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Low expression of interferon regulatory factor-1 and identification of novel exons skipping in patients with chronic myeloid leukaemia.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Tzoanopoulos, Dimitrios Speletas, Matthaios Arvanitidis, Konstantinos Veiopoulou, Christina Kyriaki, Sofia Thyphronitis, George Sideras, Paschalis Kartalis, Georgios N. Ritis, Konstantinos |
| Copyright Year | 2002 |
| Abstract | Chronic myeloid leukaemia (CML) is a malignant clonal disorder of the haematopoietic stem cell. Treatment of CML patients with interferon alpha (IFN-alpha) has induced haematological and cytogenetic remission. Interferons transcriptionally activate target genes through the JAK-STAT and interferon regulated factors (IRFs) family pathways. Interferon regulated factor-1 (IRF-1) is a transcriptional activator of genes critical for cell growth, differentiation and apoptosis. The skipping of exons 2 or 2 and 3 of IRF-1 in patients with myelodysplastic syndromes and acute myelogenous leukaemia suggests that this factor may have a critical role in leukaemogenesis. The role of IRF-1 in CML is currently unknown. Therefore, mutational analysis of IRF-1 was performed and its expression pattern was also studied in CML patients. We studied IRF-1 in peripheral blood mononuclear cells of 21 patients in chronic phase CML. No point mutations were identified at the cDNA level. Surprisingly, fourfold reduction of full-length IRF-1 mRNA expression was established in 17/21 patients compared with normal individuals. Low expression of full-length IRF-1 was observed in conjunction with high levels of aberrantly spliced mRNAs, reported for the first time. In three patients who were also analysed during blastic transformation, further reduction of full-length IRF-1 mRNA was observed. These findings demonstrate that, in CML patients, IRF-1 can produce high levels of aberrant spliced mRNAs with subsequent reduction in the levels of full-length IRF-1 mRNA. This observation is consistent with the notion that exon skipping may constitute another mechanism of tumour suppressor gene inactivation in this disease. |
| Starting Page | 46 |
| Ending Page | 53 |
| Page Count | 8 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://www.inflathrace.gr/sites/default/files/31.%20Low%20expression%20of%20interferon%20regulatory%20factor-1%20and%20identification%20of%20novel%20exons%20skipping%20in%20patients.pdf |
| PubMed reference number | 12358902v1 |
| Volume Number | 119 |
| Issue Number | 1 |
| Journal | British journal of haematology |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Apoptosis Blast Phase Chronic Lymphocytic Leukemia Clone DNA, Complementary Exons Hematopoietic System IRF1 gene Interferon Alfa-2a Interferon-alpha Leukemia, Myelocytic, Acute Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative MYELODYSPLASTIC SYNDROME Myeloid Leukemia Myeloid Leukemia, Chronic Patients Recombinant Interferon Stem cells Transcription Coactivator Transcription, Genetic |
| Content Type | Text |
| Resource Type | Article |
