Chromosomal localisation of two putative 11p oncosuppressor genes involved in human ovarian tumours

Chromosome 11 allele imbalance and clinicopathological correlates in ovarian tumours

“…Frequent LOH has been demonstrated at 1 lpl5 (Lee et al, 1989;Ehlen and Dubeau, 1990;Eccles et al, 1992a;Gallion et al, 1992;Vandamme et al, 1992;Viel et al, 1992;Kiechleschwarz et al, 1993), although not all studies have confirmed this high level of loss (Sato et al, 1991;Zheng et al, 1991;Yangfeng et al, 1992). A proximal locus at lpl3 (site of WT1) exhibits lower rates of LOH in ovarian cancer (Call et al, 1990;Vandamme et al, 1992;Viel et al, 1992;Bruening et al, 1993). A minority of these studies have proposed a correlation of I lp LOH with poorly differentiated (Zheng et al, 1991;Kiechleschwarz et al, 1993) and more advanced (Viel et al, 1992) tumours.…”

“…Minimum consensus regions of allele imbalance may lead to isolation and cloning of these 'deleted' genes, and LOH studies in many tumour types have suggested putative TSGs located on chromosome 11. In ovarian cancer, cytogenetic analysis has demonstrated partial deletions of chromosome 11 affecting both the long and short arms (Bello and Rey 1990;Pejovic et al, 1992;Jenkins et al, 1993). Frequent LOH has been demonstrated at 1 lpl5 (Lee et al, 1989;Ehlen and Dubeau, 1990;Eccles et al, 1992a;Gallion et al, 1992;Vandamme et al, 1992;Viel et al, 1992;Kiechleschwarz et al, 1993), although not all studies have confirmed this high level of loss (Sato et al, 1991;Zheng et al, 1991;Yangfeng et al, 1992). A proximal locus at lpl3 (site of WT1) exhibits lower rates of LOH in ovarian cancer (Call et al, 1990;Vandamme et al, 1992;Viel et al, 1992;Bruening et al, 1993).…”

“…A proximal locus at lpl3 (site of WT1) exhibits lower rates of LOH in ovarian cancer (Call et al, 1990;Vandamme et al, 1992;Viel et al, 1992;Bruening et al, 1993). A minority of these studies have proposed a correlation of I lp LOH with poorly differentiated (Zheng et al, 1991;Kiechleschwarz et al, 1993) and more advanced (Viel et al, 1992) tumours. Molecular studies of the proximal 1 lq region have shown low rates of both LOH and amplification of the 1 1q13 amplicon in ovarian cancer (Lee et al, 1989;Li et al, 1991;Sato et al, 1991;Viel et al, 1992;Foulkes et al, 1993).…”

“…A minority of these studies have proposed a correlation of I lp LOH with poorly differentiated (Zheng et al, 1991;Kiechleschwarz et al, 1993) and more advanced (Viel et al, 1992) tumours. Molecular studies of the proximal 1 lq region have shown low rates of both LOH and amplification of the 1 1q13 amplicon in ovarian cancer (Lee et al, 1989;Li et al, 1991;Sato et al, 1991;Viel et al, 1992;Foulkes et al, 1993). In contrast, the only study that has looked specifically at the subtelomeric region of 1llq (Foulkes et al, 1993) recorded a high rate of allele imbalance at 1 lq23.3-qter in a small sample of tumours.…”

Ovarian cancer has frequent loss of heterozygosity at chromosome 12p12.3-13.1 (region of TEL and Kip1 loci) and chromosome 12q23-ter: evidence for two new tumour-suppressor genes

“…In ovarian carcinoma, several chromosome arms have been reported to be frequently affected by allele loss (Eccles et al, 1990;Russel et al, 1990;Foulkes et al, 1991;Perez et al, 1991;Sato et al, 1991;Zheng et al, 1991;Saito et al, 1992; Jones and Nakamura, 1992;Viel et al, 1992;Yang-Feng et al, 1992Jacobs et al, 1993;Cliby et al, 1993;Foulkes et-al, 1993a,b;Takano et al, 1994;Koike et al, 1997). At most of the sites of LOH, the tumoursuppressor genes have not been identified.…”