Ovarian Endometrioid Adenocarcinoma Research Articles

The Pivotal Role of the Key Angiogenic Factors in the Development of Endometrioid Pathologies of the Uterus and Ovary.

A characteristic feature of uterine pathologies is a specific change in cell metabolism, which predominantly manifests as a shift in the need for nutrients, thereby directing cells to engage in different angiogenic marker activities. Angiogenesis is one of the main signals supporting the survival and development of cells and tissues not only under physiological conditions. Therefore, it is necessary that we understand pathological hyperactivation in all uterine diseases, from endometriosis through ovarian endometrioid adenocarcinoma to malignant transformed cells of the uterine epithelium and body. This work presents the gene expression results of selected angiogenesis targets (VEGF-A, TGF-β1, ANG1/2, and HIF-1α), cell migration, and cell-cell interaction determined in vitro. Our results suggest that angiogenesis varies in the tested pathological conditions (ectopic endometriosis-12Z; ovarian endometrioid adenocarcinoma-A2780; tumors-SK-UT-1 and RL-95-2) compared to physiological angiogenesis (HME1). The differential expression of angiogenic factors may contribute (or is a contributing factor) to the observed differences to acknowledge an inherent variability in angiogenesis among cell lines. Determining the genomic phenomena responsible for processes associated with inadequate angiogenesis in the pelvic region could help us to develop individual treatment strategies and explain resistance to treatment.

#387 : Enlightening the Management of Chocolate Cysts Before IVF Treatment: Case Reports of 3 Young Endometriosis-Associated Ovarian Cancer Patients with Ovulation Induction History

Background and Aims: Endometriosis is a common estrogen-dependent disease that occurs mostly in women of childbearing age and is characterized by ectopic growth of endometrial glands and stroma. Endometriosis may present as malignant transformation and the two most common malignancies in this situation are ovarian clear cell carcinoma and endometrioid adenocarcinoma. Rare cases of endometriosis-associated ovarian cancer (EAOC) after in-vitro fertilization (IVF) treatment were reported before, and the relationship between the usage of ovulation induction medications and the development of ovarian cancer is controversial. This study aims to summarize the characteristics of EAOC patients with IVF treatment history. Method: All history, clinical data, imaging data, operative documents, and follow-up of 3 cases of endometriosis-associated ovarian cancer with IVF treatment history were reviewed, among the 793 patients undergoing surgeries for ovarian malignancy at the Gynecology Department, Renji Hospital affiliated to Shanghai Jiao Tong University, School of Medicine, from 2019 to 2022. Results: 3 EAOC patients under the age of 40 who had undergone controlled ovarian hyperstimulation (COH) for IVF treatment were identified in the cases review. The 3 infertility women underwent 3, 4, and 6 cycles of ovulation induction and achieved 1, 0, and 1 time of pregnancy, respectively. Unfortunately, none of them reached a pregnancy outcome over 12 weeks. After staging surgery, the 3 patients were diagnosed with Stage IA clear cell carcinoma, Stage IIB clear cell carcinoma, and Stage IIB adenosquamous carcinoma, respectively. The latter two patients had undergone two times of needle aspiration and sclerosis for chocolate cysts, and the surgical records also showed more severe abdominal adhesion and poor prognosis. Conclusion: Patients with endometriosis cysts need to be very careful when seeking IVF treatment, especially in the order of treatment of cysts and ovulation induction. Repeated needle aspiration and sclerosis for ovarian cysts are not recommended.

An algorithm for the pre-operative differentiation of benign ovarian tumours based on magnetic resonance imaging interpretation in a regional core hospital: a retrospective study

