Parotid carcinoma metastasis to parietal meningioma: case report and molecular biologic considerations

A combination of factors as the meningioma's rich vascularity, its low metabolic rate, immunologic factors and the molecular pattern explains the affinity of some cancer metastasis to seed inside meningiomas. In this context, the importance of surface adhesion molecules is of rising interest.

We report the exceptional case of a parotid carcinoma metastasis within a meningioma. A 68-year old male was referred to our hospital with headache and progressive right hemiparesis. Four years before he was diagnosed with parotid gland cancer for which he had undergone parotidectomy, radiation, neck dissection and chemotherapy. MRI showed a left sided high-parietal, dural-based, extraaxial, contrast enhancing tumor which was consequently removed microsurgically. Histological examination revealed a dedifferentiated parotid carcinoma metastasis inside a microcystic meningioma WHO grade I. Mechanisms that have been suggested to be responsible for metastasis into meningioma include meningiomas' rich vascularity, slow growth, their high collagen and lipid content, immunologic factors but also the expression of certain surface adhesion molecules, in particular E-cadherin. In the presented case E-cadherin immunostaining was strongly positive in the metastatic tissue that invaded the meningioma in a droppled-like fashion. We discuss the potential role of E-cadherin, re-expression of a modified E-cadherin complex and the potential importance of mesenchymal surface proteins in the pathophysiology of carcinoma metastasis into meningioma.

Surface proteins of carcinoma cells might play a key role regarding their affinity to seed inside meningiomas. This might be a leading mechanism to the multifactorial process of carcinoma-to-meningioma metastasis.