Intraepithelial Neoplasia of the Fallopian Tube: Precursors, Field Effects, and Conceptual Traps

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Abstract

The fallopian tube hosts a range of epithelial proliferations including high-grade serous carcinoma (HGSC). Stem cell outgrowths—benign epithelial hyperplasias—are common in tubal epithelium of postmenopausal women with or without HGSC and exhibit a wild-type p53 immunohistochemical pattern. In contrast, epithelia with TP53 mutations comprise a serous carcinogenic sequence from benign epithelium to HGSC. Mild atypias with 12 to a few hundred cells and aberrant p53 immunohistochemical staining (p53 signatures) are common and carry negligible risk of an HGSC outcome. More expansile serous tubal intraepithelial neoplasias (STINs) exhibit a spectrum of atypia from low (serous tubal intraepithelial lesion) to high (serous tubal intraepithelial carcinoma) grade, the latter characterized by both atypia and loss of epithelial cell polarity. In the risk-reducing salpingo-oophorectomy for BRCA mutations (BRCA+), STINs carry a low risk of an HGSC outcome (5%–10%). Serous tubal intraepithelial carcinoma will be discovered in the fallopian tube of 40%+ of women with HGSC. Serous tubal intraepithelial carcinoma is a dualistic entity. (1) Isolated serous tubal intraepithelial carcinomas emerging in a background of low-grade STIN most certainly originate in the tube. (2) Serous tubal intraepithelial carcinomas appearing abruptly in the mucosa of women with HGSC could either be an initiating event or an intramucosal metastasis. The concept of precursor escape—implantation of tubal precursors in the pelvis leading to later extratubal malignancy—also deserves attention. Thus, the serous carcinogenic sequence must be continually revisited and reexamined, and the pathologist remains a central and critical participant in its solution.

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