname: Gastl
authors.forename: K
authors.initials: K
authors.lastname: Weyrer
authors.forename: J
authors.initials: J
authors.lastname: Thaler
authors.forename: W
authors.initials: W
authors.lastname: Aulitzky
authors.forename: F
authors.initials: F
authors.lastname: Herrmann
authors.forename: U
authors.initials: U
authors.lastname: Rapp
authors.forename: C
authors.initials: C
authors.lastname: Huber
mesh_terms: D001854:Bone Marrow Cells / Q000378:metabolism / Q000473:pathology; D016044:Fusion Proteins, bcr-abl / Q000096:biosynthesis; D006801:Humans; D007370:Interferon Type I / Q000009:adverse effects / Q000627:therapeutic use*; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000097:blood / Q000473:pathology / Q000628:therapy*; D007958:Leukocyte Count; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D009857:Oncogenes; D010976:Platelet Count; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis*; D016271:Proto-Oncogene Proteins c-myc / Q000096:biosynthesis; D012333:RNA, Messenger / Q000096:biosynthesis; D011994:Recombinant Proteins; D012307:Risk Factors; D014158:Transcription, Genetic; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis
chemical_list: D007370:Interferon Type I; D016760:Proto-Oncogene Proteins c-fos; D016271:Proto-Oncogene Proteins c-myc; D012333:RNA, Messenger; D011994:Recombinant Proteins; D016159:Tumor Suppressor Protein p53; D016044:Fusion Proteins, bcr-abl