Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Highly purified vesicular stomatitis virus (VSV) was obtained from VSV-infected SV40-transformed hamster cell lines. Immunization with this virus protected hamsters against challenge with SV40-transformed cells (TSV5-cl2). This protection was obtained regardless of the source of the SV40-transformed cells (e.g. cat, rat, hamster) used to produce VSV, and was therefore associated with the SV40 tumor-specific transplantation antigen (SV40-TSTA). Furthermore, when grown on spontaneously transformed cell lines or on cells transformed by a different oncogenic DNA virus, such as polyoma virus, the VSV failed to protect against the SV40-induced tumor. It was concluded that the SV40-TSTA activity of purified VSV is due to the incorporation of SV40-TSTA within the viral envelope. When VSV was treated with proteolytic enzymes (bromelain, trypsin) no loss of TSTA-induced tumor rejection was observed, although VSV had lost its ability to induce virus-neutralizing antibody. This clearly demonstrates that the TSTA activity is not related to the viral spikes. Phospholipase C suppressed the TSTA activity but neutralizing activity was still detectable in the anti-VSV sera. The results presented here demonstrate that the protection afforded by VSV is highly specific. It is particularly interesting that SV40-TSTA activity may be conveyed by the lipid core of the viral envelope.
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PMID:SV40 tumor rejection induced by vesicular stomatitis virus bearing SV40 tumor-specific transplantation antigen (SV40-TSTA). I. Specificity of immunoprotection and effect of enzyme treatment on TSTA activity. 7 Dec 74

Highly purified vesicular stomatitis virus (VSV) was obtained from VSV-infected SV40-transformed and from "normal" hamster cell lines. A glycolipid extract was prepared from these VSV preparations according to the Folch partition procedure. These glycolipids were rendered immunogenic to the Syrian hamsters when incorporated within liposomal membranes composed of lecithin/sphingomyelin/cholesterol (1/1/2 by weight). When the glycolipids were extracted from VSV grown on cell lines (TSV5-cl2 and EHSVi-cl1) which contained the SV40 tumor-specific transplantation antigen (SV40-TSTA), it was possible either to induce a tumor rejection or at least to slow the growth of the tumor in Syrian hamsters challenged with TSV5-cl2 cells. No protection was obtained in animals treated with liposomes containing glycolipids extracted from purified VSV grown on SV40-TSTA-negative cells (EHB). The SV40-TSTA could be a glycolipid of the transformed cell membrane which is incorporated within the VSV envelope.
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PMID:SV40 tumor rejection induced by vesicular stomatitis virus bearing SV40 tumor-specific transplantation antigen (SV40-TSTA). II. Association of SV40-TSTA activity with liposomes containing VSV glycolipids. 7 Dec 75

Crude membrane (CM) extracts from three different cultured human melanoma lines that were "virus-augmented" (infected with vesicular stomatitis virus (VSV) and subsequently inactivated by ultraviolet light) produced positive skin tests in 17 of 20 (85%), 11 of 20 (55%), and 13 of 18 (72%) tests, respectively, performed in 20 melanoma patients. Identical CM extracts from the same melanoma lines that had not been infected with VSV gave positive skin tests in 2 of 20 (10%), 4 of 20 (20%), and 2 of 18 (11%) tests, respectively, performed in the 20 melanoma patients, and no positive tests in the control patients. The 3 virus-augmented extracts were positive in only 2 of 18 (11%), 0 of 18 (0%), and 1 of 17 (6%) control subjects, respectively. The controls consisted of six normal volunteers and 12 patients with cancers other than melanoma. The "virus-augmented" CM extracts thus exhibited markedly greater sensitivity without significant loss of specificity as compared to nonvirus augmented extracts when used as tumor-specific melaonma skin test antigens.
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PMID:Melanoma skin test antigens of improved sensitivity prepared from vesicular stomatitis virus-infected tumor cells. 7 81

A combination regimen consisting of cisplatin, bleomycin, and vinblastine was evaluated in 86 patients with metastatic testicular tumors. Prior therapy included surgical resection of primary tumor (84 patients), radiotheapy (21 patients), chemotherapy (33 patients). Thirteen patients received prior bleomycin and vincristine or vinblastine. Of 80 evaluable patients 51 achieved complete response (CR) and 26 achieved partial response (PR), for an overall response rate 96.5%. There was no significant difference in response rates or survival with respect to prior therapy, sites of metastatic lesions, and tumor histology. The median survival time was not reached in an observation period of 44+ months. Sixty patients were alive 11+--44+ months, and 57 of these were free of disease. Thirty-two of the 60 patients (53%) had a survival time greater than 20 months. Toxicities included nephrotoxicity (18 patients) leukopenia, (69 patients), thrombocytopenia (nine patients), and anemia (56 patients). Bleomycin-induced pulmonary toxicity was fatal in one patient. Other toxicities included nausea and vomiting, stomatitis, fever, alopecia, and neurological effects.
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PMID:Cisplatin, bleomycin, and vinblastine combination therapy of testicular tumors: an analysis. 8 24

Pseudotypes of vesicular stomatitis virus were prepared with avian sarcoma viruses and avian leukemia viruses representing five different subgroups. These pseudotypes display a host range restricted to that of the avian tumor virus when assayed on avian cells and are neutralized by subgroup-specific antisera. The efficiency of penetration of mammalian cells was assayed by using these vesicular stomatitis virus pseudotypes. Pseudotypes of avian tumor viruses belonging to subgroup D and of B77 virus were able to plate on mammalian cells with a high efficiency, whereas pseudotypes of other strains were not. The efficiency of penetration of the vesicular stomatitis virus pseudotypes was 10-2-to 10-3-fold higher than the efficiency of transformation of the corresponding avian tumor virus strain assayed on mammalian cells, suggesting that there are postpenetration blocks to the expression of transformation in these cells.
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PMID:Virus envelope markers in mammalian tropism of avian RNA tumor viruses. 16 37