ObjectiveFor selecting minimally invasive surgery (i.e. laparoscopic ovarian cystectomy) for treating ovarian tumours (OTs) in premenopausal patients, the pre-operative differentiation of benign ovarian tumours (Be-OTs) based on magnetic resonance imaging (MRI) interpretation is important. This paper describes the authors’ 8-year experience of approximately 1000 OT cases, and provides information about a diagnostic algorithm to help other hospitals. Study designThe medical records of 901 patients aged < 50 years with OTs from 1 January 2015–31 March 31 2023 were reviewed. First, the accuracy of pre-operative differentiation between Be-OTs and borderline/malignant ovarian tumours (Bo/Ma-OTs) was compared in each type of OT. Second, to identify the factors influencing differentiation between Be-OTs and Bo/Ma-OTs in 164 serous/mucinous ovarian tumours (SM-OTs), a multi-variate logistic regression analysis was performed to assess the effect of 13 factors, including MRI findings, OT size and tumour markers. ResultsIn the comparison of diagnostic accuracy of pre-operative MRI for each OT type, accuracy was found to be notably high for ovarian endometrial cyst (OEC) (n = 409), ovarian mature cystic teratoma (OMCT) (n = 308), ovarian endometrioid adenocarcinoma (OEA) (n = 6) and ovarian clear cell adenocarcinoma (OCCA) (n = 14). On the other hand, discrepancies between MRI and pathological findings often occurred in SM-OTs, including ovarian serous cystadenoma (n = 86), ovarian mucinous adenocarcinoma (n = 61), ovarian serous adenocarcinoma (n = 12) and ovarian mucinous adenocarcinoma (n = 5). In the multi-variate logistic regression analysis of the latter 164 patients, in addition to MRI findings, OT size and carbohydrate antigen 125 also had an effect to some extent. The combination of MRI interpretation and OT size may enhance differentiation of Be-OTs and Bo/Ma-OTs. ConclusionsAmong four types of OTs (OEC, OMCT, OEA and OCCA), MRI interpretation was able to differentiate between Be-OTs and Bo/Ma-OTs almost perfectly. Additionally, to mitigate the difficulty in differentiating SM-OTs, OT size may be useful in combination with MRI findings, although further accumulation and analysis of OT cases is needed.

Ovarian Endometrioid Adenocarcinomas With Infiltrative "Adenofibroma-like" Morphology and Aberrant ß-catenin Expression: Tumors That Coexpress CDX2 and LEF1 With Frequent Neuroendocrine Marker Expression, Diminished/Lost PAX8 and Possible Association With Endometrioid Type II Stem Cell Outgrowths in the Fallopian Tube.

Ovarian Endometrioid Adenocarcinomas With Infiltrative "Adenofibroma-like" Morphology and Aberrant ß-catenin Expression: Tumors That Coexpress CDX2 and LEF1 With Frequent Neuroendocrine Marker Expression, Diminished/Lost PAX8 and Possible Association With Endometrioid Type II Stem Cell Outgrowths in the Fallopian Tube.

Patterns of spread and genetic alterations of primary endometrioid carcinomas of the ovary

ObjectiveThe primary objective was to characterize the rate of lymph node involvement in a cohort of patients with primary ovarian endometrioid adenocarcinoma. Additionally, we sought to quantify the recurrence rate,...

An Interesting Case of Synchronous Low-Grade Peritoneal Mesothelioma and Ovarian Endometrioid Adenocarcinoma

Synchronous mesothelioma with other primary malignancies has previously been reported. However, the finding of a low-grade peritoneal mesothelioma with a synchronous ovarian endometrioid adenocarcinoma remains unreported. We report a case of a 57-year-old woman presenting with distended abdomen. CT abdomen and pelvis and subsequent MRI revealed a large pelvic mass. On pathology of the exploratory laparotomy specimen, stage IIIB FIGO grade 3 right ovarian endometrioid adenocarcinoma, as well as stage 1A left ovarian endometrioid borderline tumor, were discovered. Incidentally, a low-grade mesothelioma, epithelioid type, was discovered spanning omentum, right upper paracolic gutter left upper paracolic gutter, and umbilicus. Post-surgery, chemotherapy was initiated primarily to treat the ovarian adenocarcinoma.

Investigation of nanoformulation and incorporation potential of radiolabeled curcumin using HeLa and MDAH-2774 cells

Nowadays plant origin compounds with anti-cancer properties come into prominence, among them is curcumin (CUR) with a remarkable anti-cancer activity against various cancers. CUR was nanoformulated (CUR-PLGA) by the polymer based poly(lactic-co-glycolic acid) (PLGA) and both CUR and CUR-PLGA were radiolabeled with iodine-131 radionuclide for investigation of their in vitro behaviour on Human cervix adenocarcinoma (HeLa) and Ovarian endometrioid adenocarcinoma (MDAH-2774) cell lines. The newly described radiolabeled CUR and CUR-PLGA may be initiative discovery of novel potential imaging and therapeutic agents.

