Expression of midkine in patients with acute myeloid leukemia and its significance.
- Author:
Lin YANG
1
;
Zuo-Ren DONG
;
Ling PAN
;
Jian-Min LUO
;
Shi-Rong XU
Author Information
1. Department of Hematology, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, China.
- Publication Type:Journal Article
- MeSH:
Adolescent;
Adult;
Apoptosis;
physiology;
Bone Marrow Cells;
metabolism;
Cytokines;
biosynthesis;
genetics;
Female;
Humans;
Leukemia, Myeloid, Acute;
metabolism;
Leukocytes, Mononuclear;
metabolism;
Male;
Middle Aged;
Prognosis;
RNA, Messenger;
biosynthesis;
genetics
- From:
Journal of Experimental Hematology
2006;14(3):442-445
- CountryChina
- Language:Chinese
-
Abstract:
The study was aimed to investigate the expression of midkine (MK) in bone marrow mononuclear cells (BM MNC) from 65 acute myeloid leukemia patients and 15 normal controls. The method of RT-PCR was used to examine the expression of MK mRNA in BM MNC. Parts of samples were incubated for 24 hours and the gene expression of MK in the BM MNC was detected by means of Western blot. The results showed that the expression of MK of BM MNCs in 50 newly diagnosed AML patients (0.331 +/- 0.436) and 15 AML patients in relapse (0.374 +/- 0.463) were markedly higher than that in 15 CR cases (0.067 +/- 0.190), and 15 normal controls (0), respectively. The complete remission in MK positive patients (63.16%) was significantly lower than that in MK negative group (93.55%). The patients with positive MK expression had a higher relapse rate than those with negative MK expression. The positive rate of MK gene expression in drug-resistant patients and drug-sensitive patients were 57.69% and 25.64% respectively and there was positive correlation between the gene expressions of MK and bcl-2 (P < 0.01) (r = 0.0556, P < 0.001). It is concluded that MK can be secreted by AML cells and involved in drug-resistant, its positive expression may be associated with the poor prognosis in newly diagnosed AML patients. The inhibitory effect of MK on apoptosis of leukemic cells is induced by upregulating bcl-2 expression.
