Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Granulomatous prostatitis and poorly differentiated prostate carcinoma can mimic each other both clinically and histologically. To develop criteria useful in resolving problem cases, the authors compared the reactivities of these conditions (nine cases of granulomatous prostatitis and six cases of poorly differentiated carcinoma) with a panel of antibodies to cytokeratin (AE1/3), prostate-specific antigen (PSA), prostatic acid phosphatase (PAP), lysozyme, antimacrophage M, and leukocyte common antigen (LCA). In granulomatous prostatitis, histiocytes were not immunoreactive for PAP, PSA, or cytokeratin; however, histiocytes reacted to lysozyme in nine of nine cases, antimacrophage M in seven of nine cases, and LCA in one of nine cases. Tumor cells from all six carcinoma cases reacted with PAP, PSA, and cytokeratin; all failed to react with lysozyme, LCA, and antimacrophage M. The authors conclude that granulomatous prostatitis and poorly differentiated carcinoma can be reliably distinguished with immunohistochemical methods.
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PMID:Granulomatous prostatitis and poorly differentiated prostate carcinoma. Their distinction with the use of immunohistochemical methods. 199 42

Hepatocellular carcinoma with osteoclast-like giant cells (hepatic giant cell carcinoma [HGCC]) is a rare entity, with only three cases reported. The tumor is histologically similar to giant cell tumor (GCT) of bone, and the origin of the multinucleated giant cells and mononuclear stromal cells has not been determined. The purpose of this report is to present a case of this rare tumor and compare its ultrastructural and immunohistochemical features with those of a conventional GCT of bone. Histologically, the HGCC consists of sheets of osteoclast-like giant cells with a background of mononuclear cells. The giant cells lack the pleomorphism seen in hepatocellular carcinomas with anaplastic giant cells. At the light microscopic level, most of this tumor was nearly identical to a GCT of bone, but several microscopic fields (less than 5% of the tumor) had the histologic appearance of a "usual" hepatocellular carcinoma. The hepatic tumor was negative for HAM 56, epithelial cytokeratins, muramidase, and alpha-1-antitrypsin, with only focal positivity for chymotrypsin in mononuclear and giant cells. The GCT was strongly positive for alpha-1-antitrypsin and chymotrypsin in both the mononuclear and giant cells and showed focal, weak staining for AE1 and AE3 in the mononuclear stromal cells. Ultrastructurally, both mononuclear and giant cells of the HGCC showed features typical of hepatocellular carcinoma. Although the patient presented in this report died, the pattern of growth was different from most hepatocellular carcinomas. The overall histologic features of this tumor are distinctive and appear to justify separating this variant from other types of hepatocellular carcinoma.
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PMID:Hepatic giant cell carcinoma. An ultrastructural and immunohistochemical study. 215 1

Renal disease is a common cause of morbidity and mortality in patients with plasma cell dyscrasia (PCD). We have conducted a systematic study of the formalin-fixed, paraffin-embedded renal tissues from 53 patients with plasma cell dyscrasia, 24 of whom had Bence Jones cast nephropathy (with large casts, often associated with giant cells and polymorphonuclear leukocytes). A battery of 5 immunocytochemical and lectin markers for various segments of the nephron was used [Tetragonolobus lotus, Arachis hypogaea (AH), Tamm-Horsfall protein (THP), epithelial membrane antigen (EMA), and cytokeratin (AE1/AE3)]. In particular, we sought to determine the nature of the intratubular multinucleated giant cells in Bence Jones myeloma cast nephropathy with a variety of epithelial and hematopoietic cell markers. Although tubular epithelial cells stain with their respective markers (whether inflamed, thinned, detached, or adjacent to and lining casts), true intratubular giant cells in PCD were never positive for these tubular markers. In approximately one-third of the cases studied, intratubular and extratubular giant cells stained for several of the seven hematopoietic cell markers employed [i.e., alpha 1-antitrypsin (A1AT), alpha 1-antichymotrypsin (A1ACT), vimentin, and lysozyme], suggesting that giant cells are of hematopoietic origin. The majority of the casts are present in the distal nephron, although some casts were noted in more proximal sites of the nephron. Some larger casts did not stain for THP; smaller casts often showed lamination or stratification of THP staining. Finally, in one-half of the cases, Tamm Horsfall protein (THP) and other distal tubular markers (AH, EMA, AE1/AE3) were found in Bowman's space, almost always in association with interstitial deposits of THP; these markers were virtually never noted in Bowman's spaces of PCD patients without numerous large casts. This suggests that there are communications between distal and proximal nephron, most likely by intraluminal reflux but possibly also through breaks in the tubules and via the interstitium.
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PMID:Myeloma cast nephropathy: immunohistochemical and lectin studies. 246 87

