Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histologically confirmed inadequate treatment resulted in a lower than expected recurrence percentage in dogs with haemangiopericytoma (38%) and mastocytoma (30%). Clinical suspicion of inadequate tumour treatment did not always correlate with the histologically assessed inadequacy, nor with the appearance of local recurrence. Local recurrence did not seem to be correlated with histological grade of malignancy and tumour size. Local injection of C. parvum vaccine did not result in a lower percentage of local recurrence or longer recurrence-free intervals in any of the three tumour groups (canine haemangiopericytoma, canine mastocytoma, feline mammary carcinoma). Nor was palliative local adjuvant injection of Cp successful in dogs and cats with soft tissue sarcomas or in dogs with gingival melanoma. Re-operation of locally recurrent tumour was successful in some dogs with haemangiopericytoma, in a few with mastocytoma, but not in cats with mammary carcinoma. A trend toward histological progression of recurrences and metastases, when compared with the primary tumours, was not evident. The possible reasons for the relatively low recurrence rate of some tumour types and for the failure of Cp-treatment are discussed.
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PMID:Incomplete surgery, local immunostimulation, and recurrence of some tumour types in dogs and cats. 311 58

The in vitro cytotoxicity assay and the histological in vivo analysis were used to study cell-mediated immunity in the spleen of DBA/2 mice bearing subcutaneously developing P815X2 mastocytoma. Mononuclear cells separated from the spleen showed P815X2 specific cytotoxic activity between days 10 (12) and 16 following tumor inoculation. Maximal cytotoxicity was detected on days 13 and 14. In the T cell area of the spleen white pulp (C-PALS), an increase in the proportions of T lymphocytes and mononuclear phagocytes was observed on days 10 and 12 after the injection of P815X2 cells. On day 14, the T cell level in C-PALS dropped below control values, and the cellular density in the T cell area was reduced. Tumor metastases were seen in the spleen from day 14 onwards. The results indicate, that the T cell reaction in vivo was detectable in C-PALS one to two days earlier than the in vitro cytotoxicity of the spleen cells. By the time of maximal cytotoxic activity, the in vivo reaction had disappeared.
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PMID:Immune response against P815X2 mastocytoma growing in syngeneic DBA/2 mice. V. Spleen immunoreactivity and cell mediated cytotoxicity. 311 52

The successful penetration of endothelial basement membranes is an important process in the formation of hematogenous tumor metastases. Heparan sulfate (HS) proteoglycan is a major constituent of endothelial basement membranes, and we have found that HS-degradative activities of metastatic B16 melanoma sublines correlate with their lung-colonizing potentials. The melanoma HS-degrading enzyme is a unique endo-beta-D-glucuronidase (heparanase) that cleaves HS at specific intrachain sites and is detectable in a variety of cultured human malignant melanomas. The treatment of B16 melanoma cells with heparanase inhibitors that have few other biological activities, such as N-acetylated N-desulfated heparin, results in significant reductions in the numbers of experimental lung metastases in syngeneic mice, indicating that heparanase plays an important role in melanoma metastasis. HS-degrading endoglycosidases are not tumor-specific and have been found in several normal tissues and cells. There are at least three types of endo-beta-D-glucuronidases based on their substrate specificities. Melanoma heparanase, an Mr approximately 96,000 enzyme with specificity for beta-D-glucuronosyl-N-acetylglucosaminyl linkages in HS, is different from platelet and mastocytoma endoglucuronidases. Elevated levels of heparanase have been detected in sera from metastatic tumor-bearing animals and malignant melanoma patients, and a correlation exists between serum heparanase activity and extent of metastases. The results suggest that heparanase is potentially a useful marker for tumor metastasis.
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PMID:Heparanases and tumor metastasis. 328 60

