Synchronous Endometrioid Carcinoma Research Articles

Synchronous endometrioid carcinoma of endometrium and ovary: A case report

The synchronous endometrial and ovarian cancer is a rare phenomenon with incidence of 1.4 to 3.8%. Mostly in SEOC, the ovarian endometroid carcinoma arises in background of endometriosis with endometrial carcinoma with lower stage and lower grade in premenopausal age group.Herein we present a case of 33year old female, presented with abdominal pain, underwent TAH with BSO and histopathologically uterus and ovary showing features of Synchronous endometrial and ovarian carcinoma of low grade with no nodal involvemnet in premenopausal lady.The SEOC being a rare phenomenon with different therapeutic and favorable prognostic considerations, when compared with metastatic carcinomas and hence SEOC can be managed with multidisciplinary approach and regular follow up.

Endometrioid Cancer Associated With Endometriosis: From the Seed and Soil Theory to Clinical Practice.

Endometriosis is a benign condition characterized by the presence of ectopic endometrial tissue. It is still debated whether endometriosis is a disease that can predispose to the pathogenesis of endometrial cancer outside the uterus. Deficiencies in mismatch repair (MMR) genes are a known risk factor for developing endometrioid cancer. Starting from two cases of patients with abnormal MMR endometrioid carcinoma of the uterus and synchronous endometrioid carcinoma in non-ovarian and ovarian endometriosis, we performed a somatic mutation profile and phylogenetic analysis of the lesions in order to identify if they were metastasis or primary de novo tumors. In the first case, we identified de novo activating mutations in PIK3CA and KRAS in endometrioid cancer lesions but not in endometriosis. Although the acquisition of a de novo mutation in ESR1 and a decrease in mutant allele fraction (MAF) from the endometrial tumor to the localizations in the endometriosis lesions, the clonal relationship was confirmed by the limited number of heteroplasmic mutations in D-loop mitochondrial DNA region. In the other case, the clonal behavior was demonstrated by the overlap of MAF at each site. Our data support the hypothesis of a retrograde dissemination of tumor cells, moving from the primary carcinoma in the endometrium to ectopic sites of endometriosis where localizations of tumor arise.

Concurrently Presenting Endometrial And Ovarian Endometrioid Adenocarcinomas- A Clinicopathologic Study Of 52 Cases

Abstract Introduction/Objective Concurrent presentation of endometrioid adenocarcinomas in endometrium and ovary is uncommon, but oft-noted. They may arise from ovarian metastasis of endometrial carcinoma, endometrial metastasis of ovarian carcinoma, or synchronous development of independent primary lesions. Scully and Young criteria have been widely used to differentiate the site of origin.1 Role of a field effect in the genesis of synchronous carcinomas is supported by increasing evidence that endometrioid ovarian carcinomas arise from endometriosis. 2–5 Methods All cases of concurrent endometrioid adenocarcinomas of the endometrium and ovary between 2002 and 2019 in the Mount Sinai health system New York were included, using pathology database (Powerpath) and EMR database (Epic). Results 52 cases of concurrent endometrioid adenocarcinomas of endometrium and ovary were identified between 2002 and 2019. Mean age at presentation was 54.07 years (24–80). 69.2% had synchronous origin, 21.15% had endometrial primary and 3.8% had an ovarian primary. Ovarian endometriosis was identified in 51.9% and complex atypical hyperplasia in 26.9%. Lower uterine segment involvement was seen in 26.9%, bilateral ovarian involvement in 40.3%, fallopian tube involvement in 23% and lymphovascular space invasion in 25%. Different histologic grade of ovarian and endometrial counterparts was noted in 25% cases. Synchronous endometrioid carcinomas had the following characteristics: mean age at presentation 50.6 years, associated with CAH in 33.3% and endometriosis in 66.6%, presentation at stage 1 in 63.8% and lower grade of differentiation (grade 1/2) in 80.5% cases. Conclusion In majority of cases, synchronous endometrioid carcinomas have a younger mean age at presentation, are lower grade tumors, present at stage 1 and have associated endometriosis. It can be inferred that the percentage of synchronous tumors with endometriotic foci would be even higher (with extensive sampling & assuming that the neoplastic process has replaced native benign endometriotic foci) – pointing towards the likely role of endometriosis in the genesis of these tumors.

Synchronous endometrioid carcinoma of bilateral ovaries and uterus: A case report

Synchronous endometrioid carcinoma of bilateral ovaries and uterus: A case report

Cutaneous Metastases of the Synchronous Primary Endometrial and Bilateral Ovarian Cancer: An Infrequent Presentation and Literature Review.

There are limited data about the cutaneous metastases of gynecological malignancies in the literature. Based on this limited number of studies, cutaneous metastases from gynecological malignancies are uncommon occurrences. Cutaneous metastases from the synchronous endometrioid carcinoma of the uterine corpus and bilateral ovaries arising from endometriosis are extremely rare. Herein, we report a 51-year-old woman with FIGO Stage 1A Grade 1 endometrial endometrioid-type adenocarcinoma and synchronous bilateral Stage 1B ovarian endometrioid-type adenocarcinoma who presented 34 months following total abdominal hysterectomy and bilateral salpingo-oophorectomy with skin metastases. After the patient underwent an excisional biopsy, we applied a palliative radiotherapy. The patient received the combination therapy with cisplatin and doxorubicin after the completion of radiotherapy but the disease evolution was rapidly fatal and the patient died 4 months after her admission to our department due to widely disseminated disease.