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 &amp; assuming that the neoplastic process has replaced native benign endometriotic foci) – pointing towards the likely role of endometriosis in the genesis of these tumors.

Assessing and validating housekeeping genes in normal, cancerous, and polycystic human ovaries.

Housekeeping genes (HKGs), reference or endogenous control genes, are vital to normalize mRNA levels between different samples. Since using inappropriate HKGs can lead to unreliable results, selecting the proper ones is critical for gene expression studies. To this end, normal human ovaries, as well as those from patients diagnosed with ovarian endometrioid adenocarcinoma (OEA), ovarian mucinous adenocarcinoma (OMA), ovarian serous papillary carcinoma (OSPC), and polycystic ovary syndrome (PCOS), were used to identify the most suitable housekeeping genes. RNA was isolated from 5 normal human ovaries (52-79years of age), 9 cancerous ovaries (3 OEA, 3 OMA, 3 OSPC; 49-75years of age), and 4 PCOS ovaries (18-35years of age) in women undergoing hysterectomy. cDNA was synthesized using a whole transcriptome kit, and quantitative real-time PCR was performed using TaqMan array 96-well plates containing 32 human endogenous controls in triplicate. Among 32 HKGs studied, RPS17, RPL37A, PPIA, 18srRNA, B2M, RPLP0, RPLP30, HPRT1, POP4, CDKN1B, and ELF1 were selected as the best reference genes. This study confirms recent investigations demonstrating that conventional HKGs, such as GAPDH and beta-actin, are not suitable reference genes for specific pathological conditions, emphasizing the importance of determining the best HKGs on a case-by-case basis and according to tissue type. Our results have identified reliable HKGs for studies of normal human ovaries and those affected by OEA, OMA, OSPC, or PCOS, as well as combined studies of control subjects vs. each cancer or PCOS group.

Evidence for a Novel Endometrioid Carcinogenic Sequence in the Fallopian Tube With Unique Beta-Catenin Expression.

Epithelial proliferations in the fallopian tube have been characterized by some as stem cell outgrowths (SCOUTs) and divided into type I and type II. Type II SCOUTs exhibit diffuse cellular beta-catenin nuclear staining (β-catenin), implying a CTNNB1 mutation. SCOUTs are more common in perimenopausal and postmenopausal women and are associated with ovarian cancer but have not been linked directly to malignancy. We analyzed type II SCOUTs in various gynecologic conditions, and searched for endometrioid atypical hyperplasias (tubal endometrioid intraepithelial neoplasia) or adenocarcinomas in the tube. β-catenin SCOUT frequency in cases of neoplasia was 66.7% per case and 30.7% per nonfimbrial cross-section for uterine endometrioid carcinomas versus 25% and 13.3% for controls, respectively (P=0.02 and 0.09). Multiple (3 or more) β-catenin SCOUTs in a single section were uncommon; 6 of 9 were associated with a carcinoma or proliferative lesion in the endometrium. Tubal endometrioid intraepithelial neoplasia/atypical hyperplasia displayed complex growth, including focal cribriform growth patterns and squamous morules. Two cases of type II SCOUTs associated with tubal endometrioid intraepithelial neoplasia/atypical hyperplasia and/or adenocarcinomas in the fallopian tube were identified, both of which coexisted with a separate endometrioid adenocarcinoma, one with bilateral ovarian endometrioid adenocarcinomas. Both benign and neoplastic tubal lesions were β-catenin. This report is the first to link components of a unique β-catenin endometrioid carcinogenic sequence in the fallopian tube. It further emphasizes the multifocal nature of endometrioid neoplasia in the female genital tract and poses questions regarding the frequency and biologic underpinnings of β-catenin proliferations in the oviduct.

