Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of the i.v. administration of endotoxin (6.25-50 micrograms/mouse on day 13 after tumor implantation) in mice treated orally with lysozyme hydrochloride (100 mg/kg on days 5-12 from tumor implantation) were examined using Lewis lung carcinoma in the C57Bl mouse and MCa mammary carcinoma of CBA mice. On primary tumor growth, endotoxin alone causes a dose-dependent and statistically significant reduction with a nadir on day +2 from endotoxin treatment. Combined with lysozyme, endotoxin causes an effect independent of the dose used, corresponding to the effect caused by endotoxin alone at the dose of 25 micrograms/mouse. No tumor regression was recorded in any of the treated groups. Endotoxin is virtually devoid of effects at the metastatic level. In the same conditions, lysozyme causes a reduction of primary tumor growth and a more pronounced inhibition of lung metastasis formation as expected from its already reported effects. The antitumor activity of endotoxin, unlike lysozyme, can be ascribed to tumor hemorrhagic necrosis due to tumor necrosis factor (TNF) production, as determined in tumor homogenates. Endotoxin does not increase the antitumor effects in mice treated with lysozyme, as expected from the data obtained with the more immunogenic SA1 sarcoma, although lysozyme increased the mitogenic response to ConA of ex vivo isolated splenocytes, in vitro cultured in the presence of IL-2.
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PMID:Effects of endotoxin in mice bearing solid metastasizing tumors and treated with lysozyme hydrochloride. 140 79

The oral administration of hen egg-white lysozyme to mice bearing B16 melanoma significantly reduces the formation of spontaneous lung metastases and, when combined with surgical removal of the primary tumor, prolongs the survival of the treated hosts. The antimetastatic effect, comparable with that found in the Lewis lung carcinoma and MCa mammary carcinoma systems, is independent of the direct interaction of lysozyme with tumor cells and tends to indicate the suggested intervention of an indirect action mediated by the induction of host responses.
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PMID:Reduction of B16 melanoma metastases by oral administration of egg-white lysozyme. 259 13

Dendritic cells (DC) in 121 colorectal adenocarcinomas were investigated immunohistochemically, using anti-S-100 protein antibody. S-100(+)DC were recognized among the malignant cells and/or around the tumor and differed in distribution either from lysozyme-positive macrophages or from neuron-specific enolase-positive neural tissue. Patients with many S-100(+)DC (more than 30 cells per 10 high-power fields) in the tumor survived longer than did those with few such cells (less than 30 cells), most often with no metastases (P less than 0.001). The grade of S-100(+)DC infiltration was related to both density of lymphocytic infiltration in the primary tumor and the degree of paracortical hyperplasia in the regional lymph nodes (P less than 0.05). Dendritic cells, therefore, as antigen-presenting cells, conceivably mediate cell immunity in a tumor with lymphoid infiltration and in the regional lymph nodes. The number of S-100(+) DC in the primary colorectal carcinomas represents one aspect of such a series of antitumor immunoreaction, in vivo.
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PMID:S-100 protein-positive dendritic cells in colorectal adenocarcinomas. Distribution and relation to the clinical prognosis. 291 28

The host-mediated effects of lysozyme on primary tumor growth and on the formation of pulmonary metastases were investigated in mice bearing the MCa mammary carcinoma. The oral administration of lysozyme to CBA mice for 7 consecutive days before i.v. inoculation of MCa mammary carcinoma cells causes a significant reduction in the formation of lung tumors. The growth of s.c. tumors and the development of lung metastases is also significantly lowered in mice inoculated with tumor cells previously kept at 37 degrees C for 30 min in the presence of peritoneal resident cells or whole plasma samples obtained from normal mice treated with 25-100 mg/kg/day lysozyme for 7 consecutive days. The lysozyme concentration in plasma samples of the treated mice remains undetectable even at daily dosages up to 400 mg/kg, ruling out the hypothesis of a direct effect of the ingested lysozyme. These data seem to suggest a role for host immune reactivity in the antineoplastic effects of lysozyme. The results are consistent with previously reported data and further stress the interesting antitumor properties of the oral administration of lysozyme in mice bearing solid metastasizing tumors.
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PMID:Evidence for host-mediated antitumor effects of lysozyme in mice bearing the MCa mammary carcinoma. 320 16

The pharmacological activity of orally administered lysozyme, for the control of the growth of solid tumor metastases, was examined in mice bearing Lewis lung carcinoma. Groups of at least 10 tumor-bearing mice, fed daily for three consecutive weeks from subcutaneous tumor implantation with lysozyme, prepared from hen egg-white, had a pronounced reduction of the weight of their metastatic tumor to 25-50 per cent of controls within a wide range of doses (25-200 mg/kg/day). The antimetastatic effect was not related to the length of the treatment schedule employed; a short course of 7 days, given on days 1-7 after tumor implantation, proved equally active. The inhibition of the formation of lung metastases, in mice treated with lysozyme prior to tumor inoculation, lasts for at least 2 weeks after discontinuation of treatment, indicating that the antimetastatic activity observed is not associated with cytotoxic activity of the lysozyme, and is probably mediated by the elicitation of host responses. The examination of the therapeutic potential of the antimetastatic action of lysozyme supplied through the usual diet indicates that this treatment synergizes with the antitumor effects of cisplatin, given to mice after surgical removal of the primary tumor, causing a statistically significant prolongation of the survival time of the animals as compared with chemotherapy alone.
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PMID:Antimetastatic action of orally administered lysozyme in mice bearing Lewis lung carcinoma. 334 67

