RESUMO
Gliomatosis peritonei (GP) is a rare condition characterized by mature glial tissue implants widespread in the peritoneum, which is occasionally followed by treatment for immature teratoma (IM). The present study reported a case of GP with fluorodeoxyglucose (FDG) accumulation and contrast enhancement followed by treatment for IM. A 30-year-old female, 2-gravida and 0-para, underwent laparotomy with hysterectomy, bilateral salpingo-oophorectomy, and partial omentectomy followed by four cycles of chemotherapy with bleomycin, etoposide, and cisplatin for IM (Grade 2) of stage IIIC. At the 6-month follow-up, computed tomography (CT) revealed a 1-cm mass with contrast enhancement on splenic flexure. Positron-emission tomography (PET)/CT revealed intense FDG accumulation at the same site. Although α-fetoprotein, which was elevated preoperatively, remained normal, she was diagnosed with IM recurrence. The patient underwent three cycles of chemotherapy with paclitaxel, ifosfamide, and cisplatin, but the size, the degree of contrast enhancement and FDG accumulation of the mass did not change after chemotherapy. A diagnostic laparoscopy was performed. which revealed multiple small peritoneal implants, including a 1-cm mass at the splenic flexure. The 1-cm mass was dissected at the splenic flexure and some other implants. Mature well-differentiated glial tissue with non-atypia was identified in all tissue, and a diagnosis of GP was made. The patient is currently undergoing regular follow-up. Few reports are available regarding FDG-PET/CT imaging of GP. GP should be considered as the differential diagnosis of FDG-avid mass followed by IM therapy. A laparoscopic diagnosis is useful to obtain an accurate diagnosis of GP.
RESUMO
BACKGROUND: Recently, the Eph-ephrinA system was proposed to contribute to the initial interaction between the maternal endometrial epithelium and embryonic trophectoderm. Since the Eph-ephrin interaction can induce adhesive and/or repulsive forces into the cells, we examined the possible role of this system in functional changes in endometrial epithelial cells using endometrial carcinoma-derived Ishikawa cells. METHODS: The expressions of EphA1, A2 and A4 on Ishikawa cells were examined by RT-PCR and western blotting analyses. The effects of recombinant ephrinA1 on Ishikawa cells were also examined by western blot analysis and cell attachment and aggregation assays. RESULTS: EphA1, A2 and A4 were expressed on Ishikawa cells. Recombinant ephrinA1 bound to the surfaces of Ishikawa cells and induced phosphorylation of EphA2 and A4. In bovine serum albumin-blocked nitrocellulose-coated dishes, Ishikawa cells remained floating and aggregated with each other. Under these conditions, immobilized ephrinA1 promoted Ishikawa cell attachment with increased tyrosine phosphorylation in focal adhesion kinase. In addition, immobilized ephrinA1 reversibly inhibited Ishikawa cell aggregation. Gene-reduction of EphA1, A2 and A4 by siRNAs attenuated the inhibitory effects of ephrinA1 on cell aggregation, confirming that ephrinA1 affects Ishikawa cell functions through Eph-ephrinA interaction. CONCLUSIONS: This study demonstrated that the Eph-ephrinA system can promote cell attachment along with intercellular dissociation in Ishikawa cells. These findings suggest that this system can induce functional changes in endometrial epithelial cells.