Ovarian endometrioid carcinomas resembling sex cord-stromal tumors (ECSCSs) may simulate Sertoli cell tumors, Sertoli-Leydig cell tumors (SLCTs), and adult granulosa cell tumors (AGCTs), both clinically and pathologically. Differing clinical features and histologic findings are almost always successful in distinguishing these tumor types, although in some cases the differential diagnosis is difficult. Immunohistochemical staining of 17 ECSCSs, 14 Sertoli cell tumors or SLCTs, and 15 AGCTs was performed with the use of antibodies against cytokeratins (AE1/AE3, 902, and CAM 5.2), epithelial tumor-associated antigens (EMA, OM-1, B72.3, and carcinoembryonic antigen B1.1), vimentin, S-100, neuron-specific enolase, and lysozyme to determine the immunohistochemical profile of each tumor type and to define further the nature of the sex cord-like components in ECSCSs. All 17 ECSCSs, none of the 15 AGCTs, and one of 14 Sertoli cell tumors or SLCTs stained with EMA. Staining for OM-1 was almost as helpful diagnostically, with positive results for 15 of 17 ECSCSs, 0/15 AGCTs, and 1/14 Sertoli cell or SLCTs. Antikeratins were immunoreactive with all the ECSCSs as well as some of the AGCTs and Sertoli cell tumors or SLCTs. The B72.3 and B1.1 were immunoreactive with some ECSCSs and Sertoli cell tumors, but were nonreactive with AGCTs. Neuron-specific enolase was demonstrated in 11 of 17 ECSCSs, two of 14 Sertoli cell tumors or SLCTs, and 0 of 15 AGCTs. Vimentin, S-100, and lysozyme were least helpful in the differential diagnosis. These studies suggest that an immunohistochemical approach may be useful in the differentiation of ECSCSs and sex cord-stromal tumors. Furthermore, it supports the conclusion that the sex cord-like cells in ECSCSs are not Sertoli or granulosa cells, but cells of surface epithelial type growing in architectural patterns similar to those of sex cord-stromal tumors.
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PMID:Ovarian endometrioid carcinomas resembling sex cord-stromal tumors. An immunohistochemical study. 247 93

We describe histological, immunohistochemical and ultrastructural findings in a case of littoral cell angioma of the spleen in a 44 year old man. Beside phagocytosis and heavy haemosiderin deposits in the cytoplasm, a very characteristic and hitherto undescribed feature of the littoral cells was focal accumulations of eosinophilic globules 0.5-2 microns in size, which often entirely filled the cytoplasm of the tumour cells. Ultrastructurally the globules were composed of abundant cytoplasmic deposits of lysosomes and residual bodies. The globules most probably originate from the phagocytized red blood cells, lymphocytes and plasma cells. Immunohistochemically the tumour cells reacted positively with antibodies against factor VIII-related antigen, KiM1P, KP1 and lysozyme and negatively with antibodies against cytokeratins AE1-AE3, EMA and S-100 protein. Ultrastructurally the tumour cells often formed long cytoplasmic processes without external lamina and pinocytic vesicles. Scarce and poorly formed junctions between the tumour cells were seen. Very rarely cytoplasmic rod-shaped microtubulated bodies, often difficult to distinguish from heavy accumulations of lysosomes were observed.
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PMID:Littoral cell angioma of the spleen. A case report with ultrastructural and immunohistochemical observations. 751 May 15

The formation of true synovial-lined membranes at tissue sites not intimately related to an articulation or a tendon sheath has been described in a variety of pathologic and postsurgical conditions, but until recently has not been well recognized to occur in association with tissue surrounding silicone breast implants. Of 15 cases with resected periprosthetic breast capsules, 7 (47%) demonstrated true synovial metaplasia with capsule-implant interfaces lined by typical synovial cells. Histochemical and immunohistochemical staining reactions were essentially identical to those observed in synovial control cases and featured positive reactions to Alcian blue-periodic acid-Schiff, reticulin, and vimentin. Focal positive immunoreactivity was observed with alpha 1-antitrypsin, alpha 1-antichromotrypsin, lysozyme, and CD68. No immunoreactivity was observed with cytokeratin AE1/AE3, S-100 protein, carcinoembryonic antigen, or basement membrane antigens. Transmission electron microscopy of the lining cells confirmed their true synovial nature with the type A (macrophage-like) cells, type B (fibroblast-like) cells, and intermediate forms or type AB cells identified. We conclude that the cellular lining surrounding silicone breast implants is a true synovial membrane, that synovial metaplasia may occur in nearly one half of all resected periprosthetic capsules, and that awareness of this entity will enable the surgical pathologist to render an accurate histopathologic diagnosis.
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PMID:True synovial metaplasia of breast implant capsules: a light and electron microscopic study. 779 53

