Myxopapillary Ependymoma of the Cauda Equina in a 5-Year-Old Boy

Myxopapillary ependymoma in childhood typically occurs in the central nervous system. There are few surgical cases of myxopapillary ependymoma of the cauda equina in children. We report a case of myxopapillary ependymoma of the cauda equina in a 5-year-old boy, who presented with leg pain and abnormal gait. Subtotal resection surgery was performed. Following the subtotal tumor resection, follow-up magnetic resonance imaging evaluation showed a recurrent tumor. As a result, we performed a second subtotal tumor resection and followed with postoperative radiation therapy. No further evidence of the disease has been noted elsewhere in the patient in over ten years of follow-up. Myxopapillary ependymoma of the cauda equina in a young boy was improved by subtotal tumor resection and postoperative radiation therapy.

Mice-lacking LMP2, immuno-proteasome subunit, as an animal model of spontaneous uterine leiomyosarcoma

Uterine tumors are the most common type of gynecologic neoplasm. Uterine leiomyosarcoma (LMS) is rare, accounting for 2% to 5% of tumors of the uterine body. Uterine LMS develops more often in the muscle tissue layer of the uterine body than in the uterine cervix. The development of gynecologic tumors is often correlated with female hormone secretion; however, the development of uterine LMS is not substantially correlated with hormonal conditions, and the risk factors are not yet known. Radiographic evaluation combined with PET/CT can be useless in the diagnosis and surveillance of uterine LMS. Importantly, a diagnostic biomarker, which distinguishes malignant LMS and benign tumor leiomyoma (LMA) is yet to be established. Accordingly, it is necessary to analyze risk factors associated with uterine LMS in order to establish a method of treatment. LMP2-deficient mice spontaneously develop uterine LMS, with a disease prevalence of ∼40% by 14 months of age. It is therefore of interest whether human uterine LMS shows a loss of LMP2 expression. We found LMP2 expression is absent in human LMS, but present in human LMA. Therefore, defective LMP2 expression may be one of the risk factors for LMS. LMP2 is potentially a diagnostic biomarker for uterine LMS, and gene therapy with LMP2-encording DNA may be a new therapeutic approach.