c‐myc over‐expression in human primary ovarian tumours: Its relevance to tumour progression

Abstract

Expression of the c-myc gene was analyzed in 56 human primary ovarian cancer tissues, including 51 common epithelial and 5 non-epithelial tumours to determine molecular events in the carcinogenic process in ovaries. Over-expression of the c-myc gene was found in 37.3% of all ovarian tumour tissues, and in 63.5% of serous adenocarcinoma tissues. Significant over-expression of the c-myc gene at Stage III compared with other stages, and one remarkable case of over-expression in a serous tumour of low malignant potential suggest that c-myc expression is temporarily activated at some stage(s) during tumorigenesis of ovarian cancer, especially of serous tumours.

Mutation of the nm23 gene, loss of heterozygosity at the nm23 locus and K-ras mutation in ovarian carcinoma: correlation with tumour progression and nm23 gene expression

“…In Japan, ovarian carcinoma is less common than in other Western countries (Tashiro et al, 1992) and allelic loss on chromosome 17 of Japanese ovarian cancer (Sato et al, 1991) is about half as frequent compared with other studies (Jacobs et al, 1993;Phillips et al, 1993). In the present study LOH at the nm23 locus was observed in 23.8% of informative cases.…”

The Notch pathway in ovarian carcinomas and adenomas

“…It is likely, however, that Notch alone is not capable of transforming cells but requires the functional collaboration of other oncogenes, namely from the RAS (IRK, MAP kinase, PI3 kinase) (Fitzgerald et al, 2000;Weijzen et al, 2002) and c-Myc pathways (Rao and Kadesch, 2003). PI3K (Philp et al, 2001) and c-Myc (Tashiro et al, 1992) overexpression have been reported for ovarian adenocarcinomas.…”

“…Loss of function mutations of tumour suppressor genes have been described such as p53 in late stage tumours (Kupryjanczyk et al, 1993), PTEN in endometroid ovarian carcinomas (Obata et al, 1998), BRCA1 and BRCA2 in familial ovarian cancers (Ford et al, 1998;Kote-Jarai and Eeles, 1999). Overexpression or amplification of oncogenes have been described for PI3K (Philp et al, 2001) and its downstream effector AKT2 (Cheng et al, 1992), EGF-R (Kohler et al, 1989), cMyc (Tashiro et al, 1992), K-ras (Enomoto et al, 1991) and c-erbB (HER2/neu) (Slamon et al, 1989). In a recent study we demonstrated that p73, a member of the p53 family, is expressed in ovarian adenocarcinoma but rarely in adenoma (Zwahlen et al, 2000).…”

Establishment of an immortalised human ovarian surface epithelial cell line without chromosomal instability

“…In epithelial ovarian carcinoma, numerous studies have revealed different patterns of genetic change. These include activation of oncogenes (K-ras, HER-2, Src, c-myc, AKT2, PIK3CA and STK/BTAK) through amplification, translocation, or mutation (Slamon et al, 1989;Enomoto et al, 1991;Tashiro et al, 1992;Bellacosa et al, 1995;Zhou et al, 1998;Shayesteh et al, 1999;Wiener et al, 2003), as well as inactivation of tumour suppressor genes (p53, PTEN, WT1, BRCA 1, NOEY2 and WWOX) through homozygous deletion, double mutations, or a combination of mutation and loss of heterozygosity or promotor methylation (Fujita et al, 1995;Obata et al, 1998;Yu et al, 1999;Schorge et al, 2000;Paige et al, 2001;McCoy et al, 2003). Although such genetic changes have long been identified using ovarian carcinoma tissues or cell lines, the early molecular changes in ovarian carcinogenesis have not been fully clarified.…”