Histologic typing of thymoma according to the new World Health Organization classification.

The new WHO classification scheme provides a set of simple and easily reproducible morphologic criteria for an accurate and consistent categorization of thymic epithelial tumors. This scheme should facilitate interobserver reproducibility and lead to a more precise assessment of prognosis when used in combination with the staging system.

Lymphoepithelioma-like carcinoma of the breast: lack of evidence of Epstein-Barr virus infection.

AIMS: Six cases of lymphoepithelioma-like carcinomas of the breast were studied in order to better define the morphology of this type of breast tumour and to see if these neoplastic lesions are related to Epstein-Barr virus (EBV) infection by analogy with histologically similar tumours located in other organs. METHODS AND RESULTS: The cases were studied with immunohistochemistry using several antibodies and with in-situ hybridization method employing different types of nucleotides in four cases. The cases presented the distinctive morphology of the lymphoepithelioma-like carcinomas as seen in other organs. Specifically Rigaud and Schminke's patterns of growth were observed. In addition, at the edge of the neoplastic lesions, a lymphoepithelial lobulitis was seen. In-situ hybridization failed to reveal any positivity for EBV genome. CONCLUSION: Lymphoepithelioma-like carcinoma is a specific type of breast tumour, but its relation to EBV has yet to be proven. The differential diagnosis with medullary carcinoma is discussed.

Gliomatosis peritonei with malignant transformation.

A 13-year-old girl underwent a right salpingo-o-ophorectomy and partial omentectomy for an ovarian tumor that on microscopic examination was a grade 1 immature teratoma. Mature glial implants were found in the omentum (Stage III). No additional treatment was given. Ten months later, grade 0 and grade 1 peritoneal glial implants were found on laparotomy. Chemotherapy with four cycles of vincristine/cisplatin/etoposide/bleomycin was administered. A second laparotomy 4 months later showed persistence of grade 0 and grade 1 peritoneal glial implants. The patient was well for the next 7 years, after which time she presented with a pelvic mass that on microscopic examination was a malignant neuroectodermal tumor resembling a glioblastoma multiforme. The tumor did not respond to debulking and chemotherapy, and the patient died 6 months later, 8 years after her initial presentation. This case represents the second report of malignant transformation of peritoneal glial implants.

Endothelin-A receptor antagonist BQ-610 blocks cigarette smoke-induced mitogenesis in rat airways and vessels.

To ascertain whether endothelin may play a role in cigarette smoke-induced cell proliferation in the airways and arterial vasculature of the lung, we exposed groups of seven Sprague-Dawley rats to either room air (control) plus saline infusion, an intravenous infusion of the selective endothelin A antagonist BQ-610 (control BQ-610), the smoke of 10 cigarettes (smoke only), or the smoke of 10 cigarettes after intravenous BQ-610 infusion (smoke + BQ-610). Cell proliferation was quantified by determining the percentage of cell nuclei labeled by 5-bromo-2'-deoxyuridine. We separately evaluated the cells in the epithelium and wall components of the bronchioles, and endothelium and wall components of the peribronchiolar and perialveolar ductular arteries. We found that cigarette smoke produced significant cell proliferation in the airway epithelium and wall, in the peribronchiolar arterial endothelial compartment, and in both the endothelial and wall compartments of the perialveolar ductular arteries. Pretreatment with BQ-610 reduced the peribronchiolar arterial endothelial and the perialveolar ductular arterial wall proliferation to control lev- els and reduced but did not totally abrogate the smoke-in- duced proliferation of the airway epithelial, airway wall, and perialveolar ductular arterial endothelial compartments. We conclude that cigarette smoke-induced cell proliferation of the airways and pulmonary arterial vessels is at least partially mediated through stimulation of the endothelin-A receptors.