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Query: UMLS:C1275122 (TEM)
 21,810 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There has been increasing interest regarding the use of Corynebacterium parvum (CP) with other modalities in the management of primary cancer. Due to the paucity of specific information available relative to CP toxicity, a Phase I study was carried out in patients with advanced disease. The purpose of the investigation was not to evaluate the effect of CP on tumor growth. from 273 injections of CP in 40 patients it was observed that following intravenous (i.v.) infusion of CP: a) a febrile response and chills of considerable severity occured in almost all patients and did not appreciably diminish in intensity following repetitive administrations; b) nausea, vomiting, headache, and confusion were not infrequent; c) a "flu-like" syndrome lasting 24 to 48 hours occurred following almost all courses of CP; d) blood pressure elevations occurred on occasion and were related to the severity of other-side-effects; hyper- or hypo- tension was not a problem; e) ther were no anaphalactic reactions. Pretreatment with a single administration of 100 mg of hydrocortisone prior to CP infusion markedly and in some instances dramatically diminished the toxicity and made acceptable the use of i.v. CP on an outpatient basis. The use of i.v. CP in patients with cerebral metasteses may be hazardous. Subcutaneously administered CP resulted in a significant number of undesirable local reactions. Evaluation of delayed cutaneous hypersensitivity response, immunoglobulins, complement, and E- and EAC-rosette-forming cells during CP administration failed to demonstrate significant change from injection values. Results were similar whether hydrocortisone pretreatment was or was not employed. From the standpoint of toxicity it now seems appropriate to use i.v. CP, particularly following pretreatment with hydrocortisone, in a controlled clinical trial to evaluate its therapeutic effectiveness in the management of primary cancer.
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PMID:Observations following Corynebacterium parvum administration to patients with advanced malignancy. a phase I study. 94 9

The effect of oxythiamine (400 mg/kg) on chromosomal structure of Ehrlich ascites carcinoma cells (EAC, hyperdiploid strain) and bone marrow cells was studied in intact AF mice. The influence of the antivitamin on the rate of tumor growth was investigated in tumor-bearing mice. Oxythiamine decreased transketolase activity in hepatocytes and tumoral cells and markedly inhibited tumor growth. Amount of chromosomes was unaltered both in tumor cells and in bone marrow cells, which could be manifested as increased content of cells with impairment of chromosomal set calculated per a cell. However, the oxythiamine-induced impairment of chromosomal integrity was less distinct as compared with the effect of such mutagens as urethane and cyclophosphamide; hence, the antivitamin might be used in the courses of combined chemotherapy.
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PMID:[The effect of oxythiamine on tumor growth and certain biochemical and genetic characteristics of normal and tumor cells]. 149 88

A new component of antitumor action TG has been isolated from the ethyl acetate extract of Tripterygium wilfordii (besides Triptolide, Tripdiolide and Triptonide). TG was shown in this study to have obvious antitumor effects. The average life span of H22, S180, EAC and breast carcinoma-bearing mice treated with TG ip x 2 days were 100% more than those of the control mice (P less than 0.01) TG was able to inhibit tumor growth of S37-bearing mice at the dose of 150 mg/kg per day, ig x 3, its inhibitory rate was 42% (P less than 0.01). TG could also inhibit squamous epithelial lung carcinoma induced by 3-methylcholanthrene. The inhibitory rate was 65.13% (P less than 0.05). TG had remarkable killing effect on human HL60 and Daudi cells and two direction effects on function M phi of mouse abdominal cavity in vitro.
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PMID:[Antitumor effect of Tripterygium wilfordii]. 150 34

The dynamic changes of cellular immune function and antitumor effect of GTE (green tea extract) in the BALB/c mice bearing EAC, HAC and S-180 tumor were investigated. Results showed that intraperitoneal injection GTE daily dose of 80mg/kg stimulate the proliferation of T-Lymphocyte S-180 tumor bearing mice, the 125-IudR incorporation value (cpm) of control group was 932 and that of GTE treated group increased to 2988. The Natural Killer cell's activity (cpm) of treated group was raised from 10.7% of control group to 41%. Daily dose 50mg/kg inhibited the EAC, HAC and the life span of GTE mice bearing EAC ascites tumor prolonged 128%. The GTE were effective on growth activity against mouse Ehrlich tumor at a dose of 500mg/kg by oral administration (P less than 0.05), the inhibition ratio being about 32%. The authors suggested the mechanism of antitumor effects of GTE possible included both cellular immune function and the inhibition of tumor growth.
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PMID:[Effect of Chinese tea extract on the immune function of mice bearing tumor and their antitumor activity]. 160 73

