Ovarian cancer is the 8th most common cancer type in women and the deadliest one among the gynecological malignancies. Due to its late clinical presentation, it is often diagnosed in a late stage, when the 5-year survival rate is under 30%. Despite the commonly observed initial good response to chemotherapy, chemo-resistant tumor cells can remain in metastatic sites and lead to a relapse or progressive disease.^[1,2]

Ovarian carcinoma (OC) is a broad term that encompasses both epithelial and non-epithelial subtypes. Epithelial tumors are the most common form of OC and consist of serous, endometrioid, clear-cell, mucinous, and undifferentiated carcinomas, representing about 90% of all cases.‌^[3] The main pathway for OC metastasis is through abdominal implantation, with the cancer primarily spreading to the peritoneum, pelvic organs, and lymph nodes. OC also disseminates to distant organs—liver, distant lymph nodes, lung, bones, and brain being the most frequent sites.^[4] Gastric metastases are rare in clinical practice and autopsy analyses, with an incidence ranging from about 0.2% to 0.7%, with the main origin being breast cancer, followed by malignant melanoma and lung cancer.^[2,5] Gastric metastasis from OC is extremely rare, accounting for only 0.013% to 1.6% of all gastric metastatic tumors.^[2,5-7] We herein present a rare case of single submucosal gastric metastasis from OC without ulcerations, mimicking gastrointestinal stromal tumor (GIST). The tumor was detected on a follow-up 18F-FDG PET/CT in a patient with a history of ovarian cancer. The histological diagnosis was confirmed after endoscopic ultrasound (EUS) examination and biopsy.

A 59-year-old female with a history of arterial hypertension presented to another hospital with postmenopausal vaginal bleeding. This case report was conducted at Acibadem City Clinic Tokuda Hospital in Sofia, Bulgaria, with appropriate ethical oversight and patient consent obtained. Initial imaging, including abdominal and transvaginal ultrasound, revealed a cystic tumor formation in the pelvis. Given the findings, the patient underwent diagnostic and staging laparoscopic surgery, which included total hysterectomy, bilateral adnexectomy, total omentectomy, appendectomy, and paraaortic lymph node dissection. Pathological reports showed poorly differentiated ovarian carcinoma. Six weeks after surgery, the patient underwent a diagnostic CT scan in our hospital, which revealed no evidence of distant metastases. The patient was staged as pT3N1M0. Pre-therapy CA-125 levels were in the reference range. Therapy with paclitaxel, carboplatin, and bevacizumab was initiated after a cardiac ultrasound showed no abnormalities in the heart function and kinetics. After 6 cycles of combined chemo- and targeted therapy, the patient underwent a restaging with 18F-FDG PET/CT. It showed no signs of recurrent or metastatic disease and was assessed as stable disease according to RECIST 1.1(Fig. 1) .

A non-avid FDG lesion in the brain was revealed (not shown). As indicated by the findings, an MRI brain scan was performed and ruled out a metastasis from the oncologic disease; the lesion was assessed as meningioma. The therapy was continued in the same regimen. A restaging 18F-FDG PET/CT scan was performed after 16 cycles and showed stable disease. The patients continued maintenance therapy with bevacizumab in a stable clinical condition, remaining asymptomatic. Tumor marker CA-125 levels remained in the normal range. The following two routinely performed PET/CTs showed stable disease.

She was free of disease for 3 years until a routine follow-up PET/CT form January 2024 revealed a newly detected FDG-avid lesion in the stomach measuring 12×23 mm with SUVmax 6.45. The hypermetabolic intramural formation was smoothly compressing the posterior wall of the gastric body, bulging into the gastric cavity. The metabolic activity and morphological characteristics of the lesion raised the suspicion for a neoplastic process, suggestive of a gastric submucosal tumor such as a gastrointestinal stromal tumor (GIST)(Fig. 2) .

At that time the patient reported no symptoms, exhibited overall well-being, and had no elevation in serum levels of CA-125. Based on the findings, EUS (endoscopic ultrasound) with biopsy was performed. The pathological report showed a metastasis of high-grade serous ovarian carcinoma(Fig. 3) .

A clinical tumor board stated the necessity of a subtotal gastrectomy. In March 2024 a Billroth I partial gastrectomy was performed. The resected tissue was submitted for final pathological analysis, which excluded GIST and confirmed the surgically excised mass as metastatic ovarian cancer(Fig. 4) .

The postoperative period was well-tolerated, and the patient remained stable. A diagnostic CT in April 2024 showed no abnormalities. The patient continued targeted therapy with olaparib. Our patient successfully managed maintenance therapy with the PARP inhibitor with no adverse effects. The last PET/CT scan was performed in January 2025 and showed no signs of recurrent disease and no new metabolically active lesions(Fig. 5) .

A Krukenberg tumor is a metastatic “signet ring” subtype of metastatic tumor to the ovary, which typically originates from the stomach in 70% of the cases with an incidence of 1% to 21%, with a higher frequency in Asian countries due to the greater prevalence of gastric cancer.^[8] A “Reverse Krukenberg” tumor—a gastric metastasis from ovarian cancer—is ever rarer, with few cases published.^[9] A systematic review published in 2016 described only 18 cases of gastric metastases originating from ovarian carcinoma, most of the patients being in advanced disease stages.^[10] Two additional case reports, published in 2021 and 2024, detailed newly identified patients with gastric metastasis originating from primary ovarian cancer.^[2,11]

Distant hematogenous spread has been reported in 2% to 3% of the patients.^[2] Even though the exact mechanism of gastric metastasis is not fully understood, it can be accounted for by the blood supply of the stomach, making it a potential target for metastasis. Gastric metastasis presents with nonspecific symptoms, which can include epigastric pain, melena, anemia, nausea, and vomiting. In this case, however, the patient was asymptomatic. Although the exact mechanisms of gastric metastasis from ovarian cancer remain unclear, some studies suggest specific pathways that facilitate tumor spread between the stomach and ovaries. Estrogen is likely a key factor, promoting the distant spread of ovarian cancer.^[12] Research on tumor development and metastasis in vivo found that MUC4 accelerates the metastasis of ovarian cancer cells by increasing N-cadherin expression, leading to more frequent metastasis to abdominal organs, especially the stomach.^[13] Changes in the tumor microenvironment, including MUC4, estrogen, and exosomes, are likely significant factors in the metastatic spread of ovarian cancer.^[2]

Although gastric metastasis from ovarian carcinoma is uncommon, we advise clinicians to stay mindful of the potential for gastric metastasis in patients with a history of ovarian cancer.

The clinical presentation of gastric metastasis from ovarian carcinoma can be nonspecific or vary, as presented in the current case. The combination of imaging modality plus biopsy can be a helpful tool in accurately diagnosing gastric lesions.