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:3.2.1.36 (hyaluronidase)
4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of mucosubstances in adenoid cystic carcinoma was investigated, and an attempt was made to characterize histochemically the various mucosubstances present. For these purposes the high iron diamine technique (HID), as well as the Astra blue, aldehyde fuchsin and Alcian blue staining methods were employed. Alcian blue was further combined with the periodic acid-Schiff (PAS) technique, the Alcian blue being applied at pH levels between 0.5 and 2.5. In addition the effect of neuraminidase and hyaluronidase treatment as well as methylation and acid hydrolysis procedures on the staining qualities were studied. Acidic mucosubstances with varying histochemical properties were present in different structures of the neoplasm. The characteristic pseudocyst, a major structural component of the neoplasm, stained strongly with HID, Astra blue, aldehyde fuchsin and Alcian blue at low pH. These staining reactions were markedly suppressed by hyaluronidase treatment, and are apparently attributable to the presence of chondroitin 4- and/or 6-sulfate. Employing the Alcian blue-critical electrolyte concentration technique, the basophilia of the pseudocysts was suppressed at a concentration of 0.5-0.6 M MgCl2, which might indicate polysaccharides of relatively low degree of sulfation. An additional, non-sulfated acid mucin could also be demonstrated in these structures. In certain duct and gland like structures of the tumours, a change in staining pattern from blue or blue-red to red could be observed after exposure of the sections to neuraminidase and subsequent staining with the Alcian blue (pH 2.5)-PAS sequence. Similar observations were also made when the pH of the Alcian blue was lowered to 1.5-1.0, as well as after acid hydrolysis. These findings afford evidence for the presence of a neuraminidase susceptive sialomucin in certain epithelial secretions of the tumor. At the ultrastructural level the replicated basement lamina of the pseudocysts displayed a strong positive reaction with the PA-CrA-silver staining technique. Furthermore, amorphous material within the lumina of small duct like structures also displayed a positive reaction. The amorphous material of the cystic compartments was less reactive.
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PMID:Distribution of mucosubstances in adenoid cystic carcinoma. 7 83

Six cases of primary lung cancer that closely mimic malignant pleural mesothelioma clinically and anatomically are compared with four proven cases of malignant pleural mesothelioma. Findings on roentgenograms of the chest, clinical history, and gross examination of the lung specimens are not helpful in distinguishing between these two neoplasms. Microscopic examination of the hematoxylin and eosin-stained tissues is often inconclusive. Tissues were stained with hematoxylin and eosin, PAS with and without diastase treatment (DPAS), mucicarmine, alcian blue, toluidine blue, and colloidal iron with and without digestion by testicular hyaluronidase. Among these histochemical methods, DPAS was found to be particularly useful in distinguishing the primary lung cancers from the mesotheliomas. All primary lung cancers except one showed DPAS-positive material (mucin) in both the cytoplasm of the cancer cells and within the lumina of neoplastic glands. In contrast, none of the mesotheliomas showed the presence of DPAS-positive material. Histologically, all lung cancers were glandular. Five were classified as bronchiolar carcinoma, the remaining one as poorly differentiated adenocarcinoma. In two of the bronchiolar carcinomas, a small subpleural primary focus was demonstrated. This finding suggests a possible origin of these cancers as a small subpleural tumor that became widely disseminated via the subpleural lymphatics. This form of primary lung cancer possesses sufficient gross and microscopic characteristics that recognition should be given to it as a variant of primary lung cancer, with emphasis on differentiating it from pleural mesothelioma.
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PMID:Pseudomesotheliomatous carcinoma of the lung. A variant of peripheral lung cancer. 17 52

The adherence of group A streptococci to epithelial cells was studied by using streptococcal strains labeled with [(3)H]uridine or fluorescein isothiocyanate. The ability of the labeled organisms to adhere to Detroit 562 epithelial cells, derived from a human pharyngeal carcinoma, as well as to epithelial cells scraped from the oral cavity was determined. Adherence to monolayer cultures or cell suspensions of Detroit cells compared favorably with adherence to suspensions of human oral epithelial cells. Initial experiments to determine the optimal conditions for adherence showed that adherence was temperature dependent and that the optimal incubation time was 15 min for adherence to epithelial cells in suspension and 30 to 60 min for monolayer cultures. Both streptococci and epithelial cells exhibited specificity in the adherence process. Different streptococcal strains varied in their ability to adhere. Adherence was also affected by the growth stage of the bacterial cultures. Trypsin treatment of the streptococci slightly decreased adherence, whereas hyaluronidase treatment increased the adherence of some strains. Streptococci were found to adhere to only about half of the epithelial cells. Those epithelial cells apparently have a limited number of receptor sites since they can be saturated by adding increasing concentrations of bacteria. Further support for limited receptor sites was provided by competition experiments. Adherence was inhibited by trypsin treatment of the epithelial cells, suggesting that proteins in the epithelial cell membrane may play a role in streptococcal adherence.
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PMID:Adherence of group A streptococci to human epithelial cells. 35 28