The cancer chemotherapeutic efficacy of 3,4-dihydroxybenzylamine (DHBA), a dopamine analog with reduced neurotoxic effects, was evaluated in strain A mice bearing transplantable Ehrlich's ascites carcinoma. The analog was administered intraperitoneally on day 1 post-transplantation at dose schedules of 50, 100 and 200 mg/kg/day for 7 consecutive days. The results demonstrated a significant inhibition of tumor growth and prolongation of the survival time of EAC tumor bearing mice following DHBA treatment. Diminished activity of the growth-related respiratory enzyme succinate dehydrogenase along with the stimulated activity of the lysosomal enzyme beta-glucuronidase in the DHBA-treated tumor cells indicated inhibition of tumor growth as well as active lysis of the tumor cells. Tumor inhibition was accompanied by marked improvements in hemoglobin concentration. RBC count and bone marrow cellularity. The results demonstrated that DHBA did not adversely affect hematological profile of the host while it inhibited the growth of Ehrlich's ascites carcinoma.
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PMID:Tumor inhibition and hematological improvements by dopamine analog 3,4-dihydroxybenzylamine in mice bearing transplantable carcinoma. 223

After intraperitoneal implantation into Swiss Silver rabbits, V2 rabbit carcinoma cells invade the mesentery where they form nodules of different size and texture: compact (less than 120 microns in diameter), loose (120-250 microns) and mixed (above 200 microns). Together with tumor development, certain changes take place in the loose connective tissue of the mesentery. Application of TEM, together with use of safranin O, has shown that, in areas free of tumor growth, collagen bundles become thick and heavy and proteoglycan density is increased. Concurrently, the number of fibrocytes, now transformed to fibroblasts, increases. Small, compact nodules are surrounded by a concentrically arranged extracellular matrix. Its overall density is similar to that of nodule-free areas. In the immediate vicinity of large, loose nodules, all constituents of the extracellular matrix disappear. Adjacent connective tissue is partly destroyed but still contains collagen fibers and proteoglycans. These findings suggest the following: The presence of V2 carcinoma cells induces marked alterations in the structured and non-structured components of the extracellular matrix. These changes are, at the same time, progressive and regressive and the occurrence of one or the other depends on local tumor progression. Progressive alterations may result from an increased activity of fibroblasts. Since degradative effects, on the other hand, are only seen in the immediate vicinity of larger tumor aggregates, it is assumed that a minimal number of tumor cells is essential for destruction of extracellular matrix.
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PMID:Morphology of peritumoral proteoglycan alterations in the rabbit mesentery invaded by V2 carcinoma cells. 649 Feb 6

This study describes ultrastructural alterations of the interstitial stroma in the rat bladder epithelium during N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN)-induced bladder carcinogenesis using scanning (SEM) and transmission (TEM) electron microscopy with NaOH treatment. The results obtained with SEM demonstrated the occurrence and development of stroma protrusions which exhibited pipe-like structures in the rat bladder epithelium following administration of BBN. Number and size of blood vessel sections also gradually increased both in the stroma and within the layer of the proliferated epithelial cells as examined by light microscopy (LM) and TEM. In this study stroma alterations were not only observed in malignant lesions of rat bladder, but hyperplastic lesions were also accompanied by stroma alterations. It is suggested that: (1) the interstitial stroma of the rat bladder epithelium may exhibit pathological changes in structure and these changes may correlate with the progression of epithelial cell proliferation following administration of BBN and (2) one of the most important alterations in the stroma is the occurrence of neovascularization, which may induce structural modification of the stroma in the processes of bladder tumor growth and development.
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PMID:Interstitial stroma and carcinogenesis: ultrastructural observations in the rat bladder treated with N-butyl-N-(4-hydroxybutyl)nitrosamine. 883 86

