Influence of chemotherapy on expression of TRAIL in primary acute leukemic cells.
- Author:
Yan-Fang LIU
1
;
Sheng-Mei CHEN
;
Hui SUN
;
Jian-Xi DONG
;
Qiu-Tang ZHANG
Author Information
1. Department of Hematology, The First Affiliated Hospital, Zhengzhou University, Zhenzhou 450052, China. yahfliu@yahoo.com.cn
- Publication Type:Journal Article
- MeSH:
Acute Disease;
Antineoplastic Agents;
pharmacology;
therapeutic use;
Bone Marrow Cells;
metabolism;
Etoposide;
pharmacology;
Humans;
Interferon-alpha;
pharmacology;
Leukemia;
drug therapy;
metabolism;
pathology;
TNF-Related Apoptosis-Inducing Ligand;
biosynthesis;
genetics;
Tumor Cells, Cultured
- From:
Journal of Experimental Hematology
2006;14(3):481-484
- CountryChina
- Language:Chinese
-
Abstract:
In order to explore the expression of TRAIL in primary acute leukemic cells and the effect of chemotherapeutic drug on TRAIL expression in acute leukemic cells, the expression of TRAIL was assessed by flow cytometry on day 0, day 1, day 3 and day 5 in 16 patients with acute leukemia received chemotherapy. Meanwhile, the bone marrow mononuclear cells of acute leukemia patients were cultured in vitro with VP-16 and INFalpha-2a. Expression of TRAIL was analyszed by flow cytometry at 24, 48 and 72 hours after treatment. The results showed that the expression of TRAIL in the peripheral blood mononuclear cells was upregulated significantly from day 1 after chemotherapy (P < 0.05). In in vitro culture test, VP-16 upregulated the expression of TRAIL on acute leukemia bone marrow mononuclear cells (P < 0.05). Compared with VP-16 alone, the combination of VP-16 with IFNalpha-2a showed no synergic effects on the expression of TRAIL. It is concluded that the expression of TRAIL increases after chemotherapy in vivo and after treatment with VP-16 and IFN in vitro, which suggests that the apoptosis induced by TRAIL may play an important role in chemotherapy of leukemia.
