Mutation analysis of the c-mos proto-oncogene in human ovarian teratomas

被引:9
作者
de Foy, KAF
Gayther, SA
Colledge, WH
Crockett, S
Scott, IV
Evans, MJ
Ponder, BAJ
机构
[1] Addenbrookes Hosp, CRC, Human Canc Genet Res Grp, Cambridge CB2 2QQ, England
[2] Univ Cambridge, Physiol Lab, Cambridge CB2 3EG, England
[3] Derby City Gen Hosp, Dept Obstet & Gynaecol, Derby DE22 3NE, England
[4] Univ Cambridge, Dept Genet, Cambridge CB2 1QR, England
[5] Univ Cambridge, Wellcome CRC Inst, Cambridge CB2 1QR, England
基金
英国惠康基金;
关键词
c-mos; teratoma; ovary; parthenogenesis;
D O I
10.1038/bjc.1998.269
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Female transgenic mice lacking a functional c-mos proto-oncogene develop ovarian teratomas, indicating that c-mas may behave as a tumour-suppressor gene for this type of tumour. We have analysed the entire coding region of the c-MOS gene in a series of human ovarian teratomas to determine whether there are any cancer-causing alterations, DNA from twenty teratomas was analysed by single-strand conformational analysis (SSCA) and heteroduplex analysis (HA) to screen for somatic and germline mutations. In nine of these tumours the entire gene was also sequenced. A previously reported polymorphism and a single new sequence variant were identified. neither of which we would predict to be disease-causing alterations. These results suggest that mutations in the coding region of the c-MOS gene do not play a significant role in the genesis of human ovarian teratomas.
引用
收藏
页码:1642 / 1644
页数:3
相关论文
共 18 条
[1]   ACTIVATION OF THE TRANSFORMING POTENTIAL OF A NORMAL-CELL SEQUENCE - A MOLECULAR-MODEL FOR ONCOGENESIS [J].
BLAIR, DG ;
OSKARSSON, M ;
WOOD, TG ;
MCCLEMENTS, WL ;
FISCHINGER, PJ ;
VANDEWOUDE, GG .
SCIENCE, 1981, 212 (4497) :941-943
[2]   DISRUPTION OF C-MOS CAUSES PARTHENOGENETIC DEVELOPMENT OF UNFERTILIZED MOUSE EGGS [J].
COLLEDGE, WH ;
CARLTON, MBL ;
UDY, GB ;
EVANS, MJ .
NATURE, 1994, 370 (6484) :65-68
[3]   Mutation analysis of the c-mos proto-oncogene and the endothelin-B receptor gene in medullary thyroid carcinoma and phaeochromocytoma [J].
Eng, C ;
Foster, KA ;
Healey, CS ;
Houghton, C ;
Gayther, SA ;
Mulligan, LM ;
Ponder, BAJ .
BRITISH JOURNAL OF CANCER, 1996, 74 (03) :339-341
[4]  
FEFER A, 1967, CANCER RES, V27, P1626
[5]   OVARIAN TERATOMAS IN MICE LACKING THE PROTOONCOGENE C-MOS [J].
FURUTA, Y ;
SHIGETANI, Y ;
TAKEDA, N ;
IWASAKI, K ;
IKAWA, Y ;
AIZAWA, S .
JAPANESE JOURNAL OF CANCER RESEARCH, 1995, 86 (06) :540-545
[6]   GERMLINE MUTATIONS OF THE BRCA1 GENE IN BREAST AND OVARIAN-CANCER FAMILIES PROVIDE EVIDENCE FOR A GENOTYPE-PHENOTYPE CORRELATION [J].
GAYTHER, SA ;
WARREN, W ;
MAZOYER, S ;
RUSSELL, PA ;
HARRINGTON, PA ;
CHIANO, M ;
SEAL, S ;
HAMOUDI, R ;
VANRENSBURG, EJ ;
DUNNING, AM ;
LOVE, R ;
EVANS, G ;
EASTON, D ;
CLAYTON, D ;
STRATTON, MR ;
PONDER, BAJ .
NATURE GENETICS, 1995, 11 (04) :428-433
[7]   PARTHENOGENETIC ACTIVATION OF OOCYTES IN C-MOS-DEFICIENT MICE [J].
HASHIMOTO, N ;
WATANABE, N ;
FURUTA, Y ;
TAMEMOTO, H ;
SAGATA, N ;
YOKOYAMA, M ;
OKAZAKI, K ;
NAGAYOSHI, M ;
TAKEDA, N ;
IKAWA, Y ;
AIZAWA, S .
NATURE, 1994, 370 (6484) :68-71
[8]   DEGRADATION OF THE PROTOONCOGENE PRODUCT P39MOS IS NOT NECESSARY FOR CYCLIN PROTEOLYSIS AND EXIT FROM MEIOTIC METAPHASE - REQUIREMENT FOR A CA2+ CALMODULIN DEPENDENT EVENT [J].
LORCA, T ;
GALAS, S ;
FESQUET, D ;
DEVAULT, A ;
CAVADORE, JC ;
DOREE, M .
EMBO JOURNAL, 1991, 10 (08) :2087-2093
[9]  
MICHAEL H, 1993, OVARTAN CANC, P131
[10]  
MOLONEY JOHN B., 1966, NAT CANCER INST MONOGR, V22, P139