Adjuvant chemotherapy for early stage endometrioid ovarian carcinoma: An analysis of the National Cancer Data Base

IntroductionThe benefit of adjuvant chemotherapy for Stage IC grade 1 and stage IA/IB grade 2 endometrioid ovarian adenocarcinoma (EOOC) remains unclear as the NCCN guidelines recommend either observation only or adjuvant chemotherapy. Therefore, we sought to determine whether patients with stage I EOOC had improved overall survival (OS) following receipt of adjuvant chemotherapy. MethodsPatients with pathological stage I ovarian endometrioid adenocarcinoma diagnosed between 2004 and 2014 were identified from the National Cancer Database. Demographics, pathologic factors including tumor grade, and treatment information including receipt of adjuvant chemotherapy were collected. The impact of chemotherapy on OS was evaluated with Kaplan-Meier curves, and compared with log-rank tests. Multivariate Cox analysis was performed to control for confounders. ResultsA total of 4538 patients were identified and the median age was 55 years The rate of adjuvant chemotherapy use was 50.9%. Higher rates were noted among patients with stage IC and grade 3 tumors. Following stratification by tumor grade, substage and extent of lymphadenectomy, adjuvant chemotherapy was associated with a survival benefit for patients with grade 2 tumors who did not undergo (stage IA/IB: 95.7% vs 83%, p = 0.038; stage IC: 84.5% vs 84.8%, p = 0.39) or had limited lymphadenectomy (stage IA/IB: 96% vs 89.5%, p = 0.03; stage IC: 97.2% vs 83.9%, p = 0.001). A survival difference was also seen for patients with grade 3 tumors who did not undergo lymphadenectomy but did not reach statistical significance. ConclusionAdjuvant chemotherapy was associated with an overall survival benefit for patients with inadequately-staged, grade 2 stage I ovarian endometrioid adenocarcinoma. A possible benefit for inadequately-staged patients with grade 3 tumors cannot be excluded.

Overexpression of Long Noncoding RNA E2F-Mediated Cell Proliferation Enhancing Long Noncoding RNA Is Involved in the Development of Chemoresistance of Cancer Cells to Carboplatin in Ovarian Endometrioid Adenocarcinoma.

Background: E2F-mediated cell proliferation enhancing long noncoding RNA (EPEL) is an oncogenic long noncoding RNA (lncRNA) in lung cancer, but its involvement in other malignancies is unknown. We aimed at exploring the potential role of EPEL in ovarian endometrioid adenocarcinoma. Results: Plasma levels of EPEL and p53 were significantly upregulated in ovarian endometrioid adenocarcinoma patients. In effect, EPEL overexpression distinguished ovarian endometrioid adenocarcinoma patients from the control group. Plasma levels of EPEL and p53 were reversely correlated in ovarian endometrioid adenocarcinoma patients. EPEL overexpression led to downregulated p53 expression in cells of human ovarian endometrioid adenocarcinoma cell line SNU-251, whereas no significant changes in the expression level of EPEL were observed after p53 expression. EPEL overexpression increased, whereas small interfering RNA (siRNA) silencing reduced the viability of SNU-251 cells under carboplatin treatment. In addition, p53 overexpression attenuated the effects of EPEL overexpression on cancer cell viability under carboplatin treatment. Conclusions: Therefore, the overexpression of EPEL may participate in the development of chemoresistance of cancer cells to carboplatin in ovarian endometrioid adenocarcinoma by downregulating p53.

Peritoneal Keratin Granulomatosis Is a Clinical and Radiological Mimicker of Endometrial Adenocarcinoma With Peritoneal Involvement

Peritoneal keratin granulomatosis is a rare tumor-like lesion caused by deposition of tumor-produced keratin. It may be associated with endometrial or ovarian endometrioid adenocarcinoma, atypical polypoid adenomyoma of the endometrium, or ruptured mature teratomas of the ovary. We present 2 cases of peritoneal keratin granulomatosis associated with FIGO (International Federation of Gynecology and Obstetrics) stage 1 endometrial adenocarcinoma. This entity can mimic advanced-stage disease clinically and radiologically, as it did in those cases, and constitutes a diagnostic pitfall that pathologists and surgeons must be aware.

Differential expression of mTOR components in endometriosis and ovarian cancer: Effects of rapalogues and dual kinase inhibitors on mTORC1 and mTORC2 stoichiometry

