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BACKGROUND: Solitary fibrous tumors (SFTs) are rare fibrous neoplasms. Since their initial description as arising from the pleura, SFTs have been reported at a wide range of anatomic sites. To the authors's knowledge, there are no large series reporting both thoracic and extrathoracic SFTs nor are there any large series that analyze clinicopathologic correlates of tumor behavior. METHODS: Institutional soft tissue tumor and pathology databases were reviewed to identify patients. Pathologic material was reviewed by an experienced soft tissue pathologist and scored for the presence of a histologically malignant component. Clinical information was obtained from medical records and phone calls to patients. Statistical analysis was performed using the Student t test, Pearson chi-square test, and log-rank test. RESULTS: Seventy-nine patients with SFTs treated at a single institution over an 18-year period were identified. These tumors arose in a wide range of anatomic sites. Thoracic and extrathoracic SFTs had similar clinical and pathologic features, although extrathoracic tumors were more likely to be symptomatic on diagnosis. Seventy-five patients underwent surgical excision of a SFT at our institution. Overall, SFTs had a low rate of local recurrence and metastasis after surgical treatment. Extrathoracic SFTs had an increased risk of local recurrence that was small but statistically significant. There was no difference in metastasis-free survival between thoracic and extrathoracic SFTs. Positive surgical margins and the presence of a histologically malignant component were factors predicting worse local recurrence-free survival. Positive surgical margins, tumor size greater than 10 cm, and the presence of a malignant component predicted worse metastasis-free survival. CONCLUSIONS: Solitary fibrous tumors are rare tumors that occur at all anatomic sites. Most SFT patients fare well after surgical treatment. Closer surveillance is warranted for those tumors that are larger than 10 cm or with the presence of a histologically malignant component

Gastric carcinomas are invariably accompanied by lymphoid proliferations. We studied their features in 22 resected gastric carcinomas in which the lymphoid proliferations ranged from reactive lymphoid follicles to mucosa-associated lymphoid tissue (MALT) lymphomas. In most cases, the collections of lymphocytes were abundant, which is remarkable considering the lack of lymphoid tissue in the normal stomach. They were not haphazardly located but in direct contact with the metaplastic, dysplastic, and neoplastic epithelial cells, in positions suggestive of defense barriers. They consisted of newly formed lymphoid follicles with reactive germinal centers sometimes high up in the superficial mucosa, collections of plasma cells beneath the surface epithelium, and large aggregates of B cells above and below the muscularis mucosae as well as abundant T cells. The latter, both CD4+ and CD8+, were seen within metaplastic epithelial cells as well as within carcinomatous glands that were partially destroyed, resembling apparent neoplastic lympho-epithelial lesions (LEL). In three cases, the B cells infiltrating the gastric muscular layers represented MALT-lymphomas adjacent to gastric carcinomas, as confirmed by polymerase chain reaction (PCR) analysis in two cases. In a case of lymphoepithelioma-like carcinoma, the excessive lymphoid cells were predominantly of T-CD8+ type. In this case, EBV identified by EBV-encoded RNA and latent membrane protein was present in large amounts. Helicobacter pylori was seen in only six cases in areas of chronic gastritis that were distant from carcinoma. H. pylori was not present in the areas of metaplasia, dysplasia, or carcinoma. It appears that the lymphoid proliferations accompanying these gastric changes do not arise in response to the pathogenic agent H. pylori, which caused the persistent infection leading to them yet is no longer present, but rather in response to the existence of the abnormal epithelial cells. Thus the lymphoid proliferations consistently associated with gastric metaplasia, dysplasia, and neoplasia may be regarded as immune reactions to the long-term cellular changes triggered by the initial chronic gastritis. On rare occasions, the exaggerated lymphoid proliferations may reach the end of the spectrum, resulting in MALT lymphomas coexistent with gastric carcinomas