Membranes prepared from tumor cells infected with surface budding viruses are much more immunogenic than membranes from uninfected tumor cells. Factors affecting immunization with membranes from virus-infected tumor cells were studied. Preparations made with influenza virus were clearly superior to those prepared with vesicular stomatitis virus (VSV). Membranes infected with VSV were maximally immunogenic at a dose equivalent to a 10% cell pack whereas influenza-virus-infected membranes were immunogenic at 1/100th of this dose. Subcutaneous inoculation was better than other routes of administration. Maximum protection against challenge with viable tumor cells was afforded by two inoculations of VSV-infected membranes spaced 3 days apart or a single inoculation with influenza-virus-infected membranes. Administration of membranes in complete Freund's adjuvant either had no effect of induced a slight degree of tumor enhancement. Immunization with influenza-virus-infected membranes significantly reduced tumor size and incidence even at a challenge dose of tumor cells which was 50 times the LD100.
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PMID:Augmented immunogenicity of tumor cell membranes produced by surface budding viruses: parameters of optimal immunization. 18 46

An adult male African green monkey (Cercopithecus aethiops) with an undifferentiated carcinoma, probably originating from the nasal mucosa, was received from the Akron, Ohio zoo. Cultivation of this tumor in vitro resulted in a mixture of fibroblastic and epithelial cells which was subsequently separated using differential trypsinization. The neoplastic nature of the cultured epithelial cells was verified by their ability to transplant into athymic nude, or antithymocyte serum-treated mice, where poorly differentiated carcinomas were produced, and cultures of the tumors that arose in nude mice were morphologically similar to pretransplantation cultures. Early cultures showed a normal male karyotype characteristic of the species; however, in long-term cultures, a clearly defined, small submetacentric Y chromosome was not observed. Electron microscopic examination of tumor tissue and cultured tumor cells revealed desmosomes and the presence of cytoplasmic (keratin-type) fibrils, which tended to be organized around the nucleus. In addition to the keratin-type fibrils, the cultured tumor cells also contained a large amount of cytoplasmic inclusion material that may represent keratohyalin granules. There was no evidence of a viral association with tumor material or cultured cells. The cultures were susceptible to infection by vesicular stomatitis virus, Herpesvirus hominis type 1, and H. saimiri, but were resistant to the Epstein-Barr virus.
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PMID:Characterization of a spontaneous undifferentiated carcinoma from an African green monkey (Cercopithecus aethiops). 18 33

A thermolabile as well as thermosensitive mutant of vesicular stomatitis virus, VSV-tl-17, could be thermostabilized by phenotypic mixing with avian RNA tumor viruses (ATV). Biological, immunological and morphological studies revealed that this effect is due to a replacement of the thermolabile projections of the VSV by the avian tumor viral projections. The arrangement of projections of VSV and ATV on phenotypically mixed viria was studied by electron microscopy. A-type particles were detected in chick embryo cells which were doubly infected by ATV and VSV. Their intracytoplasmic appearance seemed to be the result of a disturbed maturation of ATV due to the relative deficiency of envelope proteins which were depleted by VSV maturation in the course of phenotypic mixing.
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PMID:Biological and electron microscopic studies on the phenotypic mixing of the thermolabile mutant of vesicular stomatitis virus, tl-17, with avian RNA tumor viruses. 18 54

Homogenates of L1210 cells infected in vitro with vesicular stomatitis virus (VSV) were immunogenic agains a tumor graft of 100 times the LD50 dose of L1210 cells" whereas those of uninfected cells were not. The immunogenicity of intact X-irradiated L1210 cells was distinguishable from that of VSV-infected cell homogenates on the basis of the susceptibility of immunogenicity to experimental procedures used in preparation of the immunogenic homogenates: Homogenization of intact X-irradiated cells or their infection with VSV prior to irradiation led to loss of immunogenicity. In addition, uninfected cell homogenates were not made immunogenic nor was the immunogenicity of VSV-infected cell homogenates eliminated by X-irradiation. At the time of tumor challenge, sera from mice that were effectively immunized with VSV-infected cell homogenate showed a high VSV-neutralizing titer but no complement-dependent cytotoxicity for L1210 cells. Quantitative absorption studies demonstrated that VSV infection led to a marked reduction in L1210 surface antigens recognized by cytotoxic alloantibody; spatial association between these antigens and VSV antigens was not demonstrable on VSV-infected cells. Antigens recognized by heterologous antiserum to L1210 cells were also reduced following VSV infection.
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PMID:Vesicular stomatitis virus-infected L1210 murine leukemia cells: increased immunogenicity and altered surface antigens. 18 42

The glucagonoma syndrome is characterized by dermatitis, stomatitis, elevated serum glucagon levels, abnormal glucose tolerance, weight loss, and anemia--all in association with a glucagon-secreting alpha-cell tumor of the pancreas. A review of 21 cases showed strikingly similar features. A generalized, symmetrical dermatitis initially appeared to be asteatotic or eczematous over the perineum, buttocks, and lower extremities. Gradually, a more characteristic migratory necrolytic erythema with transient bulla formation and erosions developed in intertriginous and dependent areas. Histologically, the most specific features included necrolysis of the upper epidermis, with liquefaction necrosis of the granular cell layer and subcorneal clefting or blister formation. The dermatologist is often first to examine such patients; early recognition of this syndrome with prompt surgical removal of the primary pancreatic lesion may afford cure of the neoplasm.
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PMID:Glucagonoma syndrome. Report of two cases and literature review. 19 36


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