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Granular cell myoblastomas develop most commonly in the head and neck region, but their occurrence in the salivary glands has been reported in only one case, in the submaxillary gland. The authors report a case of granular cell myoblastoma in a previously undescribed localization, the parotid gland.
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Inflammatory myofibroblastic tumours are aetiologically enigmatic, nosologically confusing and biologically unpredictable lesions. The lungs are the organs of apparent predilection. These tumours have also been documented in a number of extrapulmonary sites including the head and neck. So far only two cases of inflammatory myofibroblastic tumour of the tonsil have been reported in the English literature. We document another case, occurring in a 41-year-old man with history of cadaveric renal transplant nine years ago. A comprehensive review of the literature is also presented.
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BACKGROUND: Peritoneal spread of tumour cells is a major source of morbidity and mortality in patients with colorectal cancer. In order to develop strategies to prevent intraperitoneal dissemination and to treat peritoneal carcinomatosis, the spread of tumour cells in the peritoneal cavity was studied. METHODS: Two million CC531 colon carcinoma cells were administered intraperitoneally in five groups of eight rats. The rats were killed after 1, 2, 4 and 8 hours and 3, 7, 14 and 21 days. After inspection of the abdominal cavity, samples of blood and ascites were taken. Liver, spleen, omentum, mesentery, diaphragm, parathymic lymph nodes and lungs were removed for histology and immunohistochemistry. RESULTS: No abnormalities were seen in the abdominal cavity until day 3. Subsequently the peritoneum and omentum became thickened and after 21 days all rats had haemorrhagic ascites and peritoneal carcinomatosis. The abdominal fluid contained tumour cells at all stages. The number of tumour cells decreased in the first 8 hours, and increased thereafter. At microscopy the peritoneum was completely covered by tumour cells after 3 days. Tumour cells concentrated in the milky spots (MS) of the omentum within 4 hours. The size of the MS increased as a result of an increase in number of tumour cells and macrophages. After 7--21 days the MS were completely replaced by tumour cells and new MS were formed. In the diaphragm tumour cells invaded the lymphatic lacunae after 8 h, and obliterated these after 3--7 days. Also invasion of the muscle fibres was seen after 3 days. Microscopically no tumour cells were found in blood, liver, spleen, parathymic nodes and lung. CONCLUSION: After intraperitoneal administration of CC531 colon carcinoma cells, tumour cells spread throughout the abdominal cavity, and concentrate in the milky spots of the greater omentum, the paracolic gutters, the subhepatic and subphrenic spaces and in the lymphatic lacunae of the diaphragm.
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UNLABELLED: Cutaneous smooth muscle is present in 3 separate locations: arrector pili muscles, blood vessel walls, and genital/areolar skin. Benign or malignant smooth muscle neoplasms may arise from each of these locations. This review discusses the pathogenesis, clinical manifestations, histologic findings, prognosis, treatment options, and controversial areas of cutaneous smooth muscle neoplasms. ( J Am Acad Dermatol 2002;46:477-90.) LEARNING OBJECTIVE: At the completion of this learning activity, participants should be able to discuss the pathogenesis, clinical manifestations, histologic findings, prognosis, and treatment options of cutaneous smooth muscle neoplasms.
We report on a case of a 40-year-old male patient who underwent a gastrectomy because of a biopsy-proven large B-cell lymphoma of the stomach. On surgery, a nodule in the spleen also was noted. Grossly and microscopically, the two lesions were different: the tumor of the stomach appeared white-gray on the cut surface and was a centroblastic variant of diffuse large B-cell lymphoma. Histologically, one perigastric lymph node was involved. Grossly, the splenic nodule was gray-yellow and had a histological appearance of an inflammatory myofibroblastic tumor (IMT). The association between malignant tumor and IMT is rare. In such an association, the latter lesion most often has been reported in the spleen. As EBV may be involved in the genesis of both lymphoma and IMT, we tested both lesions for its presence using in situ hybridization, but the tests were negative. It remains to be verified whether the association between lymphoma and IMT is more than fortuitous.
Electron-microscopic examination of a malignant granular cell tumor revealed cells with abundant granular and glycogen-containing cytoplasm and eccentric nuclei. Numerous junctional structures including desmosomes were identified between tumor cells which, moreover, displayed a pattern of gland formation with the presence of short microvilli in one pole of the cell. The presence of junctional structures may provide a feature for positive identification of this tumor by electron microscopy. The findings may also have implications to further our understanding of the histogenesis of this tumor. This case further raises the question of familiar occurrence of this tumor.
Immunosuppression is known to favor the development of various types of tumors. After organ transplantation, the risk of lymphoproliferative disease, whether clonal or not, is particularly increased and clearly associated with Epstein-Barr virus infection. We report a case of an unusual large cystic tumor of the liver with satellite hepatic and splenic nodules occurring 4 years after renal transplantation. Radiologic examination showed a rich vascularization of the tumor. Light and electron microscopy of a surgical liver biopsy, completed by an immunohistochemical study, demonstrated a well-differentiated tumor of smooth-muscle origin. Using in situ hybridization, we showed large amounts of Epstein-Barr virus messenger RNAs within the tumor cells. In addition, Southern blot analysis revealed that viral DNA was present in the form of a single monoclonal episome within the tumor. The polymerase chain reaction analysis of the genomic DNA of tumoral cells also indicated a monoclonal pattern. At last, the tumor was shown to be of host origin. Six months later, and despite three courses of chemotherapy, the tumoral lesions were unchanged. This case underlines the role of Epstein-Barr virus infection in the development of unusual and clonal smooth-muscle tumors after organ transplantation. The evolution of these rare tumors is uncertain.
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Minute uterine leiomyomas, less than 3 mm in diameter, were studied by electron microscopy. In five of 15 cases, morphologically different types of smooth muscle cell were identified. In the central region of leiomyomas, most myoma cells were characterized by filaments sporadically located in the cytoplasm and well-developed organelles. These cells were interpreted as immature smooth muscle cells. In the outer layer of nodules, the cells were a more mature form of smooth muscle cell and resembled normal myometrial cells. The differences suggest that differentiation of the smooth muscle cells occurs early in the growth of uterine leiomyoma.
This review focuses on the pathology of uterine smooth muscle tumors (SMTs), with a particular emphasis on those studies published in the past 15 years that have expanded our knowledge of these tumors which still present diagnostic challenges for the pathologist. Leiomyoma variants, leiomyosarcoma, SMTs of low or uncertain malignant potential, epithelioid SMTs, SMTs with unusual growth patterns, and mixed endometrial stromal-SMTs are discussed.
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