Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six cases of oral granular cell lesions were studied with respect to intermediate-sized filaments (IF), peanut lectin binding (PNL) and muramidase activity by means of the peroxidase antiperoxidase technique. The tumours included three granular cell myoblastomas of the tongue (GCM) two cases of congenital gingival granular cell tumour (CGGT) and one granular cell ameloblastoma (GCA). Every tumour studied showed intracytoplasmic PNL binding whereas muramidase was negative in all cases. Vimentin expression was demonstrated in the CGGT and to a lesser extent in the GCM, but was absent in the GCA which was positive for keratin. Desmin and glial fibrillary acidic protein (GFAP) were not present in any of the lesions. These data demonstrate that PNL binding might be considered to be a common feature of granular cells regardless of their histogenesis. Lysosomes are supposed to represent the intracellular binding sites for this marker. Moreover it is shown that histomorphological identity between the granular cells of CGGT and GCA does not signify identity in histogenesis since the former are of mesenchymal derivation while the latter, from their intermediate filament protein types appear to originate from epithelium.
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PMID:Oral granular cell lesions. An immunohistochemical study with emphasis on intermediate-sized filaments proteins. 631 25

Immunohistochemical and ultrastructural studies were performed on the sinusoidal lining cells of eight canine hepatocellular carcinomas. The sinusoidal endothelial cells of the tumors had a positive reaction for both Factor VIII-related antigen and peanut agglutinin, but did not bind with Ulex europaeus agglutinin-1. Desmin- and lysozyme-positive cells were present along the sinusoids and perisnusoidal spaces of the tumor tissues, respectively, but were fewer in number compared with those of normal canine liver. Alpha-Smooth muscle actin-positive cells outlining the sinusoids were frequently observed. Electron microscopy revealed that basement membranes were often formed beneath the sinusoidal endothelial cells, with rare fenestration. Macrophages were present around or within the sinusoids and tended to increase in number relative to the degree of tumor differentiation. Myofibroblast-like cells with various morphological features, consistent with alpha-smooth muscle actin-positive cells, were frequently found in the perisinusoidal space. The present study indicates that the sinusoidal lining cells of canine hepatocellular carcinoma have some phenotypic characteristics.
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PMID:Immunohistochemical and ultrastructural studies on the sinusoidal lining cells of canine hepatocellular carcinoma. 889 92

Carcinoembryonic antigen, epithelial membrane antigen, Keratin, Desmin, Vimentin, CD30, lysozyme, alpha 1-antitrypsin, alpha 1-antichymotrypsin, S-100 protein, somatostatin and glucagon were looked for using immunohistochemical methods in the epithelial component of 20 parotid gland cystadenolymphomas and 20 normal parotid glands. Carcino-embryonic antigen, ephithelial membrane antigen, S-100 protein, and somatostatin were found in the epithelial cells of most of the cystadenolymphomas. In normal parotid tissue, carcinoembryonic antigen, epithelial membrane antigen, Keratin, alpha 1-antitrypsin, alpha 1-antichymotrypsin, and S-100 protein were found in all three types of ductal cells, somatostatin only in intercalated and striated ductal cells, and lysozyme only in acinar and intercalated ductal cells. Desmin and CD30 were found in the epithelial component of seven of the 20 tumors versus none of the 20 normal parotid glands. Glucagon and Vimentin were negative both in tumor epithelial cells and in normal parotid ductal cells. Our results support the theory that cystadenolymphomas arise from epithelial cells. The presence of lysozyme in the epithelial tumor cells and in the intercalated ductal cells of normal parotid tissue suggest that cystadenolymphomas may arise from the intercalated ducts. The presence of S-100 and somatostatin may indicate that the tumor derives from neuroendocrine structures, but further studies are needed to clarify this point.
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PMID:Cystadenolymphoma of the parotid gland an immunohistochemical study of the epithelial component of twenty cases. 915 27