Glycosaminoglycans have been characterized from a normal human breast cell line (HBL-100) and two different cell lines from human breast carcinoma (MDA-MB-231 and MCF-7). The glycosaminoglycans were labeled by exposure of cell cultures to [3H]glucosamine and [35S]sulfate and then isolated from both spent media and cells by pronase digestion and cetylpyridinium chloride fractionation. They were further characterized by (a) hexosamine composition, (b) controlled-pore glass exclusion chromatography, (c) reactivity with specific enzymes (hyaluronidase chondroitinase, heparitinase, and heparinase), (d) nitrous acid degradation, and (e) DEAD-Sephadex chromatography. The results indicate that the HBL-100 line synthesizes mainly hyaluronic acid, most of which is secreted into the medium. Chondroitin sulfate and heparan sulfate are the predominant glycosaminoglycans synthesized by the cancer lines; both are found mainly in the spent medium, but the hyaluronic acid synthesized by the MDA-MB-231 line remains cell associated. The cell-associated heparan sulfate had a molecular weight in excess of 13,000 and may contain linkages susceptible to testicular hyaluronidase. The MCF-7 cells produce significantly lower amounts of glycosaminoglycans than do the other two lines.
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PMID:Glycosaminoglycans of normal and malignant cultured human mammary cells. 42 76

Mouse eggs were activated with hyaluronidase in vitro and subsequently transferred to the oviduct. In the female reproductive tract they formed morulae and blastocysts which died soon after implantation. Haploid blastocysts were transferred beneath the kidney capsule and here some formed disorganized egg-cylinder structures in a week. Morulae and blastocysts from haploid and diploid parthenogenones were also transferred beneath the testis capsule. Two to four months later the growths which had formed were sectioned. They contained neural tissue, pigment, keratinized epithelium, glandular epithelium, ciliated epithelium, cartilage, bone, muscle, adipose tissue, and haemopoietic tissue. The range of cell types was similar to that produced by fertilized control blastocysts except that the parthenogenones did not form identifiable yolk-sac carcinoma or embryonal carcinoma cells. The growths from haploid and diploid parthenogenones in the testis were stained with Feulgen and their DNA content measured. Growths from diploid embryos contained the normal diploid amount of DNA while growths from haploid embryos contained less than this amount. Cell cultures were prepared from the growths. The cells which were investigated contained no Y chromosome, suggesting that they were derived from the embryonic cells rather than the cells of the male host. These cells contained a near diploid chromosome number, although some of them were originally derived from haploid embryos.
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PMID:Development of parthenogenetic and fertilized mouse embryos in the uterus and in extra-uterine sites. 119 37

Tissue samples from 30 patients with adenoid cystic carcinoma and 20 with adenocarcinoma of salivary gland origin were studied by immunohistochemical staining with specific antibodies to the four macromolecules that are present in normal basement membranes: type IV collagen, laminin, heparan sulfate proteoglycan, and entactin. In the adenoid cystic carcinoma samples, the four proteins were localized in different types of extracellular matrices in the tumor, namely pseudocystic spaces, hyaline stroma, and around tumor cell nests. The staining intensity was enhanced by pretreatment with hyaluronidase. The tumor cells of adenoid cystic carcinoma showed a tendency to proliferate with individual cells in contact with the basement membrane and to infiltrate through basement membrane-rich tissues, such as peripheral nerves, blood vessels, and skeletal muscles. In contrast, only circumferential staining of tumor cell nests was obtained in adenocarcinoma samples. The results suggest that adenoid cystic carcinoma is a tumor with affinity for basement membranes, and this basic feature is reflected in its histology and presumably in its biologic behavior. Immunostaining with antibodies to basement membrane proteins appears to be useful for differential diagnosis of some types of these two carcinomas.
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PMID:Basement membranes in adenoid cystic carcinoma. An immunohistochemical study. 131 6

The specific binding and nature of the epitope recognized by monoclonal antibody (Mab) 1H10, which binds an antigen expressed on human cervical tumors, was characterized by enzyme digestion, lectin competition assay and immuno-electron microscopy. Membrane homogenates of CaSki cervical carcinoma cells were digested with various enzymes, then analysed by SDS-PAGE and immunoblotting. Cells grown on coverslips were treated with various enzymes and in situ binding of Mab 1H10 to cells was analysed by electron microscopy. The ability of lectin-conjugates to block Mab 1H10 binding to CaSki cells was also examined. Treatment of samples with sodium periodate abrogated antigen recognition by Mab 1H10. Neuraminidase and hyaluronidase digestion decreased but did not eliminate Mab 1H10 binding to cells in situ. Chondroitinase ABC digestion, in contrast, removed Mab 1H10 binding sites both in vitro and in situ. Trypsin and chymotrypsin digestion of cell membrane homogenates decreased the molecular weight of the Mab 1H10 antigen but did not decrease the binding intensity. Wheat germ agglutinin (WGA) strongly bound to CaSki cells and partially blocked Mab 1H10 binding, indicating that the antigen contains N-acetyl-galactosamine residues at or near the epitope recognized by Mab 1H10. Ricinus communis agglutinin (RCA) exhibited a similar binding pattern to WGA. However, concanavalin A bound only weakly to CaSki cells and was ineffective at blocking Mab 1H10 binding. The tumor-associated antigen recognized by Mab 1H10 is concluded to be a chondroitin sulphate glycoprotein or proteoglycan rather than a mucopolysaccharide or lipoprotein.
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PMID:Characterization of a human cervical carcinoma-associated antigen by lectin binding and immuno-electron microscopy. 142 5

