Ovarian Endometrioid Carcinoma
~Introduction
Ovarian cancer is a major cause of morbidity and mortality among women worldwide. Among the epithelial ovarian tumors, Ovarian Endometrioid Carcinoma (OEC) is an important histological subtype, accounting for approximately 10–20% of epithelial ovarian cancers. It closely resembles endometrial carcinoma of the uterus both morphologically and molecularly, hence the name “endometrioid.”
Ovarian endometrioid carcinoma is often diagnosed at an earlier stage than high-grade serous carcinoma and is frequently associated with endometriosis and synchronous endometrial carcinoma. Because of these features, it generally carries a better prognosis, particularly in early-stage disease.
~Epidemiology
Represents 10–20% of epithelial ovarian cancers
More common in women aged 45–60 years
Incidence is higher in women with endometriosis
Around 15–25% of patients have a synchronous endometrial carcinoma
~Etiology and Risk Factors
1. Endometriosis
Endometriosis is a well-established precursor lesion for ovarian endometrioid carcinoma. Chronic inflammation and estrogen-rich environments promote malignant transformation.
2. Hormonal Factors
Prolonged estrogen exposure
Early menarche and late menopause
Nulliparity
Obesity (peripheral estrogen conversion)
3. Genetic and Molecular Factors
Mutations in PTEN, CTNNB1 (β-catenin), and ARID1A
Microsatellite instability in some cases
Alterations in the PI3K/AKT pathway
4. Reproductive and Lifestyle Factors
Infertility
Lack of oral contraceptive use
Family history of gynecological cancers
~Pathogenesis
Ovarian endometrioid carcinoma often develops through a stepwise progression:
Benign endometriosis
Atypical endometriosis
Endometrioid carcinoma
Molecular changes such as PTEN loss, β-catenin activation, and ARID1A mutation result in increased cellular proliferation and reduced apoptosis, leading to tumor development.
~Gross Pathology
Usually presents as a solid or cystic ovarian mass
Often unilateral, though bilateral involvement may occur
Size varies from 5 to 15 cm
Cut surface appears gray-white to yellow
Frequently associated with endometriotic cysts
~Histopathology
Microscopic Features
Tumor composed of glands resembling endometrial carcinoma
Glands are tubular, cribriform, or complex
Lined by columnar epithelial cells
Moderate nuclear atypia
Mitotic figures present
Additional Features
Squamous differentiation is common and characteristic
Presence of stromal invasion
Areas of necrosis may be seen in high-grade tumors
~Immunohistochemistry
Immunohistochemistry is useful in confirming diagnosis and differentiating from other ovarian tumors.
Positive Markers:
CK7
PAX8
Estrogen receptor (ER)
Progesterone receptor (PR)
β-catenin (nuclear positivity)
Negative Markers:
WT-1 (helps distinguish from serous carcinoma)
Napsin A (helps differentiate from clear cell carcinoma)
~Clinical Features
Symptoms
Abdominal or pelvic pain
Abdominal distension
Bloating
Menstrual irregularities
Infertility
Symptoms related to coexisting endometriosis
Association with Endometrial Cancer
Patients may present with abnormal uterine bleeding
Important to evaluate uterus for synchronous malignancy
~Diagnosis
Imaging
Ultrasound: Complex ovarian mass
CT/MRI: Assessment of tumor spread and staging
Tumor Markers
CA-125 may be elevated but is nonspecific
Histopathological Examination
Definitive diagnosis requires surgical specimen analysis with histology and immunohistochemistry.
~Staging
Staged according to the FIGO staging system:
Stage I: Confined to ovaries
Stage II: Pelvic extension
Stage III: Peritoneal spread or lymph node involvement
Stage IV: Distant metastasis
Most cases are diagnosed in Stage I or II, contributing to favorable outcomes.
~Treatment
1. Surgical Management
Primary treatment includes:
Total abdominal hysterectomy
Bilateral salpingo-oophorectomy
Omentectomy
Pelvic and para-aortic lymph node sampling
Fertility-sparing surgery may be considered in young patients with early-stage disease.
2. Chemotherapy
Platinum-based chemotherapy (carboplatin and paclitaxel)
Good response compared to clear cell carcinoma
Used in advanced stages or high-grade tumors
3. Hormonal Therapy
ER/PR positivity allows the use of progestins or aromatase inhibitors in selected cases
~Prognosis
Early-stage disease: 5-year survival rate of 80–90%
Advanced-stage disease: Reduced survival
Better prognosis compared to high-grade serous carcinoma
Tumor grade and stage are key prognostic factors
~Complications
Recurrence
Spread to pelvis and peritoneum
Treatment-related side effects
Coexistence with endometrial carcinoma
~Differential Diagnosis
High-grade serous carcinoma
Clear cell carcinoma
Metastatic endometrial carcinoma
Borderline endometrioid tumors
Immunohistochemistry and clinical correlation are essential for accurate diagnosis.
~Prevention and Screening
No established screening method
Early treatment of endometriosis
Use of oral contraceptives reduces risk
Regular follow-up in high-risk women
~Recent Advances
Molecular profiling for personalized therapy
Targeted therapies focusing on PI3K/AKT pathway
Improved understanding of tumor-endometriosis link
~Conclusion
Ovarian endometrioid carcinoma is a distinct subtype of epithelial ovarian cancer with close morphological and molecular resemblance to endometrial carcinoma. Its strong association with endometriosis, early-stage presentation, and hormone receptor positivity contribute to a relatively favorable prognosis. Accurate diagnosis, optimal surgical management, and appropriate adjuvant therapy are crucial for improving patient outcomes. Ongoing research into molecular pathways offers hope for more targeted and effective treatments in the future.
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