Expression of SCL gene in bone marrow stromal cells from patients with leukemia.
- Author:
Zhen WANG
1
;
Yang-Qiu LI
;
Xiu-Li WU
;
Li-Jian YANG
;
Shao-Hua CHENG
;
Huan ZHANG
;
Kang-Er ZHU
;
Zhong-Chao HAN
Author Information
1. Institute of Hematology, Medical College, Jinan University, Guangzhou 510632, China.
- Publication Type:Journal Article
- MeSH:
Adolescent;
Adult;
Basic Helix-Loop-Helix Transcription Factors;
Bone Marrow Cells;
metabolism;
Child;
Child, Preschool;
DNA-Binding Proteins;
genetics;
Female;
Gene Expression;
Humans;
Infant;
Leukemia;
metabolism;
Male;
Proto-Oncogene Proteins;
genetics;
Stromal Cells;
metabolism;
T-Cell Acute Lymphocytic Leukemia Protein 1;
Transcription Factors;
genetics
- From:
Journal of Experimental Hematology
2004;12(1):39-43
- CountryChina
- Language:Chinese
-
Abstract:
In order to investigate expression of SCL (stem cell leukemia) gene in bone marrow stromal cells (BMSC) and bone marrow cells from patients with leukemia and normal individuals, bone marrow mononuclear cells from AML (18 cases), CML (17 cases), ALL (7 cases) and normal individuals (33 cases) were cultured long-term in vitro. Nonadherent cells (hematopoietic cells) and amplified adherent cells (BMSC) were collected respectively. RT-PCR-ELISA assay was then performed to detect expression of SCL gene. The expression ratio of SCL gene were analyzed and its expression level was normalized by beta(2)M gene acting as an internal reference for the purpose of semi-quantitative analysis. The results indicated that the expression ratio of SCL gene was lower in BMSC from AML (27.8%) and CML (11.8%) than that in normal controls (69.7%, P < 0.05), while was higher in the nonadherent cells from CML (64.3%) than that in its corresponding BMSC (P < 0.05). Semi-quantitative analysis showed that SCL gene expression level in nonadherent cells from AML was higher than that in its corresponding BMSC (P < 0.05). In conclusion, the low-level expression state of SCL gene in BMSC from patients with AML and CML may be involved in the abnormal regulation of hematopoiesis in myelocytic leukemia.