The effect of hyaluronidase and a combination of hyaluronidase with Adriamycin was investigated on several breast cancer models in vitro and in vivo. In vitro enzyme treatment (using concentrations up to 80,000 IU/1) of murine (MXT-, MXT +/-, and MXT+) and human (MCF-7, ZR-75-1 and T-47-D) breast cancer cell lines did not inhibit tumour cell proliferation (measured by a kinetic crystal violet assay) in either case. Although high-dose hyaluronidase (1.2 x 10(6) IU/kg) was ineffective, when administered peritumourally to the MXT M3.2 mammary carcinoma of the B6D2F1 mouse, it is remarkable that five "megadoses" were excellently tolerated. However, the antineoplastic activity of Adriamycin against the oestrogen-receptor-positive variant of the MXT tumour was significantly enhanced by combination with concentrations of hyaluronidase that were inactive per se, both in vitro and in vivo. Interestingly, the enhancement of the in vivo antitumour activity was not compromised by toxic side-effects.
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PMID:Hyaluronidase enhances the activity of adriamycin in breast cancer models in vitro and in vivo. 151 81

We have studied the effects of hyaluronidase (HYD) on the penetration and cell kill effect of doxorubicin (DXR) using multicellular tumor spheroids (MTS). MTS of approximately 500 microns in diameter were prepared by liquid over lay culture technique from PC-10 lung and HEp-2 laryngeal squamous carcinoma cell lines. Cells in MTS and monolayer were exposed for various durations to HYD, followed by 1 hr, rest interval, and by 1 hr. exposure to DXR. MTS and monolayer cells were then trypsinized to a single cell suspension and subjected to clonogenic assay. For PC-10 MTS, pretreatment with HYD for 24 hr. resulted in approximately 10-fold increases in DXR cell kill effects as compared to DXR alone. HEp-2 MTS were more sensitive to HYD pretreatment. Thus, 1 hr. exposure to HYD produced approximately 4-fold increases in DXR-induced cell lethality. Fluorescent microscopic study revealed that 1hr. exposure of MTS to DXR produced DXR fluorescence only 1-2 outer layer of MTS. When MTS were pretreated with HYD, there was an enhanced penetration of DXR fluorescence into the MTS core. HYD-induced enhancement of DXR penetration and its cell kill effect was dependent on the exposure time and tumor cell origin.
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PMID:[Combination chemotherapy of solid tumor--effects of hyaluronidase on doxorubicin (DXR) penetration into multicellular tumor spheroids (MTS)]. 162 55

A high molecular weight secretion product of cell lines established from duct cell-derived human pancreatic adenocarcinomas was investigated in this study. After metabolic labeling and molecular sieve chromatography of culture medium, a product appeared in the void volume of a Superose 6 column that could be labeled with [3H]glucosamine, but not with [35S]sulfate. After further purification by anion exchange chromatography it was analyzed and demonstrated to be hyaluronan (HA). CsCl density gradient centrifugation revealed a density of 1.45 g/cm3 in a 4 M guanidinium hydrochloride solution. [3H]Glucosamine-labeled material could be degraded by digestion with hyaluronidase from two sources, but not with heparitinase I or chondroitinase AC. Sugar analysis revealed glucuronic acid and glucosamine at a molar ratio of 1:1. When the amount of HA synthesized by different pancreatic adenocarcinoma cell lines was compared, the values of the cell lines PaTu 8902 and PaTu II were about five- to tenfold higher than those of the lines PaTu 8988s, PaTu 8988t or HPAF, but an order of magnitude lower than in murine 3T3 fibroblasts. HA synthesis per cell decreased with increasing cell density. In serum-free cultures of cell lines with high HA synthesis it was 3 to 5 times higher compared to cultures that were supplemented with serum. We conclude that pancreatic adenocarcinoma cells secrete hyaluronan and thus contribute to the extracellular matrix of the tumor tissue. In pancreatic carcinoma cells, regulation of HA biosynthesis seems not to be positively correlated to proliferation as has been demonstrated for fibroblasts.
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PMID:Hyaluronan is a secretory product of human pancreatic adenocarcinoma cells. 164 63


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