# Clinicopathological Diagnosis and Prognosis of Endometrioid Borderline Ovarian Tumors: Dual Case Reports and Literature Review

**Authors:** Fang Yang, Dong Chen, Qian Sun, Jingjing Yu, Xue Wang

PMC · DOI: 10.1002/cnr2.70388 · Cancer Reports · 2025-10-28

## TL;DR

This paper presents two case studies of rare endometrioid borderline ovarian tumors, highlighting their diagnosis, treatment, and genetic features to improve understanding and reduce misdiagnosis.

## Contribution

The study contributes two detailed case reports of EBOT with genetic findings (CTNNB1 and PTEN deletions) and emphasizes surgical treatment effectiveness.

## Key findings

- EBOT cases showed disorganized glands, mild epithelial atypia, and specific immunohistochemical profiles (CK, CK7, ER, PR positive; WT-1 negative).
- Genetic analysis revealed heterozygous deletions in CTNNB1 and PTEN in the two cases.
- Both patients remained tumor-free after surgery with no recurrence or metastasis during follow-up.

## Abstract

Endometrioid borderline ovarian tumor (EBOT) is rare and frequently misdiagnosed. This study aims to investigate the clinicopathological features, immunohistochemical characteristics, differential diagnosis, therapeutic approaches and disease prognosis, thereby establishing a robust foundation to mitigate misdiagnosis risks and deepen insights into the pathological diagnosis of this disease.

From May 2020 to December 2022, two female patients diagnosed with EBOT were enrolled at Ningbo Yinzhou No. 2 Hospital. The patients, aged 30 and 34 years, respectively, both underwent left adnexal resection. Microscopically, the tumors displayed disorganized crowded endometrioid glands, mild‐to‐moderate epithelial atypia, and fibrous stroma interspersed among glands. Mulberry‐like squamous metaplasia was also observed in some areas. Tumor cells were positive for cytokeratin (CK), cytokeratin 7 (CK7), estrogen receptor (ER) and progesterone receptor (PR), but negative for Wilms' tumor 1 (WT‐1). The Ki‐67 index ranged from 3% to 10%. Genetic analysis revealed a heterozygous CTNNB1 deletion in one tumor, whereas a heterozygous PTEN deletion in the other. As of the current follow‐up (ranging from 10 to 40 months), both cases remained in a tumor‐free status, with no signs of recurrence or metastasis to date.

EBOT are infrequent and may coexist with endometriosis or endometrioid carcinoma. Our cases demonstrated a heterozygous deletion of the CTNNB1 gene in one case, while a heterozygous deletion of the PTEN gene in the other. Surgery remains the main treatment, reflecting its efficacy in achieving disease control and a favorable prognosis.

## Linked entities

- **Genes:** CTNNB1 (catenin beta 1) [NCBI Gene 1499], PTEN (phosphatase and tensin homolog) [NCBI Gene 5728], CHKA (choline kinase alpha) [NCBI Gene 1119], KRT7 (keratin 7) [NCBI Gene 3855], EREG (epiregulin) [NCBI Gene 2069], PGR (progesterone receptor) [NCBI Gene 5241], WT1 (WT1 transcription factor) [NCBI Gene 7490]
- **Diseases:** endometriosis (MONDO:0005133), endometrioid carcinoma (MONDO:0005026)

## Full-text entities

- **Genes:** PGR (progesterone receptor) [NCBI Gene 5241] {aka NR3C3, PR}, PTEN (phosphatase and tensin homolog) [NCBI Gene 5728] {aka 10q23del, BZS, CWS1, DEC, GLM2, MHAM}, CMPK1 (cytidine/uridine monophosphate kinase 1) [NCBI Gene 51727] {aka CK, CMK, CMPK, UMK, UMP-CMPK, UMPK}, ESR1 (estrogen receptor 1) [NCBI Gene 2099] {aka ER, ESR, ESRA, ESTRR, Era, NR3A1}, KRT7 (keratin 7) [NCBI Gene 3855] {aka CK7, K2C7, K7, SCL}, WT1 (WT1 transcription factor) [NCBI Gene 7490] {aka AWT1, GUD, NPHS4, WAGR, WIT-2, WT-1}, CTNNB1 (catenin beta 1) [NCBI Gene 1499] {aka CTNNB, EVR7, MRD19, NEDSDV, armadillo}
- **Diseases:** endometrioid carcinoma (MESH:D018269), EBOT (MESH:D010051), metastasis (MESH:D009362), endometriosis (MESH:D004715), Tumor (MESH:D009369)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12568370/full.md

## References

12 references — full list in the complete paper: https://tomesphere.com/paper/PMC12568370/full.md

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Source: https://tomesphere.com/paper/PMC12568370