Cases reported "Carcinoma"

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1/40. An unusual cervical carcinoma showing exception to epitheliotropism of human papillomavirus.

    Human papillomaviruses (HPV) infect epithelial tissues but have not been previously detected within mesenchymal cells. During a systematic investigation of FIGO stage Ib cervical cancers with colorimetric in situ hybridization, we detected HPV 16 dna within the stromal compartment of an unusual undifferentiated carcinoma. The mesenchymal nature of the HPV-containing cells was confirmed by immunohistochemistry and electron microscopy. No viral particles were identified. Sequencing the majority of the HPV 16 genome identified few changes from the revised reference clone; all previously reported in other HPV 16 variants. These viral changes are unlikely to explain the exceptional mesenchymal localization of the HPV 16 dna in this case.
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2/40. In situ demonstration of parathyroid hormone-related protein mRNA in sclerosing hepatic carcinoma.

    A 69-year-old man had a hepatic tumour occupying the left and half of the right lobe, with portal vein thrombus. There were hypercalcaemia and hypophosphataemia with increased nephrogenous cyclic adenosine monophosphate; bone metastases were excluded. serum parathyroid hormone-related protein (PTHrP) was elevated, but no increase in intact parathyroid hormone (PTH) or vitamin D3 metabolites was found. At autopsy the histological features were typical of sclerosing hepatic carcinoma. By immunohistochemistry PTHrP was detected in cancer cell nests but not in the fibrous stroma. PTHrP transcripts were demonstrated by in situ hybridization using a polymerase chain reaction (PCR)-derived single-stranded dna probe. Tumour cells expressed AE1 and CA19-9 (markers for cholangioepithelium) and CEA (for bile canaliculi). Electron microscopy revealed microvilli on the apical surface, and secretory granules 100 nm in diameter were observed. These findings indicate that this case is one of cholangiocellular sclerosing hepatic carcinoma. The interaction between cancer and stromal cells may be the cause of PTHrP overexpression.
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3/40. Epstein-Barr virus early ribonucleic acids as a diagnostic adjunct for relapsed metastatic tumors in patients with cured primary undifferentiated nasopharyngeal carcinoma.

    PURPOSE: Epstein-Barr virus (EBV) has been consistently shown to be associated with undifferentiated nasopharyngeal carcinoma (NPC). In this article, the authors attempt to detect Epstein-Barr virus in distant relapsed metastatic sites in undifferentiated NPC patients with cured primary cancer. MATERIALS AND methods: in situ hybridization (ISH) technique is a reliable method to detect EBV early RNAs (EBERs) within NPC cells. We used a nonisotopical ISH technique to examine the presence of EBERs in paraffin-embedded tissues obtained from 1 paired specimen of primary NPC and its metastatic counterpart at liver and 2 metastatic specimens of retroperitoneal lymph nodes and bone. RESULTS: All the primary lesions and the metastatic tumors of NPC with undifferentiated histology contained EBERs that could be clearly detected in the nuclei of cancer cells. CONCLUSIONS: This article shows that EBERs can be successfully detected in cells of the distant relapsed metastatic sites. These results suggest that this nonisotopical ISH method of EBERs can be potentially used to diagnose NPC patients developing distant relapsed metastatic lesions with cured primary cancer early. It can offer quick information as to institute suitable salvage chemotherapy for these patients.
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4/40. Pleomorphic carcinoma of the pancreas with massive lymphocytic stromal infiltration and long-term survival after resection.

    BACKGROUND: Pleomorphic carcinoma of the pancreas is a rare tumor with an extremely poor prognosis. The mean survival time is reported to be approx 3 mo. CLINICAL AND HISTOLOGICAL FINDINGS: A 56-yr-old Japanese man presenting with general fatigue, loss of weight, and high fever was found to have a large hypervascular mass in the body of the pancreas with regional lymph node metastases. Laboratory investigation revealed leukocytosis, elevated erythrocyte sedimentation rate (ESR), and high serum c-reactive protein (CRP). In addition to distal pancreatectomy, splenectomy and lymph node dissection were performed. histology showed the presence of pleomorphic large cells with bizarre mono- or multinuclei, growing in sarcomatoid pattern without mutual cohesiveness. Another noticeable finding was massive lymphocytic infiltration of the stroma of the neoplasm. Immunohistochemically, the infiltrating lymphocytes consisted of cytotoxic type of T cells. In addition, in situ hybridization for Epstein-Barr virus-encoded rna (EBAR-1) was not seen in the tumor cells or in lymphocytes. After surgery the patient did not undergo chemotherapy or radiotherapy. He has been well without recurrence for 8 yr. CONCLUSION: We report a case of pleomorphic carcinoma, possibly lymphoepithelioma-like carcinoma, of the pancreas with massive lymphocytic stromal infiltration and long-term survival after resection. Cytokine responses and cellular immunoreactivity may have contributed to a long-term survival, which is unusual in the common type of pleomorphic carcinoma of the pancreas.
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5/40. prolactin-producing pituitary adenoma and carcinoma with neuronal components--a metaplastic lesion.

