BIRC6/Apollon gene expression in childhood acute leukemia: impact on therapeutic response and prognosis.
Autor: | Ismail EA; Clinical Pathology Department, Ain Shams University, Cairo, Egypt., Mahmoud HM, Tawfik LM, Habashy DM, Adly AA, El-Sherif NH, Abdelwahab MA |
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Jazyk: | angličtina |
Zdroj: | European journal of haematology [Eur J Haematol] 2012 Feb; Vol. 88 (2), pp. 118-27. Date of Electronic Publication: 2012 Jan 04. |
DOI: | 10.1111/j.1600-0609.2011.01734.x |
Abstrakt: | Objective: Although BIRC6/Apollon seems to play a critical role as an antiapoptotic regulator, its clinical relevance in acute leukemia remains largely elusive. Therefore, we aimed to investigate BIRC6 gene expression in childhood acute leukemia in relation to clinicopathological characteristics at presentation, therapeutic response, and prognosis. Methods: BIRC6 expression level was assessed in 75 children with acute leukemia; 30 patients with acute myeloblastic leukemia (AML) and 45 patients with acute lymphoblastic leukemia (ALL) using real-time quantitative reverse transcriptase-polymerase chain reaction. Results: The median level of BIRC6 expression did not differ significantly between AML and ALL patients. BIRC6 expression level was higher in patients with AML and ALL with extramedullary involvement, white blood cell (WBC) count ≥ 10 × 10(9) /L, and unfavorable cytogenetics at diagnosis. BIRC6 gene expression was higher in patients with unfavorable response to therapy at day 14, those who developed relapse or died in both leukemic groups. The best cutoff value of BIRC6 to predict therapeutic response and disease outcome was determined. AML and ALL patients with BIRC6 overexpression had significantly shorter overall and disease free survivals. Conclusions: This is the first report to study BIRC6 gene in pediatric ALL. Our results suggested that BIRC6 gene expression could be considered as an adverse risk factor in childhood acute leukemia and, hence, could be used to guide therapeutic regimens. (© 2012 John Wiley & Sons A/S.) |
Databáze: | MEDLINE |
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