Endometriosis is a well-known risk factor for ovarian cancer. The genetic changes that characterise endometriosis are poorly understood; however, the mechanistic target of rapamycin (mTOR) pathway is involved. In this study, we investigated the expression of key mTOR components in endometriosis and the effects of rapalogues using an endometrioid ovarian carcinoma cell line (MDAH 2774) as an in vitro model. Gene expression of mTOR, DEPTOR, Rictor and Raptor was assessed by qPCR in 24 endometriosis patients and in silico in ovarian cancer patients. Furthermore, the effects of Rapamycin, Everolimus, Deforolimus, Temsirolimus, Resveratrol, and BEZ235 (Dactolisib, a dual kinase inhibitor) on mTOR signalling components was assessed. mTOR showed a significant increase in the expression in endometriosis and ovarian endometrioid adenocarcinoma patients compared to non-affected controls. DEPTOR, an inhibitor of mTOR, was downregulated in the advanced stages of ovarian cancer (III and IV) compared to earlier stages (I and II). Treatment of MDAH-2774 cells with the mTOR inhibitors resulted in the significant upregulation of DEPTOR mRNA, whereas treatment with rapamycin and BEZ-235 (100 nM) resulted in downregulation of the mTOR protein expression after 48 h of treatment. None of the treatments resulted in translocation of mTOR from cytoplasm to nucleus. Upregulation of DEPTOR is a positive prognostic marker in ovarian cancer and is increased in response to mTOR pathway inhibition suggesting that it functions as a tumour suppressor gene in endometrioid ovarian carcinoma. Collectively, our data suggest the mTOR pathway as a potential connection between endometriosis and ovarian cancer and may be a potential target in the treatment of both conditions.

Perforated ovarian low-grade endometrioid adenocarcinoma: a case-report

Perforated ovarian low-grade endometrioid adenocarcinoma: a case-report

Distinct molecular pathways in ovarian endometrioid adenocarcinoma with concurrent endometriosis.

Women with endometriosis, a benign growth of endometrial tissue outside the uterine cavity, are at increased risk of specific histotypes of epithelial ovarian cancer, such as ovarian endometrioid adenocarcinoma (OEA). Women with OEA who have endometriosis at time of surgical staging demonstrate improved clinical prognosis compared to women with OEA without evidence of endometriosis. However, the molecular contributions of the endometriotic tumor microenvironment to these ovarian cancers remain poorly understood. As a starting point, we used a platform for genome-wide transcriptomic profiling to compare specimens of OEA from women with and without concurrent endometriosis and benign reproductive tract tissues, including proliferative endometrium and typical and atypical endometrioma samples (n = 20). Principle component analysis revealed distinct clustering between benign and malignant samples as well as malignant samples with and without concurrent endometriosis. Examination of gene signatures revealed that OEA with concurrent endometriosis contained a unique molecular signature compared to OEA without concurrent endometriosis, distinguished by 682 unique genes differentially expressed (fold change < or >1.5, p < 0.01). Bioinformatic analysis of these differentially expressed gene products using ingenuity pathway analysis revealed activation of NFkB signaling, an inflammatory signaling pathway constitutively active in endometriosis. DAVID functional annotation clustering further revealed enrichment in RAS signaling as both cytoskeleton organization and GTPase regulator activity relied heavily on RAS protein signal transduction. Gene set enrichment analysis highlighted immune and inflammatory nodes involved in OEA with concurrent endometriosis. These observations provide novel resources for understanding molecular subtleties potentially involved in OEA within the context of the endometriotic tumor microenvironment.

Clinicopathologic Correlation of Mucinous Differentiation in Primary Ovarian Endometrioid Adenocarcinoma

Clinicopathologic Correlation of Mucinous Differentiation in Primary Ovarian Endometrioid Adenocarcinoma

The Endometriotic Tumor Microenvironment in Ovarian Cancer.

Women with endometriosis are at increased risk of developing ovarian cancer, specifically ovarian endometrioid, low-grade serous, and clear-cell adenocarcinoma. An important clinical caveat to the association of endometriosis with ovarian cancer is the improved prognosis for women with endometriosis at time of ovarian cancer staging. Whether endometriosis-associated ovarian cancers develop from the molecular transformation of endometriosis or develop because of the endometriotic tumor microenvironment remain unknown. Additionally, how the presence of endometriosis improves prognosis is also undefined, but likely relies on the endometriotic microenvironment. The unique tumor microenvironment of endometriosis is composed of epithelial, stromal, and immune cells, which adapt to survive in hypoxic conditions with high levels of iron, estrogen, and inflammatory cytokines and chemokines. Understanding the unique molecular features of the endometriotic tumor microenvironment may lead to impactful precision therapies and/or modalities for prevention. A challenge to this important study is the rarity of well-characterized clinical samples and the limited model systems. In this review, we will describe the unique molecular features of endometriosis-associated ovarian cancers, the endometriotic tumor microenvironment, and available model systems for endometriosis-associated ovarian cancers. Continued research on these unique ovarian cancers may lead to improved prevention and treatment options.

