Craniopharyngioma is considered to be a benign intracranial tumor. Malignant transformation of craniopharyngioma has rarely been described. In this article, we report a case of ameloblastic carcinoma arising from a previously benign craniopharyngioma in a 42-year-old woman. The patient was diagnosed with craniopharyngioma in August 2004 and underwent surgical resection of a typical craniopharyngioma, the pathological result was craniopharyngioma, papillary and adamantinomatous types. During the subsequent 5 years, this patient experienced two recurrences, for which surgical resections were performed without radiotherapy. The last two pathologic diagnoses were malignant craniopharyngiomas and there was more apparent sign of malignancy in the third pathologic section. The exact pathogenesis and the biological behavior of malignant change in craniopharyngioma are not yet clear. We review the relevant literature of malignant craniopharyngioma. Histopathologic, clinical and imaging features of malignant craniopharyngioma and the possible effect of radiotherapy on the carcinogenesis are discussed.

Studies have found that LINC00467 is an important regulator of cancer. However, the function of LINC00467 in glioma cell is unclear. Therefore, this experimental design based on LINC00467 to explore its mechanism of action in glioma cell. RT-qPCR was used to detect the expression of LINC0046 and miR-200a in glioma cell lines. MTT assay, Edru assay and Transwell assay and flow cytometry were used to detect the effects of LINC0046 and miR-200a on PC cell proliferation, migration and apoptosis. Target gene prediction and screening, luciferase reporter assays were used to validate downstream target genes for LINC0046 and miR-200a. Western blotting was used to detect the protein expression of E2F3. The tumor changes in mice were detected by in vivo experiments in nude mice. LINC00467 was up-regulated in glioma cells. Knockdown of LINC00467 inhibited the viability, migration and invasion of glioma cells. In glioma cells, miR-200a was significantly reduced, while E2F3 was significantly rised. LINC00467 negatively regulated the expression of miR-200a in gliomas, while miR-200a negatively regulated the expression of E2F3 in gliomas. INC00467 promoted the development of glioma by inhibiting miR-200a and promoting E2F3 expression. LINC00467 may be a potential therapeutic target for gliomas. ARTICLE HISTORY