DNA Amplification of HER-2/neu and INT-2 Oncogenes in Epithelial Ovarian Cancer

Medl, M.; Sevelda, P.; Czerwenka, K.; Dobianer, Karl; Hanak, H; Hruza, C; Klein, Michael; Leodolter, Sepp; Müllauer-Ertl, Susanne; Rosen, Alexander C.; Sälzer, H.; Vavra, N.; Spona, J

doi:10.1006/gyno.1995.9969

Cited by 33 publications

(18 citation statements)

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“…According to the literature, the correlation between the amplification of ERBB2/NEU and histological subtype is open. Medl et al (1995) found amplification of ERBB2/NEU in 35% of serous tumours and 50% of mucinous tumours, but the difference was not statistically significant. On the other hand, Hruze et al (1993) did not find any correlation between copy number of ERBB2/NEU and the histological subtype.…”

Section: Discussionmentioning

confidence: 76%

“…The minimum overlapping region of the gain at 11 q was I1 q 13, which harbours the proto-oncogene INT2, a member of the fibroblast growth factor (FGF) family. This proto-oncogene is amplified in breast cancer (Tsuda et al, 1989) and in ovarian cancer (Medl et al, 1995), again an interesting coincidence. In breast cancer, the amplification of INT2 correlates with a poor prognosis, but it appears not to predict survival in patients with ovarian cancer (Medl et al, 1995).…”

Section: Discussionmentioning

confidence: 90%

“…This proto-oncogene is amplified in breast cancer (Tsuda et al, 1989) and in ovarian cancer (Medl et al, 1995), again an interesting coincidence. In breast cancer, the amplification of INT2 correlates with a poor prognosis, but it appears not to predict survival in patients with ovarian cancer (Medl et al, 1995). Other genes located at llql3 include HSTFI, also a member of the FGF family, PRADI, EMS and the folate receptor.…”

Section: Discussionmentioning

confidence: 90%

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Evidence for divergence of DNA copy number changes in serous, mucinous and endometrioid ovarian carcinomas

Tapper

Bützow²,

Wahlström³

et al. 1997

Br J Cancer

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Summary Comparative genomic hybridization was applied to detect and map changes in DNA copy number in 24 well or moderately differentiated epithelial ovarian carcinomas (eight serous, eight mucinous and eight endometrioid carcinomas). Twenty-three of the 24 tumours showed changes in DNA copy number in one or several regions (median 4, range 1-17). Gains were more frequent than losses (ratio 1.6:1.0). The most frequent gains occurred in chromosomes 1 q (38%), 2p (29%), 7q (25%), 8q(38%) and 1 7q (38%), and the most common losses were located in chromosomes 8p (21%), 9p (25%) and 13q (21%). High-level amplifications were detected in seven tumours at 1q22-32, 2p15-22, 3qcen-23, 6p21-22 and 8q. In the three histological subtypes the copy number karyotypes showed substantial differences. Gains at 1 q were observed in endometrioid (five cases) and serous tumours (four cases). Increased copy number at 1 Oq was seen in endometrioid tumours only (four cases), whereas gains at 11q occurred mostly in serous tumours (four cases). In mucinous tumours, the most common copy number change was a gain at 1 7q (six cases). The results show that, in epithelial ovarian carcinoma, changes in DNA copy number are a rule rather than an exception, chromosomes 1, 2, 7, 8, 9, 13 and 17 being the most frequently affected. The diverging pattern of genetic changes seen in epithelial ovarian carcinomas with different histological phenotypes suggests that various pathways may lead to tumorigenesis and/or progression in these subgroups.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 90%

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Evidence for divergence of DNA copy number changes in serous, mucinous and endometrioid ovarian carcinomas

Tapper

Bützow²,

Wahlström³

et al. 1997

Br J Cancer

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“…For HER-2/neu, 20 studies reporting results of 21 analyses in 3055 patients were subjected to final analysis (Supplementary Table 4; median study size 111 patients, range 40 -783; Berchuck et al, 1990;Fajac et al, 1995;Kaufmann et al, 1995;Medl et al, 1995;Wang et al, 1999Wang et al, , 2005Davidson et al, 2000;Skirnisdottir et al, 2001b;Camilleri-Broet et al, 2004;Nielsen et al, 2004;Verri et al, 2005;Castellvi et al, 2006;Surowiak et al, 2006;Malamou-Mitsi et al, 2007;Pils et al, 2007;Steffensen et al, 2007;Tuefferd et al, 2007;de Graeff et al, 2008;Garcia-Velasco et al, 2008;Tomsova et al, 2008). All studies were designated phase II biomarker studies.…”

