Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Small cell carcinoma of the ovary is a rare, poorly understood aggressive tumor of young women, associated with paraendocrine hypercalcemia in two-thirds of the cases. Immunohistochemical staining of 15 small cell carcinomas, one-third of which were associated with hypercalcemia, 15 adult granulosa cell tumors, 15 juvenile granulosa cell tumors, and 5 Sertoli cell tumors, was performed with the use of antibodies against cytokeratins (AE-1/AE-3, CAM 5.2, 902), epithelial tumor-associated antigens (B72.3, epithelial membrane antigen [EMA]), vimentin, S-100, neuron-specific enolase (NSE), lysozyme, parathyroid hormone, and chromogranin-A in an attempt to define histogenetically this tumor type. One-third of the small cell carcinomas were positive for EMA, whereas all of them were negative for B72.3 and S-100. In contrast, one-third of the granulosa cell tumors were positive for S-100 and all of them were negative for EMA and B72.3. One of five Sertoli cell tumors were positive for EMA and two were positive for B72.3, but all were negative for S-100. Differences existed in the frequency, intensity, and/or pattern of staining for cytokeratin, vimentin, lysozyme, and NSE among the various tumor types. A single small cell carcinoma from a patient with hypercalcemia stained focally for parathyroid hormone, whereas all 30 granulosa cell tumors and 4 of 5 Sertoli cell tumors were nonreactive. Chromogranin-A staining was noted in four of five small cell carcinomas, none of ten granulosa cell tumors, and two of five Sertoli cell tumors. These immunohistochemical findings, as well as previous light and electron microscopic data, do not clearly indicate any specific cell as the cell of origin of the ovarian small cell carcinoma.
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PMID:Ovarian small cell carcinoma. Histogenetic considerations based on immunohistochemical and other findings. 247 44

We present 22 (0.9%) cases of rhabdoid tumour of the kidney diagnosed amongst 2392 renal tumours in children. The patients ages ranged from 3 weeks to 94 months (median 7 months) and the female:male ration was 1.2:1. Clinically, they presented with an abdominal mass but four (18%) children also had hypercalcaemia and one (4.5%) developed a brain tumour (primitive neuroectodermal tumour). None of the children presented with stage I disease, five (23%) had stage II, ten (46%) stage III, and five (23%) stage IV disease. Two (9%) patients had bilateral tumours. Histologically, the vast majority (20/22) of the tumours exhibited a classical pattern but other histological patterns were also noted. Immunohistochemical studies performed in 12 cases showed vimentin positivity in all cases, CAM 5.2 in eight, epithelial membrane antigen in six, neuron specific enolase in four, S-100 protein in eight, and desmin in one case. In only 12 of the 22 tumours was there agreement between the reporting pathologist and the panel on a diagnosis of rhabdoid tumour of the kidney. Eight tumours originally diagnosed as rhabdoid tumour of the kidney were found to be other renal tumours and in another ten cases the initial diagnosis was changed by the panel to rhabdoid tumour. Metastases developed in 18 (82%) of the children--in eight they were present at the time of diagnosis and in 10 they developed from 2 weeks to 9 months after initial diagnosis. Metastases were found in the lung, abdomen, lymph nodes, liver, bone and brain. Of the 19 children with adequate follow-up, only two (10.5%) with stage II disease are alive, while 17 (89.5%) died 2 weeks to 20 months after the diagnosis.
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PMID:Rhabdoid tumour of the kidney: a clinicopathological study of 22 patients from the International Society of Paediatric Oncology (SIOP) nephroblastoma file. 873 42

We reviewed 11 cases of primary thymic neuroendocrine carcinomas with combined features ranging from well-differentiated to poorly differentiated neuroendocrine carcinoma. For 3 asymptomatic patients, tumors were discovered during routine examination. Presentation in the other patients was as follows: Cushing syndrome, 2 patients; chest pain, 3 patients; superior vena cava syndrome, 1 patient; and hypercalcemia and hypophosphatemia, 1 patient. No clinical data were available for the 11th patient. All tumors were located in the anterior mediastinum and treated by surgical excision. The lesions were large and well-circumscribed with areas of hemorrhage and necrosis. They were characterized by areas showing a proliferation of monotonous, round tumor cells adopting a prominent organoid pattern admixed with areas showing sheets of atypical cells with hyperchromatic nuclei, frequent mitoses, and extensive areas of hemorrhage and necrosis. Immunohistochemical studies performed in 6 cases showed strong CAM 5.2 low-molecular-weight cytokeratin positivity in all cases, chromogranin and synaptophysin positivity in 4, Leu-7 in 3, and focal positivity for p53 in 2. Follow-up information for 9 cases showed that all patients died of their tumors between 1 and 4 years after diagnosis. The present cases highlight the heterogeneity of neuroendocrine neoplasms and reinforce the notion that these tumors form part of a continuous spectrum of differentiation.
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PMID:Thymic neuroendocrine carcinomas with combined features ranging from well-differentiated (carcinoid) to small cell carcinoma. A clinicopathologic and immunohistochemical study of 11 cases. 1070 13

Pseudovascular squamous cell carcinoma (SCC) is a rare variant of SCC characterized by acantholysis and necrosis with preservation of vascular-like cords and spaces mimicking glands or vascular differentiation. Only three cases of this variant in the oral cavity have been reported in the literature. However, none of these cases were eosinophil-rich, which is considered to be a good prognostic indicator for conventional SCC. We report one case of an eosinophil-rich pseudovascular adenoid SCC in the oral cavity. A 38-year-old previously healthy African-American female presented with an enlarging inner left cheek mass with overlying ulcer of 2 months duration. A computed tomography scan with contrast demonstrated a large irregularly outlined peripherally enhancing mass located between the anterior margin of the ramus of the left mandible and maxilla protruding outward. An incisional biopsy was performed followed by a wide local excision 3 weeks later. She recovered well postoperatively but refused to follow-up chemoradiation therapy. Six months later, she presented with altered mental status secondary to hypercalcemia from bony metastases. She was discharged to a hospice facility as per her family's request. Histologic sections of the specimens revealed a diffuse hypercellular pleomorphic ill-circumscribed lesion with extensive necrosis. The viable areas exhibited slit vascular-like spaces and micropapillary architectural patterns with stromal eosinophilia. Focal small cellular nests with features of SCC were present. Immunohistochemistry displayed positivity for vimentin, p53, AE1/AE3 and CAM 5.2 (focally positive). All tumor cells were negative for desmin and CD34.
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PMID:Pseudovascular squamous cell carcinoma with eosinophil-rich stroma. 3096 33