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Twelve pairwise post hoc comparisons were performed for each significant model resulting in sixty post hoc contrasts. ER protein was significantly overexpressed in 47% of serous and 50% of endometrioid samples, while only elevated in only 14% of clear cell samples. Post hoc testing demonstrated the ER protein was significantly over expressed in serous and endometrioid histologies when compared to clear cell histology. The MGMT and RRM1 biomarkers were also significantly overexpressed in serous and endometrioid histologies when compared to clear cell histology. MGMT was significantly elevated in 93% of serous and endometrioid samples, compared to 62% of samples with clear cell histology. Only 14% of clear cell samples were found to have overexpression of RRM1, compared to 47% of serous and 25% of endometrioid samples.

Those pro teins most often underexpressed included Her2/neu, SPARC, and c kit, seen in less than 1%, 4%, and 5% of specimens, respectively. None of the post hoc compari sons for histology were significant for biomarkers BCRP and PTEN with the FDR correction applied. There were 88 genes evaluated by MA gene expression and included in statistical analysis for association with histology. Those genes most overexpressed, defined as a difference in expression of mRNA between tumor and control organ tissue at a significance level of P. 001, in serous histology included TOP2A, MSH2, OGFR, RRM2, GART, and PARP1. A description of proportion of positive expression is shown in Figure 1. There were fourteen genes that were never expressed in serous histology and are not shown in Figure 1 ABCG2, AR, CES2, KIT, MS4A1, PDGFRA, PDGFRB, POLA1, RXRB, SPARC, SSTR1, SSTR2, SSTR4, and TOP1. There was no differ ence in protein or gene overexpression identified when analyzed by age, FIGO stage, grade, primary or recurrent tumor, and ovary or other biopsy site.

Discussion TCGA project has analyzed post transcriptional messenger RNA expression, microRNA expression, promoter methyla tion, and DNA copy number in 489 high grade serous ovarian adenocarcinomas. They reported that high grade serous ovarian cancer is characterized by TP53 mu tations in almost all tumors. and a low prevalence but statistically significant recurrent somatic mutations in nine further genes including NF1, BRCA1, BRCA2, RB1, and CDK12. Pathway analyses suggested that homologous recombination was a potentially important pathway and was defective in about half of the high grade serous cancers analyzed. NOTCH and FOXM1 signaling were involved in serous ovarian cancer pathophysiology. Molecular PEP is a powerful approach to identify clinical markers for diagnosis and prognosis as in epithelial ovarian cancer. In a previous smaller study, a tissue array composed of 244 serous tumors of different grades and stages was evaluated by comprehensive IHC for proteins not necessarily associated with response to selective che motherapeutic agents.