Section: Study Characteristicsmentioning

confidence: 99%

Modest effect of p53, EGFR and HER-2/neu on prognosis in epithelial ovarian cancer: a meta-analysis

et al. 2009

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BACKGROUND: P53, EGFR and HER-2/neu are the most frequently studied molecular biological parameters in epithelial ovarian cancer, but their prognostic impact is still unequivocal. We performed a meta-analysis to more precisely estimate their prognostic significance. METHODS: Published studies that investigated the association between p53, EGFR and HER-2/neu status and survival were identified. Meta-analysis was performed using a DerSimonian -Laird model. Publication bias was investigated using funnel plots and sources of heterogeneity were identified using meta-regression analysis. RESULTS: A total of 62 studies were included for p53, 15 for EGFR and 20 for HER-2/neu. P53, EGFR and HER-2/neu status had a modest effect on overall survival (pooled HR 1.47, 95% CI 1.33 -1.61 for p53; HR 1.65, 95% CI 1.25 -2.19 for EGFR and HR 1.67, 95% CI 1.34 -2.08 for HER-2/neu). Meta-regression analysis for p53 showed that FIGO stage distribution influenced study outcome. For EGFR and HER-2/neu, considerable publication bias was present. CONCLUSIONS: Although p53, EGFR and HER-2/neu status modestly influences survival, these markers are, by themselves, unlikely to be useful as prognostic markers in clinical practice. Our study highlights the need for well-defined, prospective clinical trials and more complete reporting of results of prognostic factor studies.

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“…2,3 More than 90% of ovarian cancers are of epithelial cell origin and multiple genetic alterations are believed to occur during malignant transformation of ovarian epithelial cells. 4 Several oncogenes and tumor suppressor genes including HER-2/neu, 5,6 K-ras, 7,8 SPARC, 9 BRCA1, 10 and DOC-2 11 have been found to be involved in ovarian carcinogenesis. It has also been demonstrated that deregulation of the genes involved in apoptosis, such as Bcl-2 and p53, plays a crucial role in tumor formation.…”

mentioning

confidence: 99%

Bcl-2 and p53 Protein Expression, Apoptosis, and p53 Mutation in Human Epithelial Ovarian Cancers

Chan

Cheung

Schorge

et al. 2000

The American Journal of Pathology

157

110

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Bcl-2 and p53 gene products have been both linked to cell death by apoptosis. In the present study, we examined the relationship of Bcl-2 and p53 protein expression, p53 mutation and apoptosis in normal human ovaries and different types of human ovarian epithelial tumors by immunohistochemical localization, in situ terminal transferase-mediated dUTP nick end labeling and polymerase chain reaction-single strand conformation polymorphism. It was found that Bcl-2 expressed strongly in the surface epithelium of normal ovaries and benign and borderline ovarian tumors but weakly in the malignant tumors. On the contrary, strong protein expression of p53 was found in 54% (25/46) of the malignant epithelial tumors examined but similar expression of p53 was not observed in borderline and benign tumors and normal ovarian surface epithelium. A significant inverse correlation between Bcl-2 and p53 expression was found in the malignant ovarian tumors examined. p53 gene mutation at exons 5-11 was however not a pre-requisite for p53 expression in both borderline and malignant tumors.

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DNA Amplification of HER-2/neu and INT-2 Oncogenes in Epithelial Ovarian Cancer

Cited by 33 publications

References 4 publications

Evidence for divergence of DNA copy number changes in serous, mucinous and endometrioid ovarian carcinomas

Evidence for divergence of DNA copy number changes in serous, mucinous and endometrioid ovarian carcinomas

Modest effect of p53, EGFR and HER-2/neu on prognosis in epithelial ovarian cancer: a meta-analysis

Bcl-2 and p53 Protein Expression, Apoptosis, and p53 Mutation in Human Epithelial Ovarian Cancers

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