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Myoepithelial carcinoma of the vulva is extremely rare, with only five cases reported. Here, we describe a case of vulvar myoepithelial carcinoma along with a review of the literature. The patient, a 49-year-old woman, was referred for a tumor on the right labium majora. She underwent a wide local excision and bilateral inguinal lymph node dissection. Pathological examination revealed an unencapsulated, infiltrative pattern, with solid, nested and trabecular components and areas with myxoid or hyalinized stroma. The tumor consisted of oval to round epithelioid cells with moderate nuclear pleomorphism. By immunohistochemistry, the tumor cells were diffusely positive for cellular adhesion molecule (CAM) 5.2, epithelial membrane antigen (EMA), S-100 protein, and vimentin and focally positive for carcinoembryonic antigen (CEA) and p63, while negative for alpha- smooth muscle actin (SMA). The tumor was diagnosed as a myoepithelial carcinoma of the vulva, with metastases to the bilateral inguinal lymph nodes. Following completion of adjuvant radiotherapy, the patient remained alive without any evidence of recurrence at 56 months. A review of six cases of this tumor (including the present case), demonstrated variable morphology with some overlapping features. Therefore, immunohistochemistry using a panel of epithelial and myogenic markers is essential for definitive diagnosis. Two cases had inguinal lymph node metastases and received adjuvant radiotherapy or concurrent chemoradiotherapy, which resulted in good local control. One case had lung metastasis and was successfully treated by chemotherapy. Given the rarity of this disease and its uncertain prognosis, no clinical trials have been conducted regarding the necessity of adjuvant therapy. Myoepithelial carcinomas of the vulva are extremely rare making case series the most viable means of optimizing diagnosis and therapy.

Cyclooxygenase (COX)-2 inhibitors have been reported to potentially modulate the resistance of cancer cells to chemotherapeutic drugs by affecting multidrug resistance 1 (MDR1) expression. In the present study, we investigated the association between COX-2 and MDR1 expression in endometrial cancers and evaluated the effects of the COX-2 inhibitor, etodolac, in combination with paclitaxel on paclitaxel-resistant endometrial cancer cells. The relationship between COX-2 and MDR1 mRNA expression was examined by quantitative PCR in 36 endometrial cancer specimens. The paclitaxel-resistant cell line OMC-2P was established from OMC-2 cells. Paclitaxel (1 µg/ml) with or without etodolac (10 µg/ml) was added to OMC-2 and OMC-2P cells, and COX-2 and MDR1 mRNA expression levels were examined. The concentration of prostaglandin E2 (PGE2) in the supernatant of each cell line was examined by enzyme-linked immunosorbent assay. The function of MDR1 was determined by intracellular accumulation of rhodamine 123 using flow cytometry, and the concentration of intracellular paclitaxel was determined by high-performance liquid chromatography. We found a positive relationship between COX-2 and MDR1 mRNA expression in endometrial cancer. Both COX-2 mRNA expression and PGE2 production were elevated in resistant OMC-2P cells when compared to non-resistant OMC-2 cells. Additionally, MDR1 mRNA expression was markedly upregulated in OMC-2P cells. In OMC-2 cells, COX-2 and MDR1 mRNA levels were significantly upregulated by paclitaxel treatment and downregulated by co-administration with etodolac. In OMC-2P cells, COX-2 mRNA expression was also significantly upregulated by paclitaxel treatment and tended to be downregulated by co-administration with etodolac. Moreover, co-administration of paclitaxel and etodolac suppressed the induction of MDR1 mRNA. Rhodamine 123 efflux was increased in OMC-2P cells when compared to the efflux in the OMC-2 cells and was increased in response to paclitaxel treatment. Co-administration of paclitaxel and etodolac in both cell lines resulted in decreased rhodamine 123 efflux. The actual concentration of intracellular paclitaxel in OMC-2P cells was significantly lower than that in OMC-2 cells treated with paclitaxel alone and was significantly increased after co-administration of paclitaxel and etodolac. These findings suggest that paclitaxel resistance may be associated with COX-2 and MDR1 expression in cancer cells. Co-administration of COX-2 inhibitors and paclitaxel may have a key role in modulating or overcoming paclitaxel resistance in endometrial cancers.

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