The Expression of HSD17B12 Is Associated with COX-2 Expression and Is Increased in High-Grade Epithelial Ovarian Cancer

Objective: The aim of this study was to characterize the expression of hydroxysteroid (17β) dehydrogenase type 12 (HSD17B12), an enzyme involved in the synthesis of arachidonic acid (AA), in ovarian cancer, and to study its coexpression with its upstream and downstream enzymes in the AA pathway, namely elongation of very long chain fatty acids protein 5 (ELOVL5) and cyclooxygenase-2 (COX-2), respectively. Materials and Methods: Samples from benign and malignant ovarian neoplastic lesions were immunohistochemically stained with HSD17B12, ELOVL5, and COX-2. The staining intensities were quantified with the QuantCenter program, and the results were confirmed with visual inspection. Statistical significances were calculated with the Student t test, the Mann-Whitney test, linear regression, or ANOVA. Results: The expression of the HSD17B12, ELOVL5, and COX-2 enzymes increased according to the grade of the endometrioid ovarian adenocarcinomas. In contrast, in serous adenocarcinomas, staining with ELOVL5 was constantly weak, whereas the expression of HSD17B12 and COX-2 increased with the grade or FIGO stage of the cancer, respectively. Conclusions: The expression of HSD17B12 increased along with the severity of ovarian cancer, and the expression mimicked COX-2 expression and intensity. This further suggests the involvement of HSD17B12 in AA production, and its coexpression with COX-2 indicates a role for the enzyme in the increased prostaglandin production during ovarian cancer progression.

Napsin A and WT 1 are useful immunohistochemical markers for differentiating clear cell carcinoma ovary from high-grade serous carcinoma.

Clear cell carcinoma (CCC) of the ovary is an uncommon, but an aggressive epithelial ovarian cancer (EOC), which has overlapping histopathologic features with other ovarian tumours. Lately, Napsin A has been identified as its useful diagnostic immunohistochemical (IHC) marker. Fifty-eight prospectively diagnosed ovarian CCCs, 53 high-grade serous carcinomas (HGSCs), 16 endometrioid adenocarcinomas (EMACs), six mixed carcinomas, containing components of CCC and EMAC, seven metastatic mucinous adenocarcinomas and six ovarian yolk sac tumours (YSTs) were tested for Napsin A immunostaining. Fifty ovarian CCCs, 50 HGSCs, seven ovarian EMACs and five mixed carcinomas were tested for WT1 immunostaining. Napsin A was positively expressed in all 58 (100%) CCCs; was focally positive in 1 of 6 YSTs; in 1/16 EMACs and in six cases of mixed carcinomas, while it was negative in all 53 HGSCs and in seven metastatic mucinous adenocarcinomas. Other IHC markers expressed in cases of CCC ovary were CK7 (31/31) (100%), WT1 (0/50), p53 (20/26, 'wild type'), ER (4/31, focal) (12.9%), PAX8 (14/14) (100%), glypican-3 (4/10, focal) (44.4%), p16INK4 (5/5, focal) and CK20 (0/5). Various IHC markers expressed in HGSCs were WT1 (48/50) (96%), p53 (31/31, mostly 'mutation type'), CK7 (9/9) (100%) ER (13/16, variable) (81.2%) and PAX8 (14/14) (100%). IHC markers expressed in EMACs were ER (15/16) (93.7%), CK7 (2/2) (100%) and WT1 (0/7). IHC markers expressed in mixed carcinomas were CK7 (2/2) (100%), WT1 (0/2), focal Napsin A (6/6) and focal ER (5/6). The sensitivity and specificity of Napsin A for the diagnosis of CCC ovary was 100% and 90.9%, respectively. The sensitivity and specificity of WT1 for diagnosis of HGSC ovary was found to be 96% and 100%, respectively. Napsin A and WT1 are highly sensitive and specific IHC markers for diagnosing ovarian CCCs and HGSCs, respectively, and in differentiating these tumours from their mimics. Napsin A is useful in identification of component of CCC in certain EMACs.