Angiomatoid "malignant" fibrous histiocytoma (AMFH) has been considered to be a low-grade sarcoma of childhood, and, with its fibrous pseudocapsule, angiomatoid change, dense lymphoplasmacytic response, and proliferation of spindled or round cells, has been classified as a fibrohistiocytic neoplasm. We wanted to study the clinicopathologic and immunophenotypic features of a large number of these tumors and to especially further explore their myoid differentiation. Cases coded as AMFH from 1979 to 1995 were retrieved from the Soft Tissue Registry of the AFIP. Only cases that met the criteria for AMFH by light microscopy were included, a total of 158 cases. Immunohistochemistry was obtained on 98 cases. Clinical history on 92% of all cases revealed a gender ratio of 1.3 females: males, age range of 2 to 71 years, median size of 2.0 cm, and a distribution of extremities > trunk > head and neck, with 66% lesions occurring in areas of normal lymphoid tissue. All tumors with available margins were well-circumscribed. Eighty percent of cases had some degree of lymphoplasmacytic infiltration; 50% cases had pseudovascular spaces filled with blood. Fifty-two percent had predominantly round cell morphology; 48% had a predominantly spindle cell pattern. Desmin positivity was noted in 51% cases and occurred in both predominantly round cell and spindle cell tumors. Most of the desmin-positive cases with adjacent lymphoid infiltrate (67%) showed scattered similar, desmin-positive cells in the surrounding lymphoid infiltrate, adjacent to the tumor. Muscle-specific and smooth-muscle actins were seen in 14% cases. Heavy-caldesmon was strongly positive in 3%, and calponin was focally positive in 73% and extensively positive in 12% cases. MyoD1, myoglobin, and myogenin (myf4) were negative in all tumors studied. Forty-five percent of cases were positive for CD99; 52% of these had round cell morphology. Fifteen percent of cases were positive for KP-1. All tumors were positive for vimentin and negative for CD21, CD35, S100 protein, CD34, keratins 8/18, and lysozyme. Clinical follow-up on 86 patients indicated that only 1 patient was alive with a local nodal metastasis (1% frequency of metastasis) within 1 year, and 2 others had local recurrence, all over a mean follow-up period of 6 years. The myoid, primarily myofibroblastic, phenotype of these lesions is supported by desmin, calponin, and occasional actin positivity. The occasional heavy-caldesmon and smooth muscle actin additionally suggest rare smooth muscle phenotype; however, lack of skeletal muscle markers indicate no relationship of AMFH to skeletal muscle tumors. The resemblance of these lesions to lymph nodes, clinically and morphologically, the finding of similar desmin positive cells in the adjacent lymphoid infiltrate, and the fact that 66% cases were found in sites of normal lymphoid tissue raise the possibility that some of these lesions may arise from or be related to myoid cells of lymphoid tissue. AMFH has an almost invariably benign behavior, but the 1% metastatic rate warrants its classification as low-grade "malignant." The predominantly round cell, CD99-positive and desmin positive AMFH cases, respectively, should not be confused with Ewing's sarcoma/PNET or rhabdomyosarcoma, respectively.
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PMID:Angiomatoid "malignant" fibrous histiocytoma: a clinicopathologic study of 158 cases and further exploration of the myoid phenotype. 1057 14

An 87-year-old woman not known to have either a lymphoma or leukemia developed a left multinodular, fish-flesh superior epibulbar and forniceal mass. A biopsy disclosed a blastic tumor with scattered multinucleated immature megakaryoblasts. Immunophenotyping of bone marrow cells revealed strong positivity for CD7, CD31, CD43, CD45, CD61, and CD117; CD71, myeloperoxidase, and lysozyme were also positive in scattered cells. Forty percent of the neoplastic cells were Ki-67 positive. Cytogenetic studies indicated a trisomy 8 (associated with worse prognosis) and a t(12; 17) translocation. Desmin, smooth muscle actin, pancytokeratin, CAM 5.2, adipophilin, tryptase, S100, SOX10, MART1, and E-cadherin were negative, ruling out a nonhematopoietic tumor. The conjunctival lesion was diagnosed as a myeloid sarcoma with megakaryoblastic differentiation, a rare variant. It probably arose from a myelodysplastic syndrome. This is the first case of its type to develop in the conjunctiva.
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PMID:Myeloid Sarcoma with Megakaryoblastic Differentiation Arising in the Conjunctiva. 3067 74