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)

Clinical trials to evaluate the potential of adoptive immunotherapy in cancer patients have been restricted to the use of lymphoid effector cells. Of the other probably even more important host defense system against tumor growth, the mono-nuclear phagocyte system, only monocytes (mo) have been reinfused which, however, represent immature precursor cells and acquire full functional competence only upon further maturation. This is a report on 7 patients who received autologous macrophages (MO) grown in vitro from blood mo and activated by interferon-gamma (IFN gamma). Mononuclear cells were isolated from whole blood by cytapheresis and cultured for 7 days with 2% autologous serum on hydrophobic Teflon foils. Eighteen house before cell harvest, recombinant human IFN gamma was added at 200 IU/ml. Mo-derived MO were purified by counter-current elutriation. Starting with 10(8) MO cells, therapy was escalated up to the maximal number of MO obtainable from one single preparation cycle. Currently, 26 therapies have been performed with the maximal dose being 1.7 x 10(9) MO per infusion. Except for low grade fever (less than 38 degrees C), MO autografts were well tolerated, with no side effects observed. Biological response was followed by analyzing the serum levels of beta 2-microglobulin, neopterin, interleukin-6, tumor necrosis factor, and lysozyme. While in 3 out of 7 patients serum neopterin increased in response to MO therapy, other biological response parameters remained at pretreatment levels. Radiolabeled MO were shown to first accumulate in the lungs, then to pool into liver and spleen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A new approach to adoptive immunotherapy of cancer using tumorcytotoxic macrophages grown from peripheral blood monocytes. 175 53

Mouse lung tumors were induced transplacentally in offspring by treating C3H/HeNCrMTV- and Swiss Webster [Tac:(SW)fBR] mice during different periods of gestation with a single i.p. injection of N-nitrosoethylurea (ENU) at 0.5 mmol or 0.74 mmol/kg. Quantitative and qualitative evaluation of the lung tumors in the offspring at ages ranging from 1 week to 52 weeks was carried out by light microscopic study of hematoxylin and eosin-stained (H&E) serial and step sections. By nitroblue tetrazolium enzyme histochemistry, 3-hydroxybutyrate dehydrogenase (seen predominantly in Clara cells) was localized in frozen tissue sections. By avidin-biotin peroxidase complex immunohistochemistry, various specific cellular and nuclear markers were investigated on paraffin sections (antisera against surfactant apoprotein, Clara cell antigen, lysozyme, and 5-bromo-2' deoxyuridine). Normal lung and lung tumors were also studied by electron microscopy. A histological method was developed to assess all lesions present in the entire lung. It was shown that solid and papillary tumor types arose individually and that mixed solid/papillary forms represented a progression of the benign solid adenoma to the malignant papillary carcinoma. Immunocytochemical localization of DNA synthesis with 5-bromo-2' deoxyuridine gave the highest labeling indices at early stages of tumor growth. As the size of the papillary tumors increased, fewer nuclei were labeled/mm2 of tumor section. Lack of both specific Clara cell antigen and 3-hydroxybutyrate dehydrogenase and the absence of typical nonosmiophilic Clara cell granules indicated a cell of origin other than Clara cells. Evidence for alveolar type II cell origin of both solid and papillary neoplasms in spontaneous and induced tumors was found in the expression of surfactant apoprotein, the presence of mature lamellar bodies (solid tumors) or small lamellar bodies, and immature stages of lamellar bodies (papillary tumors). Lysozyme was present in mature alveolar type II cells and solid tumors but absent in fetal lung and papillary neoplasms. Tumors induced on gestation day 14 or day 16 had all developed by 2 weeks of age and generally did not increase in multiplicity with age, whereas those induced on day 18 showed a protracted development with regard to frequency, growth (size), and progression. The multiplicity of mouse lung tumors induced at different stages of fetal development paralleled the number of alveolar type II precursor cells (i.e., followed a bell-shaped pattern peaking on day 16 of gestation).
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PMID:Origin of spontaneous and transplacentally induced mouse lung tumors from alveolar type II cells. 205 24

