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The presence and frequency of lipoblasts (LPB) in spindle cell lipomas (SCL) and pleomorphic lipomas (PL) has never been studied in detail on a histologically, immunohistochemically and molecular genetically validated set of tumors. The authors investigated this feature by reviewing 91 cases of SCL and 38 PL. When more than 3 unequivocal LPB were found, the case was regarded as positive for the presence of LPB. All positive cases were then stained with CD34 and retinoblastoma (Rb) protein antibodies and tested by fluorescence in situ hybridization for MDM2 and CDK4 amplifications and the FUS gene rearrangements. The patients with SCL and PL containing LPB were 14 women and 47 men, the rest were of unknown gender. The cases usually presented as superficial, well-circumscribed soft tissue masses and most commonly occurred in the upper back and neck. CD34 was expressed in all cases, while Rb protein was consistently absent in all. Molecular genetic results, when available, were in concordance with the morphological diagnosis of SCL/PL. LPB were found in 37 (41%) cases of SCL and 25 cases of PL (66%). While in many cases they are inconspicuous, in some others they constitute a very prominent component of the tumor. It is important to be aware of this fact in order to avoid misinterpretation as liposarcoma., (Copyright © 2017 Elsevier Inc. All rights reserved.)

We present a case of a 24-year-old man with a right testicular mass, 2.5 cm in largest diameter. Before orchiectomy, the serum level of beta-human chorionic gonadotropin (hCG) was elevated, whereas that of alpha-fetoprotein was normal. Histologic examination showed a malignant germ cell tumor with a unique and hitherto unpublished combination of placental site trophoblastic tumor and teratoma. Testicular tubules adjacent to the tumor contained intratubular germ cell neoplasia. All cells of placental site trophoblastic tumor were immunohistochemically cytokeratin 7, 18, and pancytokeratin positive and cytokeratin 20, S-100 protein, alpha-fetoprotein, placental alkaline phosphatase, p63, OCT3/4, Nanog, and calretinin negative. Ten percent of the placental site trophoblastic tumor stained with hCG, 30% with epithelial membrane antigen and human placental lactogen, and 80% with inhibin antibodies. FISH study showed a gain on the short arm of chromosome 12 in the placental site trophoblastic tumor, proving that this component is of germ cell origin. The patient is alive and well 3 years after the orchiectomy without additional treatment., (Copyright 2010 Elsevier Inc. All rights reserved.)

A distinctive variant of basal cell adenoma called membranous basal cell adenoma is well recognized in salivary glands. It appears identical to cutaneous cylindroma, hence the synonym dermal analogue tumor. We present a case of a tumor involving the parotid gland that appeared identical to cutaneous spiradenoma. In addition, the lesion had a malignant component identical to basal cell adenocarcinoma. The patient had no features suggestive of Brooke-Spiegler syndrome. Analysis of the CYLD gene revealed polymorphisms. This is the first report of a "dermal analogue tumor" of the salivary gland that resembled a cutaneous spiradenoma and not a cylindroma.

Normal medullary interstitial cells regulate blood flow, water and salt absorption, and ultimately blood pressure through synthesis and secretion of prostanoids in which cycloxygenases play the rate-limiting steps. We found that most renomedullary interstitial cell tumors overexpressed cycloxygenase-2 (COX-2), with concomitant expression of microsomal prostaglandin E synthase-1 and the receptor for prostaglandin E2. Prostaglandin E2 is the major prostaglandin product of COX-2/microsomal prostaglandin E synthase-1 enzymatic pathway in medullary interstitial cells, and concomitant expression of COX-2, microsomal prostaglandin E synthase-1, and prostaglandin E2 receptor on interstitial cell tumors implies the presence of an autocrine growth loop important in pathogenesis of these tumors. Furthermore, overexpression of COX-2 protein was observed in association with homozygosity in several polymorphic sites within COX-2 gene (promoter region sites -1186 T/T and -765 G/G, intron 5 IVS5-275 T/T, and exon 10 Ex10+837 T>C), indicating their role in development of these tumors.