Molecular pathology of endometrial carcinoma: practical aspects from the diagnostic and therapeutic viewpoints

This article reviews the main molecular alterations involved in endometrial carcinoma. Five molecular features (microsatellite instability, and mutations in the PTEN, k-RAS, PIK3CA and β-catenin genes) are characteristic of endometrioid...

Synchronous endometrioid carcinomas of the uterine corpus and ovary: alterations in the β-catenin ( CTNNB1) pathway are associated with independent primary tumors and favorable prognosis

Diagnosis of synchronous endometrioid carcinomas of the uterine corpus and ovary as either separate independent primary or as metastatic tumors requires careful consideration of a number of gross and histological features. Although such assessment is often sufficient, recent evidence has suggested that molecular analysis may facilitate the diagnosis in problematic cases. Furthermore, as independent synchronous tumors limited to the uterus and ovary are generally associated with favorable outcome, determination of genetic alterations associated with this group of neoplasms may indicate molecular markers of less aggressive behavior. We examined 12 cases of synchronous carcinomas of the uterus and ovary, correlating conventional gross and histological parameters with molecular genetic alterations common to single endometrioid carcinomas occurring in these sites. We identified a frequency of molecular alterations in both independent and metastatic tumors, including microsatellite instability (uterine tumors, 50% and 67%, respectively; ovarian tumors, 33% and 67%) and PTEN mutations (uterine tumors, 38% and 100%; ovarian tumors, 33% and 83%) that is higher than that observed in single sporadic tumors. Loss of heterozygosity for chromosome 17p and 10q was also frequently observed. Nuclear immunoreactivities for beta -catenin and CTNNB1 mutations were restricted to independent uterine and ovarian tumors and were absent in all of the metastatic tumors, providing direct evidence for a divergence of molecular oncogenetic mechanisms in the subset of synchronous endometrioid carcinomas. Furthermore, our data show that molecular genetic classification of synchronous independent versus metastatic tumors based on beta -catenin expression/mutation correlates with clinical outcome.

PTEN as a molecular marker to distinguish metastatic from primary synchronous endometrioid carcinomas of the ovary and uterus.

The distinction between two primary carcinomas on the one hand and a metastatic disease on the other hand in patients suffering from synchronous endometrioid carcinomas of the uterus and ovary is difficult. Exclusive histopathologic analysis appears to be insufficient and sometimes misleading. The tumor suppressor PTEN was found to be important in early neoplastic transformation in endometrioid carcinomas of the uterus. In this study, we screened synchronous endometrioid carcinomas of the uterus and ovary of 10 patients for loss of heterozygosity using seven different microsatellite markers at 10q23.3 and for mutations in the entire coding region of PTEN. Point mutations or microdeletions/insertions were found in six patients. Allelic loss at 10q23.3 was detected in eight patients. Based on conventional histology, a metastatic disease was diagnosed in seven patients and a concomitant uterine and ovarian carcinoma in three patients. After molecular analysis, the histopathologic diagnosis of three patients had to be revised. Histopathology represents the standard method to process tumor specimens from these patients. Nevertheless, mutation screen for PTEN and LOH analysis at 10q23.3 provide helpful genetic tools to establish a correct final diagnosis, which is important in view of prognosis and therapeutic implications.

Genetics of synchronous uterine and ovarian endometrioid carcinoma: Combined analyses of loss of heterozygosity, PTEN mutation, and microsatellite instability

Synchronous development of carcinomas in the endometrium and ovaries is a fairly common phenomenon, but distinction of a single clonal tumor with metastasis from 2 independent primary tumors may present diagnostic problems. To determine clonality and the occurrence of progression, we microdissected multiple foci from 17 cases of synchronous endometrioid carcinomas and studied loss of heterozygosity (LOH), microsatellite instability (MI), and PTEN mutations. In 14 of the 17 cases, genetic alterations were either homogeneous or found in only some of the foci. LOH was detected for 10q (4 cases), 17p (2 cases), and 2p, 5q, 6q, 9p, 11q, 13q, and 16q (1 case each). Four cases had the MI phenotype with discordant MI patterns between both tumor sites, thus indicating a biclonal or triple clonal process. In 3 of 6 cases with PTEN mutations, identical mutations in both tumor sites indicated a single clonal neoplasm. Altogether, 14 synchronous tumors were genetically diagnosed as follows: single clonal tumor, characterized by concordant genetic alterations in both tumor sites, including identical LOH, identical PTEN mutations, and/or identical sporadic allelic instability patterns (4 cases); single clonal tumor with genetic progression, homogeneous LOH or identical PTEN mutations in both tumor sites and progressive LOH in ovarian metastatic foci (2 cases); and double (7 cases) or triple clonal tumors (1 case), determined by discordant PTEN mutations, heterogeneous LOH, and/or discordant MI patterns. Thus, 35% of synchronous tumors were monoclonal, 47% were polyclonal, and 18% were undetermined. The favorable prognosis of synchronous endometrioid carcinomas may be due to the occurrence of PTEN mutations in both independent and metastatic tumors, the MI-positive independent primary tumors, and the low frequency of LOH. HUM PATHOL 33:421-428. Copyright 2002, Elsevier Science (USA). All rights reserved.