The antitumor effects of egg-white lysozyme, at dosages between 25 and 100 mg/kg/day given for 5 to 14 days, was examined in CBA mice bearing MCa mammary carcinoma or TLX5 lymphoma. At early stages of tumor growth the antitumor action of lysozyme is statistically significant, independently from the route of administration (e.g., i.v. and oral admixed with food). With larger tumor masses, oral administration of lysozyme is effective on s.c. tumor growth but not on i.m. tumors. The effects of lysozyme in mice bearing TLX5 lymphoma consist of reduction of the capacity of tumor cells to form brain metastases: the effect is mediated by spleen cells. Dietary intake of lysozyme is also active in prolonging the survival time of animals treated with surgery and postsurgical cisplatin treatment. These effects indicate lysozyme to be an active substance, effective on the growth of malignant tumors and capable of synergizing with conventional therapies such as surgery plus cisplatin for the control of disseminated tumors in mice.
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PMID:Antineoplastic action of egg-white lysozyme on the growth of MCa mammary carcinoma and TLX5 lymphoma in the CBA mouse. 262 98

Current knowledge about the etiology and histogenesis of keratoacanthoma (KA) is first reviewed, after which the various clinical and histological patterns of this tumor are presented. The differential diagnosis, particularly against spinocellular carcinoma (SCC), and possible forms of therapy are discussed. A series of 90 KAs seen in the period 1976-1986 were investigated histopathologically with reference to the overall architecture, the epithelial differentiation, the behavior towards the adjacent tissue, and the extent and composition of the cellular infiltrate. In addition to routine staining with hematoxylin-eosin and Giemsa, several files have been subjected to immunohistological analysis by means of the peroxidase-antiperoxidase method (PAP) (keratin, lysozyme, epithelial membrane antigen, tissue polypeptide antigen). In 79 cases (88%) the overall architecture found was that of an endo-exophytic, dome-shaped structure with a central crater filled with a plug and with epithelial "lips" at the margins. In 3 KA (3%) a more endophytic picture was seen though no ulceration was observed. In 2 tumors in the very early stages (2%), there was no formation of horn crater and no epithelial lips. Similarly, 5 flat, plaque-like KA (6%) also showed no horn crater. With the exception of 3 aggregated (and/or multicentric) KA (3%), no solitary or multiple types were found. In 88 cases (98%), proliferation of the epidermis was observed mainly in the lateral and basal parts. In 86 KA (96%) there was a relatively well-demarcated, sharp border to the basal tumor portions. In 4 cases (4%) a less precise definition of the outer tumor margins was observed, because of a considerable pseudocarcinomatous, though not truly infiltrative, growth pattern. In 24 KA (27%) there was a strong tendency to formation of one or more sequesters. In the majority of cases, maturation of the epithelial cells was normal. Abnormal multipolar mitoses (7 cases; 8%) and relatively pronounced cellular atypies (8 cases; 9%) were occasionally observed. There was a clear correlation between the composition and extent of the inflammatory infiltrate and the tumor growth stage. In 78 KA (87%) large numbers of intraepithelial neutrophilic microabscesses were shown. In only 13 cases (14%) were substantial numbers of eosinophilic leukocytes observed, and 3 of these tumors (3%) later developed eosinophilic microabscesses.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Keratoacanthoma and its clinical variants. Review of the literature and histopathologic analysis of 90 cases]. 265 49

We describe an unusual type of carcinoma of the parotid gland in a 67-year-old man. Because of rapid tumor growth, radical parotidectomy was done. Light microscopic study of the tumor revealed focal gland formation with transition to anaplastic carcinoma. Among the undifferentiated mononuclear cells and bizarre large cells were scattered many osteoclastlike multinucleated giant cells. Immunohistochemical studies on paraffin sections revealed positive staining for epithelial membrane antigen in the epithelial component; however, the multinucleated giant cells were clearly negative for this antigen. Reactions for other cell constituents (carcinoembryonic antigen, alpha 1-antitrypsin, alpha-1-antichymotrypsin, Leu-M1, Leu-M3, lysozyme, and factor VIII-related antigen) were negative in both epithelial and giant cell components of the tumor. Electron microscopy revealed poorly formed cell junctions and numerous microvilli on the surface of the mononuclear tumor cells and multinucleated giant cells, features considered not of diagnostic significance. Similar to carcinomas with osteoclastlike multinucleated giant cells in other organs, this parotid gland tumor has shown clinical and morphologic evidence of aggressive growth; pulmonary metastases developed and the patient died 28 months after radical surgery.
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PMID:Carcinoma of the parotid gland with osteoclastlike giant cells. Immunohistochemical and ultrastructural observations. 383 77

