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Journal of Leukemia & Lymphoma ; (12): 733-738, 2016.
Artigo em Chinês | WPRIM | ID: wpr-506813

RESUMO

Objective To investigate the expression of SOX4 and C/EBPα mRNA in chronic myeloid leukemia (CML) and their clinical significances. Methods Bone marrow samples from 68 cases of CML including 57 newly diagnosed patients and 11 patients treated with imatinib were collected, and peripheral blood mononuclear cells from 30 healthy people were collected as healthy control. The expression of SOX4 and C/EBPαmRNA and protein levels were detected by RT-PCR and Western blot, respectively. The relations between the expression of SOX4 and C/EBPα and the influences of imatinib on SOX4 and C/EBPα were analyzed. Results The expression level of SOX4 mRNA was increased in newly diagnosed CML patients compared with that of normal control group (6.545 5±1.495 2 vs. 0.059 6±0.018 8, t=3.139, P=0.002 3), but the expression level of C/EBPαmRNA was significantly decreased (0.238 8±0.033 8 vs. 0.810 5±0.056 2, t=9.240, P0.05). The expression level of SOX4 mRNA in 5 patients treated with imatinib was decreased (0.120 6 ±0.044 9 vs. 0.557 9±0.144 8, t=2.885, P=0.020 4), and the expression level of C/EBPαmRNA was increased (0.330 3±0.042 4 vs. 0.150 5±0.046 5, t=2.855, P=0.021 3). The expression level of SOX4 mRNA in 6 patients who developed blast phase during the treatment of imatinib was increased (0.469 9±0.123 0 vs. 0.050 2±0.036 6, t=2.370, P=0.039 3), and the expression level of C/EBPα mRNA was decreased (0.197 9 ±0.064 7 vs. 0.378 7±0.042 9, t=2.327, P=0.042 3). The expression of SOX4 mRNA was negatively correlated with C/EBPα mRNA (t=-0.554 6, P=0.002 8). Conclusions In newly diagnosed CML, the expression level of SOX4 is increased, C/EBPα is decreased compared with that of healthy control, and both have negative correlation. In the patients in blast phase after imatinib treatment, SOX4 gene is up-regulated, and C/EBPα is down-regulated. C/EBPα-SOX4 axis may play a role in the occurrence and development of CML. SOX4 may be a new molecular target for the treatment of CML.

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