Fifty breast capsules surrounding smooth and textured breast prostheses were reviewed histologically, immunohistochemically, and ultrastructurally, and findings correlated with patient data. The histology of the capsules varied; although most consisted of a simple fibrocollagenous membrane, some were lined by organized, round to polyhedral cells similar to synovium. Histologically, the lining of the synovial type consisted of epithelioid cells overlying parallel bands of collagen, with basally located nuclei and cytoplasmic processes directed toward the surface and arranged within a well developed reticulin network. Immunohistochemically, the cells were vimentin positive, weakly positive focally for alpha-1-antitrypsin, alpha-antichymotrypsin, and lysozyme, and negative for EMA and AE1/AE3. Scanning electron photomicrographs showed a bosselated luminal lining overlying parallel bands of collagen. By transmission electron microscopy, both secretory and phagocytic cells could be distinguished. Some of the former were multinucleated. No basement membrane material could be identified, and cell junctions were rare. Histologically, immunohistochemically, and ultrastructurally the lining appeared identical to synovium and to the synovial metaplasia that has been described in sutured skin, after repeated subcutaneous injections of air, the bone-cement interface of loose hip prostheses and adjacent to gliding silastic tendon reconstruction rods. The physical and chemical composition of the prostheses, the mechanical forces, and the developmental response of the host mesenchymal tissue are thought to influence the formation and maintenance of the synovial metaplasia of the breast capsule.
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PMID:Histological assessment of fifty breast capsules from smooth and textured augmentation and reconstruction mammoplasty prostheses with emphasis on the role of synovial metaplasia. 805 2

We herein describe two unusual neoplasms showing histopathologic features consistent with those of giant cell angiofibroma, which was originally described as a neoplasm arising in the orbit in adults: one of them arose in the right submandibular region of a 48-year-old woman and the other in the right parascapular region of a 49-year-old woman. Macroscopically, although the latter was characterized by a lymphangioma-like cystic appearance, both tumors were well circumscribed and encapsulated. Microscopically, in both cases, pseudovascular spaces lined by a discontinuous row of multinucleated cells were seen against a background of spindle-shaped fibroblastic cell proliferation. In the second case, the tumor presented increased cellularity and plump and somewhat atypical nuclei of proliferating fibroblastic cells, compared with the tumor in the first case. Immunohistochemically, the mononuclear and multinucleated cells within these tumors were positive for vimentin and CD 34 but negative for any other antigens, including Factor VIII-related antigen, desmin, alpha smooth muscle actin, myoglobin, S-100 protein, LeuM1, lysozyme, alpha-1-antitrypsin, and cytokeratins (AE1/AE3 and CAM5.2). The features in these cases indicate that giant cell angiofibroma can arise in an extraorbital site in middle-aged patients and presents some histopathologic diversity.
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PMID:Extraorbital giant cell angiofibromas. 938 57

Middle ear adenoma (MEA) is a rare tumor postulated to take origin from the lining epithelium of the middle ear cavity. The authors report on a case of MEA arising in a 53-year old woman suffering from a sensation of fullness in her left ear, otalgia, and light left-sided hearing loss. Histopathologically, the lesion was composed of cuboidal and polygonal cells displaying a trabecular, tubulo-glandular, and solid pattern of growth. Immunohistochemically, neoplastic cells diffusely stained with anti-vimentin antibodies and were focally positive for chromogranin A, neuron-specific enolase, lysozyme, and cytokeratins AE1/AE3. The majority of tumor cells showed weak and diffuse staining with both anti-PP and anti-ACTH antibodies and intense positivity with anti-glucagon and anti Leu-7 antibodies. Ultrastructural investigation revealed both mucinous-glandular and neuroendocrine differentiation. The authors suggest that the appropriate terminology would be adeno-carcinoid or amphicrine tumor of the middle ear rather than "adenoma," a term that does not reflect its dual nature.
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PMID:Middle ear adenoma is an amphicrine tumor: why call it adenoma? 1129 23

We describe the morphology and comparative genomic hybridization findings in a tumor for which we propose the term "spiradenocylindroma" of the kidney. The tumor arose in the wall of a renal cyst in an otherwise healthy male patient who had a favorable clinical course after nephrectomy. Tumor cells formed either large nodules exhibiting a solid or trabecular architecture with conspicuous perivascular spaces or cylindromatous small tumor cell islands arranged in a jigsaw pattern. Focally, there were interspersed tubular structures and tumor cell rosettes with central deposits of periodic acid-Schiff-positive material. A minor tumor component showed epidermoid differentiation. The tumor cells were strongly positive for cytokeratins 5/6, high molecular weight cytokeratins 34betaE12 and AE1/3, and E-cadherin, but only weakly positive for cytokeratins 7, 8, 18, 19, and epithelial membrane antigen. Focal reactivity for actin, vimentin, and S-100 protein or lysozyme and alpha 1 -antichymotrypsin within tubular and cylindromatous areas suggested myoepithelial and apocrine differentiation, respectively. By comparative genomic hybridization, the only abnormality was loss of the long arm of chromosome 16 and gain of genetic material on the short arm of chromosome 16, suggesting isochromosome i(16p). This finding is unique among renal neoplasms and implies loss of heterozygosity at 16q12-13 of the CYLD1 gene that is critically involved in the oncogenesis of familial cylindromatosis and some sporadic spiradenocylindromas. We conclude that somatic mutation of the CYLD1 gene outside the skin can have a role in the oncogenesis of tumors with cylindromatous features.
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PMID:Spiradenocylindroma of the kidney: clinical and genetic findings suggesting a role of somatic mutation of the CYLD1 gene in the oncogenesis of an unusual renal neoplasm. 1175 79


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