Intracranial tumor-to-tumor metastasis: Metastatic pulmonary adenocarcinoma to a diffuse astrocytoma (WHO grade II).
Two pathologic phenomenon, "collision tumor" and "tumor to tumor metastasis" both result in the intermingling of two separate primary neoplasms. While "collision tumor" results from growth of neighboring tumors within a shared space, "tumor to tumor metastasis" results from hematogenous spread of a primary donor usually extracranial tumor to a recipient/host tumor. The criteria used to defined "tumor to tumor metastasis" are as follows: (i) more than one primary tumor must exist; (ii) the recipient tumor must be a true neoplasm; (iii) the metastatic neoplasm should show established growth in the recipient tumor, not resulting from contiguous growth of an adjacent tumor or tumor embolism; and (iv) lymphatic metastasis to a site of pre-existing lymphoid malignancy are excluded (1, 7). Tumor to tumor metastasis is an unusual phenomenon. The most common donor tumors are breast and lung carcinoma (7),while the most common benign and malignant recipient tumors are meningioma and renal cell carcinoma, respectively (7, 10). Metastasis to primary intracranial glioma is exceptionally rare and to our knowledge represents the first report of metastatic carcinoma to an IDH1mutant low-grade diffuse glioma (9). To date, 14 cases of tumor metastasis to glioma, including our case, have been reported in the literature (5-8). The three most common donors are lung carcinoma, melanoma, and breast carcinoma in descending order. The top three most common recipients are oligodendroglioma, anaplastic astrocytoma, and ependymoma. Nonetheless, some of the older reports are questionable and poorly substantiated given the lack of immunohistochemical and genetic tools of those times. For example, malignant epithelioid cells could represent epithelial-like areas or frank epithelial metaplasia within an anaplastic astrocytoma or glioblastoma (2, 6). Similarly, without appropriate immunohistochemical confirmation, metastatic melanoma may occasionally mimic diffuse glioma (6). Although in general, the pathogenesis of cancer metastasis has been described using the "seed and soil" hypothesis (3, 4), there are currently no proven molecular explanations for "tumor-to-tumor metastasis" and why gliomas so rarely serve as recipients in this phenomenon.
Contributed by Jantima Tanboon, MD, Ananya Pongpaibul, MD, Orasa Chawalparit, MD, Jitladda Wasinrat, MD, Theerapol Witthiwej, MD, Arie Perry, MD