Clinical implications of aberrant TSG101 transcripts in acute myeloblastic leukemia

被引:10
作者
Lin, SF [1 ]
Lin, PM [1 ]
Liu, TC [1 ]
Chang, JG [1 ]
Sue, YC [1 ]
Chen, TP [1 ]
机构
[1] Kaohsiung Med Univ Hosp, Dept Internal Med, Div Hematol Oncol, Kaohsiung, Taiwan
关键词
TSG101; acute myeloid leukemia; aberrant transcripts; clinical implication;
D O I
10.3109/10428190009148393
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Tsg101 is a mouse tumor suppressor gene whose homozygous deletion produces transformation of NIH3T3 cells and leads to metastases in nude mice. The human homologue of the gene, TSG101, is localized in chromosome 11p15.1-p15.2. Reduced TSG101 expression may cause the defect of the cell cycle checkpoint that leads to genetic instability and consequently to the progression of neoplasia. Aberrant TSG101 transcript have been identified in many types of cancers, and the relaxation of RNA splicing fidelity may be an onco-developmental marker in cancers and could play a general role in tumorigenesis. In our previous study, smaller TSG101 transcripts were found in AML specimens, hematopoietic cell lines and normal controls. The aberrant transcripts occurred more frequently in the AML cases and cell lines. The patients with aberrant TSG101 transcripts had higher initial white cell count, lower LDH level, and lower complete remission rate after induction chemotherapy. However, further multivariate analysis of clinical data revealed that there was no relationship to the TSG101 aberrant transcripts. The clinical significance of TSG101 aberrant transcript in AML needs further evaluation.
引用
收藏
页码:463 / 466
页数:4
相关论文
共 25 条
[1]   REDUCTION TO HOMOZYGOSITY OF GENES ON CHROMOSOME-11 IN HUMAN-BREAST NEOPLASIA [J].
ALI, IU ;
LIDEREAU, R ;
THEILLET, C ;
CALLAHAN, R .
SCIENCE, 1987, 238 (4824) :185-188
[2]   CANCER - THE RISE OF THE GENETIC PARADIGM [J].
BISHOP, JM .
GENES & DEVELOPMENT, 1995, 9 (11) :1309-1315
[3]   Presence of a p53 gene deletion in patients with multiple myeloma predicts for short survival after conventional-dose chemotherapy [J].
Drach, J ;
Ackermann, J ;
Fritz, E ;
Krömer, E ;
Schuster, R ;
Gisslinger, H ;
DeSantis, M ;
Zojer, N ;
Fiegl, M ;
Roka, S ;
Schuster, J ;
Heinz, R ;
Ludwig, H ;
Huber, H .
BLOOD, 1998, 92 (03) :802-809
[4]   A GENETIC MODEL FOR COLORECTAL TUMORIGENESIS [J].
FEARON, ER ;
VOGELSTEIN, B .
CELL, 1990, 61 (05) :759-767
[5]   Expression of a new isoform of the tumor susceptibility TSG101 protein lacking a leucine zipper domain in Burkitt lymphoma cell lines [J].
Ferrer, M ;
López-Borges, S ;
Lazo, PA .
ONCOGENE, 1999, 18 (13) :2253-2259
[6]   Aberrant splicing of the TSG101 and FHIT genes occurs frequently in multiple malignancies and in normal tissues and mimics alterations previously described in tumours [J].
Gayther, SA ;
Barski, P ;
Batley, SJ ;
Li, LM ;
deFoy, KAF ;
Cohen, SN ;
Ponder, BAJ ;
Caldas, C .
ONCOGENE, 1997, 15 (17) :2119-2126
[7]   Evidence that TSG101 aberrant transcripts are PCR artifacts [J].
Hampl, M ;
Hampl, J ;
Plaschke, J ;
Fitze, G ;
Schackert, G ;
Saeger, HD ;
Schackert, HK .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1998, 248 (03) :753-760
[8]   TSG101 may be the prototype of a class of dominant negative ubiquitin regulators [J].
Koonin, EV ;
Abagyan, RA .
NATURE GENETICS, 1997, 16 (04) :330-331
[9]  
Ku WH, 1997, INT J CANCER, V72, P270, DOI 10.1002/(SICI)1097-0215(19970717)72:2<270::AID-IJC12>3.0.CO
[10]  
2-K