Extra‐axial mass in a 72‐year‐old woman

Access at https://isn-slidearchive.org/?col=ISN&fol=Archive&file=BPA-24-08-CIR-235.svs. A 72-year-old lady presented with complaints of slurring of speech, loss of appetite, sleep disturbance for the past 1 month. Magnetic resonance imaging brain showed a large extra-axial space occupying lesion noted along left frontal convexity, measuring 47 × 70 × 36 mm. The lesion was hyperintense on T2 and hypointense on T1 and showed diffusion restriction and contrast enhancement (Figure 1). Cerebrospinal fluid (CSF) cleft sign and buckling of adjacent white matter (anterior) and pial vessels were noted around the lesion. The lesion showed few prominent intralesional flow voids. The overall imaging features favored a meningioma. She underwent left frontoparietal craniotomy and Simpson's Grade II excision of lesion (Box 1). Histopathological examination showed a meningothelial tumor composed of neoplastic meningothelial cells with mild nuclear anisonucleosis, arranged as whorls and syncytium. Embedded and admixed within this meningothelial neoplasm were deposits from an epithelial neoplasm comprising of tumor cells arranged in acini of varying sizes and papillae (Figure 2A,B and Box 1). These cells were polygonal with vesicular nuclei, visible nucleoli and moderate amounts of eosinophilic cytoplasm. Mitoses were noted within both the components, and atypical mitotic figures were seen in the epithelial component (Figure 2C). The mitotic activity in the meningothelial component was 1–2/10 high power fields. On immunohistochemistry, the meningioma component was positive for Vimentin, EMA (epithelial membrane antigen), and SSTR2A (somatostatin receptor 2A) (Figure 2D). The epithelial component was positive for EMA, CK (cytokeratin; Figure 2E) and CK7. TTF-1 (thyroid transcription factor) showed diffuse moderate to strong positivity in the epithelial component, indicating a primary carcinoma from lung or thyroid origin (Figure 2F). The tumor cells were negative for CK20. MIB1 labeling index was 5%–6% in the meningothelial component and 20%–25% in the epithelial component. Subsequently the patient underwent an 18F-fluorodeoxyglucose positron emission tomography-computed tomography (18F-FDG PET-CT) of the whole body, which showed a hypermetabolic perihilar mass lesion in the left lung infiltrating the mediastinum, encasing and severely narrowing the left pulmonary artery, suggestive of bronchogenic carcinoma. Enlarged hypermetabolic left supraclavicular, mediastinal, and left hilar lymph node metastasis were also noted, indicative of a metastatic disease process. Metastatic adenocarcinoma, consistent with lung primary to transitional meningioma (CNS WHO grade 1). This case is an example of tumor-to-tumor metastasis (TTM). Tumor-to-meningioma metastasis (TTMM) refers to a phenomenon where a tumor metastasizes to a meningioma, also known as intrameningioma metastasis. It is important to distinguish TTM from collision tumors. Collision tumors are tumors that grow adjacent to each other and infiltrates into one another. The first tumor-to-tumor phenomenon was reported in 1902 by Berent. The criteria for TTM proposed by L.V. Campbell are: at least two primary tumors must exist; the host tumor must be a true neoplasm; the metastatic focus must show established growth inside the host tumor, and not be of contiguous growth; the host tumor cannot be a lymph node involved in leukemia or lymphoma [1]. The most common tumors associated with TTMM are breast carcinoma and lung carcinoma. Other tumors associated with TTMM are esophageal carcinoma, renal cell carcinoma, prostatic adenocarcinoma, thyroid carcinoma, angiosarcoma, and malignant melanoma [2]. Because meningiomas have a rich vascular supply and a high collagen content, it permits the establishment of metastatic tumor deposits and provide an ideal environment for metastasis. Another interesting finding is, meningiomas that give shelter to metastases are more likely to express E-cadherin than meningiomas in general, indicating that E-cadherin may play a role in TTMM. This could also explain why breast carcinoma is the most common tumor associated with TTMM. E-cadherin is a tumor suppressor gene, implicated in breast carcinogenesis. E-cadherin is a cell-adhesion molecule and its loss or reduced expression in tumor cells is essential for local invasion and first step of metastasis. Contrarily, its expression may promote in cell adhesion and aid in TTM. The other tumors that act as recipient in TTM are renal cell carcinoma and pancreatic carcinoma. In the present case, the metastatic tumor was a lung carcinoma, which is one of the common malignancies to metastasize to the brain, with approximately 10% to 36% of all lung carcinomas developing brain metastasis over the course of disease [3]. The overall prognosis of cases with TTMM is very poor. The present case represents a rare occurrence of TTMM and emphasizes the need for clinicians and pathologists to be well aware of the entity as the prognosis of meningioma and TTMM are at the opposite extremes. TTMM may rarely present as the first clinical manifestation of occult primary lung carcinoma. In the era of molecular diagnosis, histopathology remains the gold standard for the diagnosis of TTM, supported by immunohistochemical studies. S. Rima analyzed the data and wrote the draft. B. N. Nandeesh, Mangalkumar Raachatte, and Anil Pande analyzed the data and reviewed the article. All authors approved the final version of the article. The authors declare no conflicts of interest. All data related to this case are deidentified. The data that support the findings of this study are available from the corresponding author upon reasonable request.