The differential effects of the i.v. administration of egg-white lysozyme on primary tumor growth and on the formation of spontaneous and artificial lung metastases have been determined in mice bearing two rodent metastasizing tumors: Lewis lung carcinoma and MCa mammary carcinoma. The depression of metastasis formation was particularly pronounced at 50 and 100 mg/kg/day given on days 1,5,10,15 after tumor transplantation, causing a correspondent prolongation of the life-span of the animals carrying artificial induced lung metastases. Contact between tumor cells and egg-white lysozyme seems at least partially responsible for the observed antitumor effects, although no direct cytotoxicity for tumor cells has been detected yet.
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PMID:Antineoplastic effects of egg-white lysozyme in mice bearing solid metastasizing tumors. 370 53

Few published reports describe patients with giant cell fibroblastoma, a rare, benign soft-tissue tumor that recurs locally and predominantly arises in children. A 4-year-old boy underwent surgery for removal of a giant cell fibroblastoma in the paranasal region, an unusual site. Six months after excision the tumor recurred locally. Immunohistochemical examination of the primary tumor and recurrence revealed vimentin positive staining in the cytoplasm of all the cells. The multinucleated giant cells and the flat cells bordering the vessel-like spaces were negative for Factor VIII-related antigen, S-100 protein, actin and desmin. Some histiocytes stained positively for alpha-1-antitrypsin, alpha-1-antichymotrypsin, antimacrophage and lysozyme antibodies. These immunoreactions indicate that giant cell fibroblastomas have a fibrohistiocytic origin.
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PMID:Paranasal giant cell fibroblastoma: case report and immunohistochemical findings. 804 95

The oral administration of 100 mg/Kg/day of hen egg-white lysozyme (Lysozyme) for 8 consecutive days to mice bearing advanced MCa mammary carcinomas and treated with 5-fluorouracil (5-FU) increases the efficacy of 5-FU on primary tumor growth and on lung metastasis formation and particularly on the postsurgical survival time. These effects are accompanied by the correction of the reduced in vitro response to ConA of lymphocytes obtained from the spleen of the treated mice. In vitro, lysozyme is capable of inducing proliferative activity in a population of blast cells, obtained by a mixed population of mononuclear cells harvested from the spleen of healthy mice, and of evoking a marked proliferative effect to IL-2 in a condition in which, in lysozyme untreated lymphocytes, IL-2 is completely uneffective. These data stress the effects of lysozyme on host immunity following oral administration and moreover indicate the beneficial role of this peptide in conditions in which the increase of host responses can significantly contribute to the success of the treatment.
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PMID:Lysozyme stimulates lymphocyte response to ConA and IL-2 and potentiates 5-fluorouracil action on advanced carcinomas. 857 73

Human acinic cell adenocarcinoma cell (HACC) line was established from the pleural effusion that contains metastatic tumor cells of acinic cell adenocarcinoma of papillary and microcystic type originating from the parotid gland. The HACC cells grew in an adherent monolayer with a doubling time of 66 h. Implanted tumor of SCID mice revealed similar histological findings to that of the primary tumor. The HACC cells produced mucin and expressed epithelial markers as well as alpha1-antitrypsin and lysozyme, whereas salivary peptide P-C was expressed in cultured HACC cells but not in the primary and implanted HACC cell tumors. S-100 protein was also expressed in both the primary tumor and HACC cell line. Neither amplification of common oncogenes nor expression of p53 was observed. The receptor for epidermal growth factor (EGF) was expressed, indicating EGF and transforming growth factor-alpha (TGF-alpha) enhanced the growth of the HACC line. Unexpectedly, tumor necrosis factor-a (TNF-alpha) also enhanced the growth of the HACC line significantly. However, there was no evidence of autocrine growth using these growth factors. In contrast, TGF-beta1 inhibited the growth of the HACC cell line through apoptosis. The HACC cell line has features similar to both acinar and intercalated ductal cells of the salivary gland. Epidermal growth factor, TGF-alpha and TNF-alpha are potential growth factors for the HACC cell line. The HACC cell line may be a good model for studying the biological behavior of salivary gland neoplasms.
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PMID:Characterization of a newly established human acinic cell adenocarcinoma cell line (HACC) originating from the salivary gland: morphological features and role of various growth factors on the growth of the HACC cell line. 978 63

A 70-year-old Japanese man presented to our hospital with a 1-month history of progressive general fatigue and anorexia. A physical examination revealed severe anemic condition, mild persistent splenomegaly, and no palpable surface lymph nodes. He had pleural effusion and ascites, though no malignant cells were detected in the effusion. He eventually died without any diagnosis of his disease. Immunohistochemical staining of his tumor after autopsy showed atypical cells that were negative for epithelial membrane antigen (EMA), keratin (AE1/3), keratin-20, vimentin, factor VIII, leukocyte common antigen (LCA/T200; CD45), myeloperoxidase (MPO), terminal deoxynucleotidyl transferase (TdT), lysozyme, CD1a, CD3, CD4, CD10, CD15, CD20 (L26), CD21, CD23, CD34, CD43, CD56, CD68, CD79a, CD138, and EBER-1 in situ. Only a few scattered cells expressed CD30, but they showed no staining for anaplastic large-cell lymphoma kinase (ALK). A few scattered cells expressed S-100 antigen and the majority of cells dominantly expressed dendritic cell-associated antigens (CD35, FDC, Ki-M1p). In conclusion, we found this unknown primary tumor to be consistent with a follicular dendritic cell tumor with anaplastic features.
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PMID:Follicular dendritic cell tumor as an unknown primary tumor. 1738 Apr 43


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