The ip inoculation of inactivated Brucella abortus, strain B19 R, protected mice against a subsequent graft of an ascites lymphoma. The bacterial components responsible for this effect were investigated. Centrifugation supernatants of sonicated bacteria supposed to contain mainly cytoplasmic products did not offer protection against the lymphoma. Cell walls (CW's) prepared by enzyme digestion of pellets of lysed bacteria and checked for purity by electron microscopy prolonged survival of mice and induced cytotoxic macrophages in their peritoneal cavities. CW peptidoglycan (PG) did not seem to play an important part in this effect. Enzyme digestion of CW, in particular by lysozyme, was found to reduce a PG characteristic component (diaminopimelic acid) without altering CW antitumor activity. Conversely, a purified PG preparation did not influence tumor growth. Extraction of CW by an ether:water mixture did not alter its antitumor activity, while incubation in NaOH abolished its activity almost completely. All CW preparations were found to elicit hypersensitivity reactions in Brucella-infected animals.
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PMID:Antitumor activity of cell walls from Brucella abortus. 641 57

The ability of differently structured, purified peptidoglycans (PG) to induce interleukin 1 (IL1) secretion was compared. PG from Bacillus megaterium and Staphylococcus aureus stimulated the production of IL1 by mouse peritoneal macrophages and human adherent mononuclear cells, whereas PG from Micrococcus lysodeikticus and Corynebacterium poinsettiae were inactive. There was a correlation between the ability of PG to induce IL1 secretion and previously demonstrated immunoenhancing activities (adjuvant effect, increase of resistance to tumor growth) of PG. PG solubilization by lysozyme decreased but did not abolish the PG effect on IL1 secretion. Active PG induced IL1 production in nude mice and in the C3H/HeJ strain (which is unresponsive to lipopolysaccharides).
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PMID:Induction of interleukin 1 secretion by adjuvant-active peptidoglycans. 660 29

Effects of lysozyme(LY) alone and combination with various antitumor agents were examined using syngeneic tumors mainly Meth-A and MH 134 transplanted into Balb/c and C3H/He mice, respectively. The effects of LY on pulmonary metastases were also examined in BDF1 mice bearing Lewis lung carcinoma (3LL). LY inhibited the growth of Meth-A tumor and enhanced antitumor effects of mitomycin C (MMC). bleomycin (BLM) and 5-fluorouracil (5-FU), LY activated antitumor effects of MMC, BLM and 5-FU on MH 134 tumor, however, LY alone did not show any significant antitumor effect on it. The combination treatments using LY with MMC or 5-FU showed a marked inhibition on pulmonary metastases of 3LL. The pre-treatment of LY inhibited the tumor growth of Sarcoma-180 in ICR mice.
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PMID:[Experimental studies on antitumor effects of lysozyme]. 718 34

Nocardia lysozyme digest (NLD), a particulate fraction from Nocardia opaca, is able to induce antitumor activity to SaL-1 tumor cells (lung sarcoma) in Balb/c mice. In mice immunized with NLD inhibition of tumor growth and prolonged survival of tumor bearing animals was observed. Macrophages isolated from peritoneal cavity and stimulated with NLD release a few arachidonic acid metabolites, mostly PGE 2. Macrophages from tumor bearing mice are more sensitive to Nocardia antigens than normal. Both in vitro and in vivo experiments have documented that Nocardia is an active immunomodulator.
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PMID:Immunomodulatory activities of Nocardia opaca. 750 60

Six well-characterized specimens of cultured astrocytoma cells were investigated with a panel of macrophage markers. Our results show that the macrophage markers OKM-1(CD11b), OKM5(CD36), EBM11(CD68), HAM56, Factor 13, alpha-1-antichymotrypsin, alpha-1-antitrypsin, ferritin and lysozyme are clearly reactive to neoplastic astrocytes whereas astrocytes in normal brain specimens are not reactive. In order to obtain further confirmation concerning the reactivity of tumor cells in vivo, we simultaneously measured by flow cytometric analysis DNA content and HAM56 immunoreactivity in a freshly obtained tumor specimen. In this experiment we found a marked reactivity of aneuploid cells to HAM56. The macrophage phenotype of malignant astrocytes may reflect a similarity in functions of these cells and tumor-associated macrophages which promote tumor growth via the production of growth factors and angiogenic factors. Furthermore, our findings implicate that demonstration of macrophages within malignant astrocytomas by using macrophage-specific antibodies must be cautiously considered.
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PMID:Human malignant astrocytes express macrophage phenotype. 782 78


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