The behavior of rhabdoid meningiomas otherwise lacking malignant features remains unknown as most of the originally reported aggressive cases showed anaplastic histologic features independently of rhabdoid phenotype. We studied 44 patients with rhabdoid meningiomas lacking anaplastic features. Median age at diagnosis was 48.6 years (range 10-79). Location was supratentorial in 28 (63.6%), skull base in 15 (34.1%), and spinal in 1 (2.3%). Tumor grade was otherwise World Health Organization grade I (n = 22, 50%) or II (n = 22, 50%). Rhabdoid cells represented <20% of the tumor in 12 cases (27.3%), 20% to 50% in 18 (40.9%), and >50% in 14 (31.8%). Median clinical follow-up, available for 38 patients, was 5.0 years (range 0.17-14.2). Recurrence occurred in 9 patients (5-year recurrence-free survival, 73.7%) with a significantly higher risk in subtotally resected tumors (p = 0.043). Rhabdoid cell percentage was not associated with recurrence. Six patients died (4 of disease, 2 of unclear causes); 5-year overall survival was 86.7%, a mortality in excess of that expected in grade I-II meningiomas but much lower than originally reported. Review of 50 similar previously reported cases confirmed our findings. We suggest that rhabdoid meningiomas be graded analogously to nonrhabdoid tumors, with caution that some may still behave aggressively and close follow-up is recommended.

Pigment deposition is occasionally seen in hepatocellular adenomas. Several reports suggest that pigmented hepatocellular adenomas have increased risk of malignancy, but these tumors remain incompletely understood. To determine the frequency of pigment deposition, we evaluated and classified 109 well-differentiated hepatocellular neoplasms that were originally diagnosed or submitted in consultation as hepatocellular adenomas and found 27 (25%) pigmented tumors. All were negative on iron stain and in three cases electron microscopy confirmed the pigment was lipofuscin. The lipofuscin intensely stained with glypican-3 in most cases (89%). Of the 27 pigmented tumors, 11 cases (41%) were classified as hepatocellular adenomas, 7 cases (27%) were classified as atypical hepatocellular adenomas/hepatocellular neoplasms of uncertain malignant potential, and 9 cases (33%) were reclassified as well-differentiated hepatocellular carcinomas. Four (of 9) hepatocellular carcinomas arose in pigmented hepatocellular adenomas, giving a rate of malignant transformation in pigmented hepatocellular adenomas of 27%. Of the total 27 pigmented tumors, 78% were in women and 22% in men, but interestingly only men had tumors classified as hepatocellular carcinoma or hepatocellular neoplasm of uncertain malignant potential. Also of note, a total of 10 individuals (37%) had multiple hepatocellular neoplasms but in 9 of these cases the other adenomas were non-pigmented. Importantly, in cases with multiple hepatocellular neoplasms, only the pigmented hepatocellular neoplasms had atypia or malignancy. Genotype-phenotype classification of the pigmented tumors showed different subtypes: HNF1α inactivated (48%), β-catenin activated (26%), inflammatory (15%), concurrently β-catenin activated and inflammatory in 1 hepatocellular adenoma, concurrently HNF-1α inactivated and β-catenin activated in 1 hepatocellular adenoma, and unclassified in 1 hepatocellular carcinoma. In conclusion, hepatocellular adenomas with lipofuscin pigment are a heterogeneous group of adenomas, with HNF-1α inactivation being the commonest genotype. They have an increased risk of atypia and malignancy, especially in males.

A n 80-year-old woman presented with complaints of a cough associated with increasing fatigue and weight loss. Her past medical history was significant for Stage I (T1 N0 M0) breast cancer for which she underwent a left modified radical mastectomy followed by immediate reconstruction with a Siltex Becker dual-lumen implant, 15 years previously. Physical examination was essentially negative. There was no evidence of splenomegaly or cervical, supraclavicular, axillary, or inguinal lymphadenopathy. Laboratory evaluation was negative for pulmonary pathology, sarcoidosis, fungal infection, or hematologic dyscrasia. Chest X-ray was unremarkable, but CT scan of the chest demonstrated mediastinal lymphadenopathy that was a new finding when compared to a CT scan obtained 9 years previously. The new chest CT scan also revealed irregularity of the left breast implant capsule with extra capsular fluid, suggesting implant rupture (Fig. 1). The patient underwent mediastinoscopy with excisional biopsy of the enlarged lymph nodes. Auramine-rhodamine and Gomori's methenamine silver (GMS) special stains and cultures were negative for aerobic and anaerobic bacteria, Mycobacteria, Legionella, Actinomyces, and fungi. Light microscopy of hematoxylin-eosin fixed tissue demonstrated diffuse involvement by a multinucleated giant cell foreign-body reaction in all specimens. Inclusions were seen that were consistent with silicone (Fig. 2). All samples were negative for neoplasm. Refractile material within vacuoles was seen by TEM and EDX confirming the presence of silicon (Fig. 3).Silicone (polymers of dimethysiloxane) has become one of the most popular utilized materials for the manufacture of prostheses because it is non-biodegradable and biologically stable, even though it behaves as a foreign body and stimulates a cell-mediated immune response. Silicone migration through regional lymphatic channels is a rare and unique complication that has been reported to be associated with silicone Figure 1. Selected axial images from computed tomography of the chest demonstrate moderate lymphadenopathy throughout the mediastinum. Irregularity of left breast implant capsule with extra capsular fluid is suggestive of implant rupture.