Taisuke Mori

Computed tomography, magnetic resonance imaging, and positron emission tomography/computed tomography findings for the diagnosis of malignant struma ovarii: A case report

AbstractMalignant struma ovarii (MSO) is an extremely rare disease arising from struma ovarii. Preoperative diagnosis is still challenging due to the lack of criteria for imaging findings. Herein, we report a case of MSO with suggestive imaging findings for a 50‐year‐old woman who presented with a pelvic tumor. The tumor did not typically show characteristic imaging findings of struma ovarii; however, the findings implied colloids of thyroid tissue within solid components on the magnetic resonance imaging (MRI) and computed tomography. Additionally, the solid components showed hyperintensity on diffusion‐weighted image and hypointensity on apparent diffusion coefficient maps. Total abdominal hysterectomy, bilateral salpingo‐oophorectomy, and omentectomy were performed. Histopathological examination revealed MSO of the right ovary, pT1aNXM0. The distribution of papillary thyroid carcinoma tissue corresponded to restricted diffusion area on MRI. In conclusion, the coexistence of imaging findings suggesting thyroid tissue and restricted diffusion in the solid component on MRI could indicate MSO.

A case of ovarian carcinosarcoma with germline BRCA2 pathogenic variant

AbstractOvarian carcinosarcoma in hereditary breast and ovarian cancer syndrome is rare. A 43‐year‐old woman with a family history of prostate and uterine or ovarian cancer had an 8‐cm mass in the right ovary. Although computed tomography suggested peritoneal dissemination to the Douglas pouch, she wanted to preserve her fertility; therefore, she underwent a right salpingo‐oophorectomy. Histopathological diagnosis was carcinosarcoma consisting of high‐grade serous carcinoma and sarcomatous components, including cartilage. Three weeks later, she underwent radical surgery. The disease was classified as advanced stage IIIB (FIGO 2014). A germline BRCA2 pathogenic variant was identified. After postoperative adjuvant chemotherapy, maintenance therapy with a poly(adenosine diphosphate‐ribose) polymerase (PARP) inhibitor was continued for 25 months without recurrence. A detailed examination of a mass in her left breast at her first visit revealed a ductal carcinoma in situ. PARP inhibitors may be effective as maintenance therapy for advanced ovarian carcinosarcoma with germline BRCA mutations.

Low-Nutrient Environment-Induced Changes in Inflammation, Cell Proliferation, and PGC-1α Expression in Stromal Cells with Ovarian Endometriosis

Although nutrient status plays an important role in cell metabolism, its significance in endometriosis is obscure. Herein, we investigated the effects of a low-nutrient microenvironment on endometriosis. Stromal cells (SCs) from ovarian endometrioma (OESCs) or normal endometrium without endometriosis (NESCs) were isolated and cultured. A low-nutrient microenvironment was replicated by replacing the culture medium with Hank's balanced salt solution. OESC and NESC proliferation under the low-nutrient condition was measured. The expression of exacerbating factors in endometriosis under the low-nutrient condition was examined at the mRNA and protein levels. OESCs showed higher proliferation than NESCs under the low-nutrient condition. In OESCs, the low-nutrient condition upregulated the mRNA expression of vascular endothelial growth factor (VEGF), interleukin-6 and -8, aromatase, Bcl-2, and peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) and downregulated that of BAX and induced transcription of PI.3, PII, and exon II. Western blotting revealed elevated VEGF and PGC-1α expression under the low-nutrient condition in OESCs. These changes coincided with the elevated expression of PGC-1α, which was reduced at the mRNA level upon nutrient status rescue. Endometriosis is exacerbated by altered angiogenesis, inflammation, anti-apoptosis, and local estrogen production while trying to survive under a low-nutrient microenvironment; it may be attributed to PGC-1α-mediated metabolic mechanisms.