PTEN/MMAC1/TEP1 involvement in primary prostate cancers

被引:112
作者
Pesche, S
Latil, A
Muzeau, F
Cussenot, O
Fournier, G
Longy, M
Eng, C
Lidereau, R
机构
[1] Ctr Rene Huguenin, Lab Oncogenet, F-92211 St Cloud, France
[2] CHU St Louis, Dept Urol, F-75010 Paris, France
[3] Hop Cavale Blanche, Dept Urol, F-29609 Brest, France
[4] Ctr Reg Lutte Canc, Inst Bergonie, F-33076 Bordeaux, France
[5] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA
[6] Univ Cambridge, CRC, Human Canc Genet Res Grp, Cambridge CB2 2QQ, England
关键词
prostate cancer; chromosome arm 10q; LOH; PTEN;
D O I
10.1038/sj.onc.1202081
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The PTEN/MMAC1/TEP1 gene, located at 10q23.3, is a tumor suppressor gene responsible for the familial cancer syndromes Cowden disease and Bannayan-Zonana syndrome, and is commonly somatically mutated in several types of cancers. Mutations of the PTEN gene have been found in prostate cancer cell lines and LOH at 10q22-24 in prostate tumors have also been described with a high frequency. To determine the role of this gene in prostate tumorigenesis, we therefore analysed 22 primary tumors for loss of heterozygosity (LOH) within the 10q22-23 region such that tumors hemizygous at those loci may be examined for somatic PTEN mutations. Losses of heterozygosity of at least one locus was found in 12 (55%) of the 22 tumors DNAs. Among these, six tumors exhibited allele loss in the interval between D10S1765 and D10S541 wherein lies the PTEN gene. We searched the entire coding region of PTEN for somatic mutations in these six tumors. One somatic mutation (17%), a 1 bp deletion, was detected in exon 7 of the gene, in ode tumor, indicating that somatic mutations of the PTEN gene may occur in primary prostate tumors.
引用
收藏
页码:2879 / 2883
页数:5
相关论文
共 48 条
[1]  
ALBRECHT S, 1992, CANCER-AM CANCER SOC, V70, P869, DOI 10.1002/1097-0142(19920815)70:4<869::AID-CNCR2820700424>3.0.CO
[2]  
2-E
[3]   DELETION MAPPING OF CHROMOSOME-8, CHROMOSOME-10, AND CHROMOSOME-16 IN HUMAN PROSTATIC-CARCINOMA [J].
BERGERHEIM, USR ;
KUNIMI, K ;
COLLINS, VP ;
EKMAN, P .
GENES CHROMOSOMES & CANCER, 1991, 3 (03) :215-220
[4]  
BOVA GS, 1993, CANCER RES, V53, P3869
[5]  
CAIRNS P, 1994, CANCER RES, V54, P1422
[6]  
Cairns P, 1997, CANCER RES, V57, P4997
[7]   Frequent loss of heterozygosity on chromosome 10q in muscle-invasive transitional cell carcinomas of the bladder [J].
Cappellen, D ;
deMedina, SGD ;
Chopin, D ;
Thiery, JP ;
Radvanyi, F .
ONCOGENE, 1997, 14 (25) :3059-3066
[8]   ALLELIC LOSS OF CHROMOSOME-16Q AND CHROMOSOME-10Q IN HUMAN PROSTATE-CANCER [J].
CARTER, BS ;
EWING, CM ;
WARD, WS ;
TREIGER, BF ;
AALDERS, TW ;
SCHALKEN, JA ;
EPSTEIN, JI ;
ISAACS, WB .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (22) :8751-8755
[9]   INTEGRINS AND SIGNAL-TRANSDUCTION PATHWAYS - THE ROAD TAKEN [J].
CLARK, EA ;
BRUGGE, JS .
SCIENCE, 1995, 268 (5208) :233-239
[10]  
Cooney KA, 1996, CANCER RES, V56, P1142