Histologic and Immunohistochemical Analyses of Endometrial Carcinomas: Experiences From Endometrial Biopsies in 358 Consultation Cases

Abstract

Context.-Uterine serous carcinoma is biologically more aggressive than the endometrioid carcinoma. Because uterine serous carcinoma has a high propensity for lymphovascular invasion and intraperitoneal and extraabdominal spread, accurate diagnosis of this tumor type in endometrial biopsies/curettings is critical for appropriate clinical management.Objective.-To share our experience in the evaluation of endometrial biopsy specimens in type I and type II endometrial adenocarcinoma.Design.-We retrospectively reviewed 358 biopsies containing endometrial carcinoma during a recent 3 year period of our consultation records. In cases in which our interpretation differed from the submitting diagnosis, a panel of immunostains was performed. The performance characteristics of each antibody in our panel was calculated in this group of challenging cases.Results. 2,3 For example, the most common genetic alterations in EMC include microsatellite instability, mutations of PTEN, b-catenin, PIK3CA, and K-ras. 4 In contrast, in the case of ESC, p53 mutations are common 3 and ERBB2 (formerly HER2) overexpression or amplification is also frequently seen. 2Clinically, ESC has a higher propensity for lymphovascular invasion and intraperitoneal as well as extra-abdominal spread than EMC.5 During presentation, approximately 40% to 70% of women with ESC will have disease beyond the uterus.6 Furthermore, although tumor grade and depth of myometrial invasion are not predictive of extrauterine spread for ESC, the incidence of extrauterine spread in endometrioid cancers correlates with both tumor grade and depth of myometrial invasion. Based on data from the Surveillance, Epidemiology and End Results database (National Cancer Institute, Bethesda, Maryland), among all cases of endometrial carcinoma, ESC represents 50% of stage III or IV disease and nearly 40% of all deaths 7 although comprising only 10% of cases by incidence. Because of the high propensity for lymphovascular invasion, intraperitone-

Adenomyosis and Endometrial Cancer: Literature Review

“…These rare tumour types are biologically distinct from the more common endometrioid carcinoma and generally carry a worse prognosis. Endometrial serous carcinoma is recognised with a higher propensity to lympho-vascular invasion and spread [116]. Endometrioid cancer is linked to alterations in PTEN gene silencing, defects in DNA mismatch repair genes, microsatellite instability and mutations in KRAS and of β-catenin.…”

Current recommendations and recent progress in endometrial cancer

“…[19][20][21] Mutational assays that can help include p53, PTEN, phosphoinositide 3-kinase (PIK3) catalytic subunit α (PIK3CA), PIK3 regulatory subunit 1 (PIK3R1), fibroblast growth factor receptor 2 (FGFR2), ARID1A, catenin β1 (CTNNB1), Kirsten rat sarcoma viral oncogene homolog (KR AS), and protein phosphatase 2 scaffold subunit Aα (PPP2R1A). No single marker is sensitive and specific enough to reliably define a histotype 22 and, although numerous panels have been proposed that improve histologic interobserver agreement, the specific elements of such a panel are not universally agreed upon.…”

Median Survival Time of Endometrial Cancer Patients with Lymphovascular Invasion at the Hospital Universiti Sains Malaysia

“…The mortality was higher for patients with type II rather than patients with type I (5) because type I cancers are more likely to grow and spread outside the uterus. However, this type is only presented in 20% of all endometrial cancer cases, which consists of less common histological subtypes such as serous carcinoma, clear cell carcinoma and carcinosarcoma (6). Although endometrioid types are more common in endometrial cancer patients (80%-85% of all cases) (6), they are not outcome factor was survival time, defined as the time to death of patients due to endometrial cancer or its complications.…”