Correlation of C/EBPα expression with response and resistance to imatinib in chronic myeloid leukaemia.
Jpn J Clin Oncol
; 45(8): 749-54, 2015 Aug.
Article
em En
| MEDLINE
| ID: mdl-25920395
ABSTRACT
OBJECTIVE:
Altered differentiation is a common feature of haematopoietic malignancies with poor prognosis. CAAT/enhancer binding protein alpha (C/EBPα) is a key transcription factor that regulates myeloid differentiation. This study is aimed to know the prognostic value of CAAT/enhancer binding protein alpha expression and correlate its expression with response to imatinib therapy.METHODS:
We quantified the expression of C/EBPα gene in 126 chronic myeloid leukaemia samples (82 from newly diagnosed and 44 from imatinib-resistant patients) and 20 control samples. C/EBPα mRNA level was measured by real-time quantitative polymerase chain reaction using the ΔΔCT method.RESULTS:
C/EBPα expression level was significantly lower in the imatinib-resistant group than in the pretreatment and control group (P = 0.0398). Low CAAT/enhancer binding protein alpha levels in the imatinib-resistant group were significantly associated with advanced phase (P = 0.04), with more peripheral blasts (P = 0.0001), high BCR-ABL levels (P = 0.018) and T315I and P-loop mutations (P = 0.0002). In the pretreatment group, low expression showed association with high EUTOS risk score (P = 0.03) and possible partial cytogenetic response (P = 0.010).CONCLUSIONS:
Our results suggest that low expression of CAAT/enhancer binding protein alpha might have a role in the response to imatinib and progression of disease in patients with chronic myeloid leukaemia.Palavras-chave
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Piperazinas
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Pirimidinas
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Benzamidas
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Leucemia Mielogênica Crônica BCR-ABL Positiva
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Resistencia a Medicamentos Antineoplásicos
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Proteína alfa Estimuladora de Ligação a CCAAT
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Antineoplásicos
Tipo de estudo:
Prognostic_studies
Limite:
Adult
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Aged
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Jpn J Clin Oncol
Ano de publicação:
2015
Tipo de documento:
Article