程序性细胞死亡5基因在急性和慢性髓系白血病中的异常表达。

Abnormal expression of the programmed cell death 5 gene in acute and chronic myeloid leukemia.

作者信息

Ruan Guo-Rui, Qin Ya-Zhen, Chen Shan-Shan, Li Jin-Lan, Ma Xi, Chang Yan, Wang Ya-Zhe, Fu Jia-Yu, Liu Yan-Rong

机构信息

Institute of Hematology and People's Hospital, Peking University, 11 Xi-zhi-men South Street, Beijing 100044, China.

出版信息

Leuk Res. 2006 Sep;30(9):1159-65. doi: 10.1016/j.leukres.2005.12.028. Epub 2006 Feb 28.

DOI:10.1016/j.leukres.2005.12.028

PMID:16507320

Abstract

To clarify whether expression of the programmed cell death 5 (PDCD5) gene in leukemic cells is abnormal, real-time quantitative reverse transcription polymerase chain reaction (RQ-RT-PCR) was used to examine its expression in marrow cells from leukemia patients. We found lower PDCD5 in both AML and CML marrow cells than in normal donor marrow cells. A negative correlation was found between relative levels of PDCD5 and BCR/ABL expression in all CML patients and in CML patients in the advanced phase. Treatment with the ABL tyrosine kinase inhibitor Imatinib mesylate increased PDCD5 expression in K562 and MEG-01 cells. These findings suggest that abnormal expression of PDCD5 in leukemia may be involved in the pathomechanism of AML and CML.

摘要

为明确白血病细胞中程序性细胞死亡5（PDCD5）基因的表达是否异常，采用实时定量逆转录聚合酶链反应（RQ-RT-PCR）检测白血病患者骨髓细胞中该基因的表达。我们发现，急性髓系白血病（AML）和慢性髓系白血病（CML）骨髓细胞中的PDCD5水平均低于正常供体骨髓细胞。在所有CML患者及晚期CML患者中，PDCD5相对水平与BCR/ABL表达之间呈负相关。用ABL酪氨酸激酶抑制剂甲磺酸伊马替尼治疗可增加K562和MEG-01细胞中PDCD5的表达。这些发现提示，白血病中PDCD5的异常表达可能参与了AML和CML的发病机制。