1998
DOI: 10.1002/(sici)1097-0215(19980220)79:1<61::aid-ijc12>3.3.co;2-e
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p16MTS1 inactivation in ovarian carcinomas: High frequency of reduced protein expression associated with hyper‐methylation or mutation in endometrioid and mucinous tumors

Abstract: Inactivation of the tumor-suppressor gene p16 (MTS1/ CDKN2/INK4a) has been described in various human malignancies. Although p16 deletion has been found in various ovarian tumor cell lines, p16 inactivation by homozygous deletion or mutation has been reported only sporadically in primary ovarian carcinomas. In a comprehensive study, we analyzed p16 protein expression by immuno-histochemistry (IHC) on paraffin sections of 94 primary ovarian carcinomas of different histological subtype. Loss of expression was de… Show more

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(3 citation statements)
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“…Furthermore, seven of the 11 Rb-positive tumors overexpressed p16 protein, relative to normal ovarian tissue controls. These data support the high frequency of p16 expression in ovarian tumors observed by Dong et al (1997), Milde-Langosch et al (1998) and Marchini et al (1997). The expression of both Rb and p16 proteins in four of the six ovarian cancer cell lines further indicated that the transformation of ovarian cancer cells frequently occurs in the absence of the loss of either one of these two negative regulators of the G1 checkpoint.…”
Section: Discussionsupporting
confidence: 76%
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“…Furthermore, seven of the 11 Rb-positive tumors overexpressed p16 protein, relative to normal ovarian tissue controls. These data support the high frequency of p16 expression in ovarian tumors observed by Dong et al (1997), Milde-Langosch et al (1998) and Marchini et al (1997). The expression of both Rb and p16 proteins in four of the six ovarian cancer cell lines further indicated that the transformation of ovarian cancer cells frequently occurs in the absence of the loss of either one of these two negative regulators of the G1 checkpoint.…”
Section: Discussionsupporting
confidence: 76%
“…Three independent studies found no evidence of p16 hypermethylation in a total of 115 ovarian tumors and three ovarian cancer cell lines (Shih et al, 1997;Marchini et al, 1997;Ryan et al, 1998). By contrast, McCluskey et al (1999) and Milde-Langosch et al (1998) identi®ed p16 hypermethylation in 2/29 and 12/94 ovarian tumors, respectively. Notably, the majority of tumors that showed p16 hypermethylation in the latter two studies were of the endometriod or mucinous histopathological sub-types.…”
Section: Introductionmentioning
confidence: 98%
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