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

被引:81
作者
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
[1] Peking Univ, Inst Hematol, Beijing 100044, Peoples R China
[2] Peking Univ, Peoples Hosp, Beijing 100044, Peoples R China
[3] Peking Univ, Sch Basic Med, Dept Immunol, Ctr Human Dis Genom, Beijing 100083, Peoples R China
基金
中国国家自然科学基金;
关键词
acute myeloid leukemia (AML); chronic myeloid leukemia (CML); programmed cell death 5 (PDCD5); real-time quantitative reverse transcription; polymerase chain reaction (RQ-RT-PCR); apoptosis; imatinib mesylate;
D O I
10.1016/j.leukres.2005.12.028
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
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. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1159 / 1165
页数:7
相关论文
共 18 条
[1]
BCR-ABL-MEDIATED INHIBITION OF APOPTOSIS WITH DELAY OF G2/M TRANSITION AFTER DNA-DAMAGE - A MECHANISM OF RESISTANCE TO MULTIPLE ANTICANCER AGENTS [J].
BEDI, A ;
BARBER, JP ;
BEDI, GC ;
ELDEIRY, WS ;
SIDRANSKY, D ;
VALA, MS ;
AKHTAR, AJ ;
HILTON, J ;
JONES, RJ .
BLOOD, 1995, 86 (03) :1148-1158
[2]
Evaluation of candidate control genes for diagnosis and residual disease detection in leukemic patients using 'real-time' quantitative reverse-transcriptase polymerase chain reaction (RQ-PCR) - a Europe against cancer program [J].
Beillard, E ;
Pallisgaard, N ;
van der Velden, VHJ ;
Bi, W ;
Dee, R ;
van der Schoot, E ;
Delabesse, E ;
Macintyre, E ;
Gottardi, E ;
Saglio, G ;
Watzinger, F ;
Lion, T ;
van Dongen, JJM ;
Hokland, P ;
Gabert, J .
LEUKEMIA, 2003, 17 (12) :2474-2486
[3]
The biology of CML blast crisis [J].
Calabretta, B ;
Perrotti, D .
BLOOD, 2004, 103 (11) :4010-4022
[4]
Nuclear translocation of PDCD5 (TFAR19): an early signal for apoptosis? [J].
Chen, YY ;
Sun, RH ;
Han, WL ;
Zhang, YM ;
Song, QS ;
Di, CH ;
Ma, DL .
FEBS LETTERS, 2001, 509 (02) :191-196
[5]
Bcr/Abl activates transcription of the Bcl-X gene through STAT5 [J].
Gesbert, F ;
Griffin, JD .
BLOOD, 2000, 96 (06) :2269-2276
[6]
Bcl-2 and c-myc expression, cell cycle kinetics and apoptosis during the progression of chronic myelogenous leukemia from diagnosis to blastic phase [J].
Handa, H ;
Hegde, UP ;
Kotelnikov, VM ;
Mundle, SD ;
Dong, LM ;
Burke, P ;
Rose, S ;
Gaskin, F ;
Raza, A ;
Preisler, HD .
LEUKEMIA RESEARCH, 1997, 21 (06) :479-489
[7]
Gene-expression profiles in hereditary breast cancer. [J].
Hedenfalk, I ;
Duggan, D ;
Chen, YD ;
Radmacher, M ;
Bittner, M ;
Simon, R ;
Meltzer, P ;
Gusterson, B ;
Esteller, M ;
Kallioniemi, OP ;
Wilfond, B ;
Borg, Å ;
Trent, J ;
Raffeld, M ;
Yakhini, Z ;
Ben-Dor, A ;
Dougherty, E ;
Kononen, J ;
Bubendorf, L ;
Fehrle, W ;
Pittaluga, S ;
Gruvberger, S ;
Loman, N ;
Johannsoson, O ;
Olsson, H ;
Sauter, G .
NEW ENGLAND JOURNAL OF MEDICINE, 2001, 344 (08) :539-548
[8]
TFAR19, a novel apoptosis-related gene cloned from human leukemia cell line TF-1, could enhance apoptosis of some tumor cells induced by growth factor withdrawal [J].
Liu, HT ;
Wang, YG ;
Zhang, YM ;
Song, QS ;
Di, CH ;
Chen, GH ;
Tang, J ;
Ma, DL .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1999, 254 (01) :203-210
[9]
Moriai R, 2001, ANTICANCER RES, V21, P595
[10]
Ravandi F, 2001, CANCER-AM CANCER SOC, V91, P1964, DOI 10.1002/1097-0142(20010601)91:11<1964::AID-CNCR1221>3.0.CO