    Recent studies indicate that cells of various epithelial tumors are capable of transformation to neurons. Observing both neurons and neuropil in two prolactin-producing adenohypophyseal tumors, one benign and one malignant, we sought to assess their cellular differentiation, the presence of nerve growth factor receptor, and expression of the dopamine receptor gene using immunocytochemistry, electron microscopy, and in situ hybridization. light and electron microscopy clearly revealed cells morphologically transitional between adenoma/carcinoma cells and neurons. Large neurons lacked proliferative activity. neurons in varying number showed immunoreactivity for pituitary hormones including prolactin, growth hormone and alpha subunit in the adenoma and prolactin alone in the carcinoma. The distribution of nerve growth factor receptor staining was similar. In both tumors, in situ hybridization showed mRNAs for prolactin and dopamine receptor within adenohypophyseal cells and neurons. Our results indicate that the occurrence of neurons and neuropil in growth hormone and prolactin-producing pituitary tumors appears to be the result of metaplasia. The process is not limited to benign tumors and may be due to the production of tropic substances by the adenohypophysial cells, which by paracrine/autocrine mechanisms result in transformation of adenoma cells to nerve cells.
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6/40. Solitary fibrous tumour of the urinary bladder with expression of bcl-2, CD34, and insulin-like growth factor type II.

    We describe a solitary fibrous tumour of the urinary bladder wall removed from a 50-year-old man with a history of pelvic pain, dysuria, and urinary bleeding. Anamnesis revealed a weight increase during the preceding 3 months, but no apparent episodes of biochemical hypoglycaemia or hormonal abnormalities. The patient is alive and well 18 months after surgery. Pathological examination revealed a 6.5-cm well-circumscribed nodular mass composed of uniform spindle cells arranged in bundles and fascicles with varying amounts of collagen and a typical haemangiopericytoma-like vascular pattern. The tumour cells were positive for bcl-2, CD34, and vimentin and ultrastructurally showed mesenchymal-myofibroblastic traits. These cells produced insulin-like growth factor type II mRNA as demonstrated by non-isotopic in situ hybridization. This rare case with a solitary fibrous tumor suggests that insulin-like growth factor type II could join CD34 and bcl-2 as markers for postoperative differential diagnosis.
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7/40. Chromosomal imbalances in gastric cancer. Correlation with histologic subtypes and tumor progression.

    dna copy number changes were analyzed by comparative genomic hybridization (CGH) in 38 gastric carcinomas and correlated with tumor histologic type and progression. Gains of copy numbers were observed in all tumors, affecting all chromosomes except chromosome 16. The average number of copy number gains was 7 (range, 1-13), most frequently located on chromosomes 11, 12, 15, 17, and 20 in 45% to 97% of tumors. High-level amplifications were found on chromosomes 12, 15, 17, and 20; the latter was affected most frequently (66%). Loss of dna copy numbers was detected in 14 tumors affecting 7 chromosomes. No statistically significant differences in the frequency and pattern of chromosomal imbalances were observed in tumor histologic type (Lauren classification) and grade of differentiation, as well as the prognostic parameters depth of invasion (pT) and lymph node involvement (pN). Our results indicate that in gastric cancer there is no specific recurrent pattern of dna aberrations to be correlated with tumor histologic type or stage. However, CGH analysis could reveal new, recurrent genetic changes in gastric cancer affecting chromosomes sites that harbor genes known to participate in tumorigenesis and progression of several human malignant neoplasms.
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8/40. Chromosomal aberrations in pituitary carcinoma metastases.

