Precursor Lesions and Prognostic Factors in Primary Peritoneal Serous Carcinoma

Abstract

Primary peritoneal serous carcinoma (PPSC) is uncommon and precursor lesions and prognostic factors are incompletely understood or described. Charts of 22 women with PPSC were reviewed for clinical and pathology data. Glass slides were reviewed for areas of PPSC, ovarian surface epithelium (OSE), ovarian cortical inclusion cysts (OCICs), tubal epithelial atypia (TEA), and serous tubal intraepithelial carcinoma (STIC). p53 and p16 immunohistochemical staining was scored and expression between the sites was compared. PPSC outcome was correlated with biomarker expression and clinicopathologic variables. p53 and p16 scores were significantly higher among PPSC and tubes than OSE and OCICs. Approximately 64% of PPSC, 46% of fallopian tubes, and none of the OSE overexpressed both biomarkers. OCICs were more frequently negative. Tubal pathologies of STIC, TEA and/or p53 signatures were present in approximately 46% of PPSC cases and the association with tubal p53 overexpression was significant. Statistically significant associations between tubal pathologies, OSE and OCICs biomarker expression profiles and their PPSC expression profiles did not occur. The median overall survival was 53 months and low-grade tumors had a better prognosis (P=0.02). A role for p53 and p16 overexpression in the formation of some PPSC, and p53 overexpression in the generation of precursor tubal pathology was identified. The high frequency of tubal pathology overexpressing p53 and low frequency of OSE and OCICs expressing either biomarker highlights a possible precursor role for the tube in some PPSC. Tumor grade was the only significant prognostic factor.

The PAX2‐null immunophenotype defines multiple lineages with common expression signatures in benign and neoplastic oviductal epithelium

“…Not surprisingly, no marker in this group separated STINs or HGSCs from SCOUTs. This is in contrast to other published markers such as Ki67, cyclin E, p16, and others, which are significantly more commonly expressed in STINs and HGSCs relative to benign Fallopian tube mucosa .…”

Opportunistic salpingectomies for the prevention of a high-grade serous carcinoma: a statement by the Kommission Ovar of the AGO

“…• 2-7 % in risk-reducing salpingo-oophorectomies (BRCA1/2 positive or familial risk) [18], • up to 80 % in surgical specimens of BRCA1/2 patients with HGSOC, • 46 % in patients with sporadic ovarian cancer [16,19].…”

“…The lesion, 'Secretory Cell Outgrowth' (SCOUT) equals a proliferation of secretory cells and is often regarded as a surrogate marker for precursor lesions. Due to their stemcell-like features, these lesions may also have a potential role in the pathogenesis of EOC [6][7][8][9][10][11][12][13][14][15][16][17].…”

Risk‐reducing salpingectomy: Let us be opportunistic

“…In addition, molecular markers and gene expression profiles of high‐grade serous carcinoma support a tubal origin, with lineage continuity of specific TP53 mutations between high‐grade serous carcinoma and the accompanying STIC lesion. TP53 mutations result in an abundance of nonfunctional p53; this is referred to as a “p53 signature,” and is commonly identified adjacent to STIC lesions …”