In order to investigate possible differences in sugar binding activities of strongly versus weakly metastatic tumors, sugar-binding molecules (endogenous lectins) of murine tumor cells differing in metastatic capacity were analyzed by affinity chromatography on supports with immobilized sugars or glycoproteins and compared. After elution with specific sugar in the absence of Ca2+-ions, the proteins were separated by sodium dodecyl sulfate-polyacrylamide slab gel electrophoresis. In comparison to a weakly metastatic subline (Eb) spontaneous strongly metastatic variants (ESb) of a murine lymphoma contained additional sugar receptors for N-acetylglucosamine (Mr 30 kDa) and maltose (Mr 64 kDa, 62 kDa, 54 kDa and 32 kDa), and lacked one sugar receptor for myoinositol (Mr 85 kDa), N-acetylglucosamine (Mr 23 kDa) and maltose (Mr 22 kDa), respectively. The strongly metastatic variant ESb expressed the common beta-galactoside-specific lectin to a higher extent and receptors for myo-inositol, melibiose and mannan to a lower extent. In another model system derived from the murine mastocytoma cell line P 815 X 2A, biochemical analysis of the liver-metastasizing variant P 815 X 2B revealed additional characteristic N-acetylgalactosamine- and maltose-specific binding proteins. This variant had reduced amounts of receptors for beta-galactosides and fucose in comparison to the parental clone. In a third tumor system a similar qualitative difference was disclosed: a metastatic variant derived from spleen metastases displayed a sugar receptor profile with 5 additional beta-galactoside-binding proteins when compared to its parental clone 6-6#3 + F, which is a virally transformed fibroblast line. The results show that metastatic variants of 3 murine tumor models consisting of lymphomas, mastocytomas and sarcomas are characterized by qualitative and quantitative alterations in the profiles of sugar-binding proteins.
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PMID:Differential expression of endogenous sugar-binding proteins (lectins) in murine tumor model systems with metastatic capacity. 357 May 57

The antineoplastic activity of hexaziridinocyclotriphosphazene (Myko 63) has been investigated in a panel of murine ascitic and solid tumors. Myko 63 was found to significantly retard primary and secondary tumor growth and to prolong the survival rates in each of the nine models employed. These included the L1210 and P388 leukemias, P815 mastocytoma, the 3LL and Madison 109 carcinomas, M5076 reticulum cell sarcoma, the line 26 colon and line 16 mammary carcinomas, and an intracranially implanted ependymoblastoma. The possible modes of action of this compound and the potentials of cyclophosphazenes, a chemical class largely unexplored as antitumor agents are discussed.
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PMID:The antineoplastic activity of hexaziridinocyclotriphosphazene (Myko 63) in murine tumors. 623 Sep 86

An extract of the meningococcus antigens (MA) prepared from N. meningitidis was tested for an anti-tumor effect in rat and murine metastasizing tumor models. Effectiveness of MA in each model varied with dose and was manifested as significantly improved survival of the treated animals. Growth of the primary Fischer bladder carcinoma (FBCa) and metastases to lungs and lymph nodes were significantly inhibited in F344 rats treated weekly with 1 mg MA. Administration of MA at 100 micrograms per animal significantly prolonged survival of P815 mastocytoma-inoculated DBA/2 mice. Survival of C-26 colon adenocarcinoma-bearing Balb/c mice was significantly improved in animals that received weekly injections of 20 micrograms MA, without significant effect on the development of local tumor. The meningococcal antigens demonstrate strong mitogenic activity in B-cell-enriched murine spleen cultures. Thus the immunostimulatory activity of MA in experimental malignancy could involve, directly or indirectly, activation of B lymphocytes.
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PMID:Menningococcal antigens (MA): a novel immune stimulant in experimental neoplasia. 641 53