Ninhydrin (2,2-dihydroxy-1,3-indane dione) was evaluated for its antitumor and cytotoxic properties in Ehrlich ascites carcinoma cell (EAC Cell)-bearing mice. The rationale behind this study has been mainly the literature reports of its characteristic interference with DNA synthesis and calcium homeostasis. Antitumor activity was evaluated from the total count and viability of EAC cells in addition to their nucleic acid, protein, non-protein sulfhydryls (NP-SH) and malondialdehyde (MDA) contents. The EAC cell-bearing animals were also observed for the effect on their survival and body weight variations. In addition, the tumors grown at the site of injection were evaluated for histopathological changes. Ninhydrin treatments (5, 10 and 20 mg/kg/day) abate the increase in body weight and advanced the duration of survival in EAC cell-bearing mice. The results on histopathological investigations show retardation in tumor growth, decreased frequency of mitotic figures and hair follicles and an increased necrosis in the tumor by ninhydrin treatment. Our results on cytotoxicity, which demonstrated compression in the number of EAC cells and their viability substantiate these data. The results of biochemical studies on EAC cells exhibit a reduction in the levels of DNA, RNA, proteins and NP-SH with a subsequent increase in the concentrations of MDA after ninhydrin treatment. Inhibition in tumor growth was dose dependently significant with the same dose regimen. The observed cytotoxic and antitumor activity of ninhydrin was comparable to cyclophosphamide. The possible mode of action of ninhydrin-induced cytotoxic and antitumor activity appear to be due to its interference with mitochondrial function resulting in inhibition of DNA synthesis, an effect that is being investigated further.
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PMID:Studies on the cytotoxic, biochemical and anti-carcinogenic potentials of ninhydrin on Ehrlich ascites carcinoma cell-bearing Swiss albino mice. 1095 90

The involvement of PRL in regulating monocyte/macrophage functions is suggested by the presence of PRL-Rs in these cells. Here, we show that PRL, though it failed to activate mouse peritoneal resident macrophages (RMs), acted as a second signal and activated mouse peritoneal inflammatory macrophages (EMs) to a tumoricidal state. The cytotoxicity of mouse tumor-associated macrophages (TAMs) isolated at day 1 of tumor (Ehrlich ascites carcinoma, EAC) growth was enhanced by PRL. However, with progression of tumor growth, TAMs became nonresponsive to the hormone. PRL-induced killing of P815 target cells by EMs and TAMs was independent of TNF but correlated with the hormone-induced augmentation of NO2(-) and O2(-) release in these macrophages. Administration of PRL in vivo inhibited EAC growth and augmented NO2(-) release by TAMs. PRL synergized with the TH1 cytokine IFN-gamma, a known activator of macrophages, in inducing tumor killing and release of NO2(-) from EMs and TAMs. The hormone might activate macrophages at least partially, through the release of IFN-gamma as anti-IFN-gamma blocked IFN-gamma- as well as PRL-induced cytotoxicity in EMs. The TH2 cytokine IL-4 suppressed PRL-induced activation of macrophages. PRL induced release of IL-12 from EMs also, which suggested that the hormone might drive the TH1 response through IL-12. Our observations further suggest that PRL alone and in synergy with IFN-gamma, released through induction of IL-12, may generate tumoricidal macrophages and thus regulate the antitumor immune response of tumor hosts.
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PMID:Prolactin regulates antitumor immune response through induction of tumoricidal macrophages and release of IL-12. 1180 12

In this study the enzyme glutaminase, purified from the ascites fluid of ovarian cancer patients, was analysed for its antiangiogenic activity. Intraperitoneal administration of this enzyme reduces the number of tumor directed capillaries in solid and ascites tumor bearing Swiss mice induced by transplantation of Ehrlich ascites cells. The enzyme has a critical role in regulating the secretion of vascular endothelial growth factor (VEGF) from tumor cell and in turn tumor growth. Glutamine analogue like 6-diazo, 5- oxo L-norleucine (DON) is also found to be effective in regulating vascular endothelial growth factor (VEGF) secretion from tumor cells in vitro. Treatment with enzyme reduced serum VEGF levels of the tumor induced animals. In vitro VEGF production by EAC cells was reduced in a concentration dependent manner in presence of glutamine analogue.
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PMID:Modulation of tumor induced angiogenesis in Ehrlich ascites tumor. 1574 40


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