    Four pituitary carcinoma metastases [two adrenocorticotropic hormone (ACTH) and prolactin cell tumors each] were studied by comparative genomic hybridization. Chromosomal gains were found in all four carcinoma metastases, but losses only in the two prolactin cell carcinoma metastases. overall, pituitary carcinoma metastases showed an average of 8.3 chromosomal imbalances per tumor (7 gains vs 1.3 losses), 10 in prolactin cell carcinoma metastases (7.5 gains vs 2.5 losses) and 6.5 in ACTH cell carcinoma metastases (6.5 gains vs 0 loss). The most common changes were gains of chromosome 5, 7p, and 14q (in three tumors each). High-level gains were found on 13q22-qter and 14q (two cases each) and on 1q, 3p, 7, 8, 9p, and 21q (one case each). To date, gains of chromosome 14q have not been reported among pituitary tumors. It remains to be shown whether gain of 14q is associated with malignant progression and metastatic dissemination of pituitary carcinomas.
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9/40. Upper respiratory tract carcinoma with chromosomal translocation 15;19: evidence for a distinct disease entity of young patients with a rapidly fatal course.

    BACKGROUND: Carcinoma of the upper respiratory tract is rare in childhood, and cytogenetic aberrations have not been characterized in this population. The chromosomal translocation 15;19 has been reported four times previously. All patients were young and had tumors arising in the thorax. The three reports that provide clinical follow-up all describe superior vena cava syndrome and death soon after presentation. All tumors were diagnosed as carcinoma (three undifferentiated, one mucoepidermoid), and the authors suggested thymus, lung, or germ cell origin. methods: The authors investigated the clinical and pathologic findings in two patients with poorly differentiated carcinoma showing evidence of t(15;19). This included a 13-year-old girl with a rapidly growing epiglottic mass, leading to superior vena cava syndrome and death and a 12-year-old girl with an aggressive nasopharyngeal mass showing intracranial extension. RESULTS: The laryngeal tumor was poorly differentiated, with vesicular nuclei, prominent nucleoli, extensive necrosis, and a lymphoplasmacytic infiltrate; cells were positive for cytokeratin and negative for lymphoma, melanoma, germ cell, and endocrine markers. Electron microscopy showed rare intermediate junctions and basal lamina. The nasopharyngeal tumor was poorly differentiated with areas of obvious squamous differentiation observed histologically, immunophenotypically, and ultrastructurally. Cytogenetic and fluorescent in situ hybridization studies were consistent with t(15;19)(q13;p13.1) in both cases. Both children received chemo- and radiotherapy. The first child died of disease after 36 weeks; autopsy revealed tumor in the larynx with spread to the skin/subcutis (neck and thorax) and lymph nodes (cervical, subcarinal, and pulmonary hilar). The second child developed widespread bony metastases and died of disease after 13 weeks. CONCLUSIONS: In conjunction with previous reports, the authors' findings show that t(15;19) is part of a distinct clinicopathologic entity characterized by young age, midline carcinoma of the neck or upper thorax, and a rapidly fatal course. female gender and superior vena cava syndrome are common. The histogenesis of these distinctive tumors is unknown. The authors' findings suggest origin in the upper airway, perhaps from submucosal glands.
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10/40. collagen type xviii/endostatin is differentially expressed in primary and metastatic colorectal cancers and ovarian carcinomas.

    collagen type xviii (C18) is a nonfibrillar collagen of basement membranes. Its C-terminal fragment, endostatin, has been identified as an inhibitor of angiogenesis. C18 is predominantly expressed by hepatocytes of normal, cirrhotic and neoplastic liver. We compared the patterns of C18 rna-expression in colonic adenocarcinoma metastases, which represent the most frequently occurring liver tumours, to normal colon mucosa, to primary colon cancers and to ovarian cancers which are often morphologically similar to colonic cancer or metastasis. Two C18-specific rna-probes were generated to perform in situ hybridization combined with immunohistochemistry for cytokeratin, vimentin and the endothelial marker CD31, in order to characterize the C18-expressing cells. C18/endostatin protein was localized by immunohistology. In colorectal carcinomas and their liver metastases high levels of C18 transcripts were observed in endothelial cells and fibroblasts/myofibroblasts, whereas C18 rna was virtually absent from carcinoma cells. Ovarian carcinomas displayed high C18 rna expression both in carcinoma and stromal cells, indicating that induction of C18 transcription in tumour stromal cells is independent of the ability of carcinoma cells to express C18. While the role of tumour cell derived C18 in cancer growth regulation remains unknown, stimulation of proteolysis of the locally strongly expressed C18 to endostatin could offer an attractive approach for a targeted antineoplastic therapy.
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