Intracameral inoculation of allogeneic P815 mastocytoma cells (DBA/2) into BALB/c mice resulted in progressively growing intraocular tumors. Intraocular tumor cells disseminated rapidly to the spleen and cervical lymph nodes, yet extraocular nests of tumor cells never developed into fulminant tumors. Further experiments showed that tumor cells were continuously seeded from the primary intraocular tumor and were rapidly cleared from extraocular sites. Hosts harboring intraocular P815 mastocytomas rejected tumorigenic doses of P815 cells inoculated subcutaneously or even into the contralateral anterior chamber. This systemic tumor immunity was found to be radiosensitive and T cell dependent. Spleen cells from animals with progressively growing intraocular tumors protected recipient mice challenged with intracamerally inoculated tumor cells and thus suggests that a cell-mediated mechanism is the underlying basis for this form of tumor immunity. The data indicate that mice harboring progressively growing intraocular tumors develop a potent state of "concomitant immunity," that prevents the development of metastases, yet is ineffective in controlling the primary tumor.
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PMID:Intracamerally induced concomitant immunity: mice harboring progressively growing intraocular tumors are immune to spontaneous metastases and secondary tumor challenge. 641 74

Progressive growth of the P815 mastocytoma in semisyngeneic mice evokes the generation of a T cell-mediated mechanism of immunosuppression that inhibits the capacity of passively transferred, tumor-sensitized T cells from regressing this tumor in recipient mice. This conclusion is based on two findings: (a) that it is possible to demonstrate adoptive T cell-mediated regression of established tumors, but only if the tumors are growing in T cell-deficient recipients, and (b) that adoptive T cell-mediated regression of tumors in these recipients can be inhibited by the infusion of splenic T cells from T cell-intact, tumor-bearing donors. The results of additional experiments designed to measure the effect of decreasing the number of suppressor cells and the time that they are infused, relative immune cells, indicate that the function of suppressor cells in this model is to inhibit the replication of passively transferred immune T cells. The results obtained with the P815 mastocytoma are similar to those obtained previously with a chemically induced fibrosarcoma. They show, in addition, that passively transferred immune cells are capable of destroying already seeded metastases in T cell-deficient recipients.
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PMID:T cell-mediated immunosuppression as an obstacle to adoptive immunotherapy of the P815 mastocytoma and its metastases. 645 75

Systemic mastocytosis is a rare disorder that infrequently affects the GI tract. Bowel involvement in mastocytosis is characterized by thickened folds and small mucosal nodules, and there is an increased incidence of peptic ulcer disease and malabsorption. This paper describes a new case of mastocytosis that presented radiographically as 1.0-1.5 cm gastric and duodenal nodules. Some of the duodenal nodules were bull's-eye lesions with central collections of barium. Mastocytosis, along with primary neoplasms, aberrant pancreas, eosinophilic granuloma, and metastases should be included in the differential for bull's-eye lesions of the GI tract.
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PMID:Bull's-eye lesions: a new gastrointestinal presentation of mastocytosis. 672 33

The effects of the specific active cancer immunotherapy utilizing autologous tumor tissue particles polymerised with ethylchlorformiate, and used in combination with PPD tuberculin, were studied with respect to the growth of mastocytoma (P-815 X 2) in DBA/2 mice. As a control material, animals not immunised or immunised only with the nonspecific reticuloendothelial system stimulator, PPD tuberculin, were used. The frequency of the tumor metastases in the organs surveyed (lymph nodes, spleen, liver, kidney, lung and thymus) was lowest in mice having received the specific immunotherapy regimen. Similarly, the signs of tumor rejection by the host (tumor-associated fibrous scar, lymphocyte and plasma cell infiltration, and disappearance of the tumor tissue totally or subtotally) were found to be most pronounced in this series of mice. The findings were discussed against the background of the successful clinical trials made with this mode of specific cancer immunotherapy during the recent few years in patients whose neoplasia had escaped the reach of conventional cancer therapy. The findings were also discussed in the light of the mechanisms involved in cancer immunity in general, and a conclusion was drawn that this kind of specific active cancer immunotherapy seems to exert beneficial effects on the host's immune system, and thus seems to contribute to tumor rejection by the host.
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PMID:Experimental cancer immunotherapy in DBA/2 mouse-mastocytoma model utilizing autologous tumor tissue polymerised with ethylchlorformiate. 677 79


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