Endometrioid Carcinomas of the Ovaries and Endometrium Involving Endocervical Polyps: Comprehensive Clinicopathological Analyses

Abstract

While synchronous ovarian and endometrial endometrioid carcinomas (ECs) have long been described in the literature, ovarian or endometrial EC involving concomitant endocervical polyp (ECP) has not yet been reported. This study aimed to investigate the histological types and prevalence of gynecological tumors co-existing with ECP and to comprehensively analyze the clinicopathological characteristics of ovarian and endometrial ECs involving ECPs. We searched for ECP cases associated with premalignant lesions or malignancies of the female genital tract occurring between March 2019 and February 2022. We then investigated the histological types and prevalence of gynecological tumors co-existing with ECP. In addition, we reviewed electronic medical records and pathology slides to collect the clinicopathological features of four patients with ovarian or endometrial EC involving ECP. We found 429 ECPs over the three-year study period. Of these, 68 (15.9%) were associated with premalignant or malignant lesions occurring in the uterine cervix, endometrium, and ovaries. Four of these cases, including two (0.5%) ovarian grade 3 ECs and two (0.5%) endometrial grade 1 ECs, involved ECPs. In the former cases (cases 1 and 2), ECs involving ECPs exhibited similar morphology and immunohistochemical staining results to those of advanced-stage ovarian EC. In the latter cases (cases 3 and 4), the histological and immunophenotypical features of EC involving ECP were identical to those of primary endometrial EC, despite the lack of tumor involvement in the myometrium, lower uterine segment, and cervical stroma as well as the absence of lymphovascular invasion and lymph node metastasis. In all cases, no evidence of benign endometriosis, endometrial hyperplasia without atypia, or atypical hyperplasia/endometrial intraepithelial neoplasm within ECP or the adjacent endocervical tissue was noted. Considering our results, the involvement of ECP by EC may have been caused by an implantation metastasis from the ovarian (cases 1 and 2) or endometrial (cases 3 and 4) EC. To the best of our knowledge, this is the first exploration of the synchronous occurrence of endometrial or ovarian EC and ECP involvement. Implantation metastasis via transtubal and trans-endometrial cavity migration may have been the pathogenic mechanism of ECP involvement.

Mesonephric-like Adenocarcinoma of the Uterine Corpus: Genomic and Immunohistochemical Profiling with Comprehensive Clinicopathological Analysis of 17 Consecutive Cases from a Single Institution

“…The Proactive Molecular Risk Classifier for Endometrial Cancer introduced four subgroups of EC: (1) DNA polymerase epsilon, catalytic subunit ( POLE )-mutant subgroup, harboring mutations in the exonuclease domain in exons 9–14; (2) MMRd subgroup, showing the loss of expression for one or more MMR proteins; (3) p53-abnormal subgroup, demonstrating aberrant p53 expression pattern indicating pathogenic TP53 mutation; and (4) no specific molecular profile (NSMP) subgroup [ 63 , 64 , 65 ]. Even though the vast majority of NSMP ECs is low-grade endometrioid carcinoma, the NSMP subgroup also encompasses high-grade EC, clear cell carcinoma, undifferentiated carcinoma, carcinosarcoma, and MLA [ 36 , 40 , 50 , 51 , 53 , 57 , 65 , 66 , 67 , 68 ]. In this study, the majority of MLA cases harbored activating KRAS mutations but not POLE -mutant signatures, MMR deficiency, or TP53 mutation; confirming that these cases belong to the NSMP subgroup.…”

“…In this study, the majority of MLA cases harbored activating KRAS mutations but not POLE -mutant signatures, MMR deficiency, or TP53 mutation; confirming that these cases belong to the NSMP subgroup. Since the biological behavior of uterine MLA is consistently described as aggressive [ 36 , 67 , 69 ], the inclusion of this entity in the high-risk non-endometrioid group appears to be justified. Several studies have identified that the high expression of the L1 cell adhesion molecule (L1CAM) and CTNNB1 mutation can add significant prognostic information to the molecular classification of EC [ 70 , 71 , 72 , 73 , 74 ].…”

“…Our group has steadily documented the clinical manifestations, cytological and histological features, immunophenotypes, and mutational profiles of uterine MLA using IHC and molecular analyses [ 2 , 3 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 ]. However, get a deep insight into their relevance, the results need to be consolidated and completely analyzed.…”

Dedifferentiated Leiomyosarcoma of the Uterine Corpus with Heterologous Component: Clinicopathological Analysis of Five Consecutive Cases from a Single Institution and Comprehensive Literature Review

“…Immunostaining was performed using whole-tissue sections containing >80% viable tumor tissue, as previously described [24][25][26][27][28][29][30][31][32]. In brief, 4 µm thick FFPE tissue sections were deparaffinized and rehydrated using a xylene and alcohol solution.…”

Endocervical Adenocarcinoma Showing Microcystic, Elongated, and Fragmented (MELF) Pattern of Stromal Invasion: A Single-Institutional Analysis of 10 Cases with Comprehensive Clinicopathological Analyses and Ki-67 Immunostaining

“…Immunostaining for Ki-67 was performed using whole-tissue sections as described previously [16][17][18][19][20][21][22][23][24]. For each case, the most representative slide containing >80% of viable tumor tissue was chosen for immunostaining.…”