Role of Immunohistochemistry to Distinguish Grade 3 Endometrioid Carcinoma and Uterine Serous Carcinoma

Abstract

Aim: The categorization of endometrial carcinomas into endometrioid and serous categories has prognostic implications but many-a-times, it is difficult to categorize based solely on morphology. The present study was conducted to determine an appropriate immunohistochemical panel to distinguish grade 3 endometrioid carcinoma from serous carcinoma. Experimental Design: This study was a retrospective and a prospective study including 63 cases of endometrial carcinoma diagnosed on morphology as either grade 3 endometrioid (n=29) or serous endometrial carcinomas (n=34). Immunohistochemistry (IHC) was performed using tissue microarrays for 8 immunomarkers on 60 cases. Results: The mean age of presentation was not significantly different for both types of carcinomas and the most common presentation was postmenopausal bleeding (93% of the total cases, P=0.66). Obesity (P=0.038), lymph nodal involvement (P=0.044), and stage at presentation (P=0.042) were found to be significantly different among the 2 types of carcinomas. Estrogen and progesterone receptor (ER, PR) positivity was more common (47.6% and 28.2%, respectively) in endometrioid carcinomas as compared with serous. Mutation type (diffuse or null) p53 staining was a powerful predictor of serous carcinomas. IMP3 and p16 were found to be positive in most cases of serous carcinoma (64.1% and 79.5%, respectively). Vimentin and β-catenin were found to be of limited utility. On the basis of IHC, 21 cases could be categorized as grade 3 endometrioid carcinomas and 39 as type 2 carcinomas (serous and clear cell carcinoma). Conclusions: The most appropriate IHC panel to differentiate endometrioid and serous endometrial carcinomas includes ER, PR, IMP3, p53, and p16.

New Pathological and Clinical Insights in Endometrial Cancer in View of the Updated ESGO/ESTRO/ESP Guidelines

“…It is unclear whether p53abn EEC and serous carcinoma have the same prognosis, since the results in this regard appear conflicting [ 23 , 24 ]. However, given the possibility of mixed EEC and serous carcinoma and the possible difficulties in differentiating between p53abn EEC and serous carcinoma, considering a different management for these two entities might not be appropriate [ 20 , 25 ]. For the MMRd and NSMP groups, which have intermediate prognosis, FIGO grade, LVSI, and depth of myometrial invasion are crucial factors for the ESGO/ESTRO/ESP risk stratification.…”

“…Distinctive features of SEC are a scalloped epithelial surface with exfoliation of tumoral cells, a lack of polarization with striking nuclear atypia, and a high mitotic index [ 9 , 20 ]. SEC have shown a quite homogeneous molecular background characterized by TP53 mutations, which can be detected by p53 immunohistochemistry and is useful for differential diagnosis in difficult cases [ 4 , 20 , 25 ]. Consistently, SECs almost invariably fall into the p53abn TCGA group, which has indeed been termed the “serous-like” group [ 12 , 33 ].…”

Deep Learning-Based Classification of Uterine Cervical and Endometrial Cancer Subtypes from Whole-Slide Histopathology Images

“…Although serous carcinoma typically shows a predominant papillary growth pattern, which is also found in some endometrioid carcinomas. Antibodies for p53, p16, IMP2, and IMP3 can help to distinguish serous endometrial adenocarcinoma, but the markers are not definitive [ 19 ]. Therefore, there is an opportunity for DL-based classifiers to improve the diagnostic accuracy of subtypes of endometrial cancers.…”

Endometrial Metaplastic/Reactive Changes Coexistent with Endometrial Hyperplasia and Carcinoma: A Morphological and Immunohistochemical Study

“…p53 was dichotomized as “mutant-pattern” (overexpression in >80% of cells, complete absence, or cytoplasmic expression) vs. “wild-type (wt)-pattern” (focal expression or diffuse expression with variable intensity) [ 22 ]; the wt pattern was further subdivided into “wt-low” (expression in <5% of cells), “wt-intermediate” (expression in 5–50% of cells), and “wt-high” (expression in >50% of cells). P16 expression was categorized as “diffuse”, “patchy”, or “negative”; a uniformly strong and diffuse expression of p16 was labeled “block-type” [ 23 ]. Vimentin expression was categorized as “positive”, “heterogeneous”, or “negative”.…”