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)

We have previously reported that phytic acid (inositol hexaphosphate or InsP6), a natural constituent of cereal diet, when administered in drinking water exerts a consistent antitumor effect on experimental colon cancer in vivo. The objective of this study was to determine whether InsP6 has similar anti-neoplastic effect on other tumor models, such as murine fibrosarcoma. We report that intraperitoneal injection of InsP6 reduces growth of subcutaneously transplanted fibrosarcoma (FSA-1) in mice, prolongs survival of tumor-bearing mice and reduces the number of pulmonary metastases. Since InsP6 is a common constituent of our diet and has very little or no toxic effects, in addition to being chemopreventive, it could have potential use in therapy of cancer as well.
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PMID:Antitumor activity of phytic acid (inositol hexaphosphate) in murine transplanted and metastatic fibrosarcoma, a pilot study. 151 13

Two years after an orthotopic liver transplantation, a multifocal hepatic tumor with lymphonodular metastases, identified as a fibrosarcoma, developed in a 4-year-old girl being treated with cyclosporine. On a needle biopsy sample, genetic typing of the HLA-DR group revealed that tumoral cells were from the recipient.
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PMID:Hepatic localization of a fibrosarcoma in a child with a liver transplant. 153 93

Various forms of stress have been shown to alter natural killer (NK) cell activity and tumorigenesis; however, few studies have measured these two variables simultaneously. Isolation of mice was utilized as a model of stress by which to study NK cell activity and pulmonary metastatic response following a tumor challenge. Male C3H mice were group or individually housed for 3 weeks, after which CIRAS 3 fibrosarcoma tumor cells or the tumor vehicle was injected intravenously (tail vein), NK cell activity, pulmonary metastasis, and plasma corticosterone were measured 1, 7, and 21 days following tumor cell inoculation. Individually housed mice, irrespective of tumor or vehicle condition, had a higher NK response on Day 1 relative to group-housed animals (P less than 0.001). By Day 21, tumor condition, rather than housing, was the major significant factor affecting NK activity (P less than 0.001). Nevertheless, individually housed, tumor-injected mice still had higher NK activity compared with the other treatment groups on Day 21. No effect of housing condition was present for the incidence of pulmonary metastases or frequency of metastases in affected animals. Plasma corticosterone levels generally increased over the study period, with no housing or injection effects at Days 1 and 7. Individually housed, vehicle-injected mice had higher corticosterone levels at Day 21 (P less than 0.01). These data suggest that in response to housing condition, NK cell activity differs in tumor-bearing mice and vehicle controls. Furthermore, CIRAS 3 pulmonary tumor formation is not affected by differences in NK activity consequent to housing condition. Plasma corticosterone does not appear to be a major in vivo regulator of NK activity in this experimental tumor system. Finally, the interpretation of housing effects on NK activity and plasma corticosterone levels depends on the temporal window in which sampling occurs.
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PMID:Effect of differential housing in mice on natural killer cell activity, tumor growth, and plasma corticosterone. 153 37

The effect of combined hyperthermia and intratumoral administration of OK-432 (Picibanil) on the development of spontaneous lung metastases was studied. The spontaneous non-immunogenic fibrosarcoma, FSa-II, transplanted into the right foot of C3Hf/Sed mice, was used throughout. Hyperthermia was given locally by immersing the animal foot in a water bath set at 44.0 degrees C for 30 min. OK-432 in the dose of 2.5 KE was injected into the tumour 3 h before hyperthermia. This treatment has been shown to strongly inhibit local tumour growth. Sham hyperthermia, i.e. restraining the mice in holders, as well as local injection of saline solution, increased metastases incidence. The high incidence of metastases following combined sham hyperthermia and saline injection was substantially reduced by intratumoral administration of OK-432 given alone or combined with hyperthermia.
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PMID:Effect of thermoimmunotherapy with OK-432 on the development of spontaneous lung metastases in mice. 157 11

Tumor cells must attach themselves to basement membranes, through which they degrade and migrate, in order to spread to distant sites. If vascular endothelial cells are damaged by pretreatment with anticancer drugs and the subendothelial basement membranes are exposed, the attachment of malignant cells to basement membranes and subsequent metastasis formation in some tissues may be enhanced. In this study, the pretreatment of endothelial cell monolayers and mice with cyclophosphamide (CPA) was respectively shown to promote the adhesion of HT1080 human fibrosarcoma cells to endothelial cell monolayers in vitro and lung colonization in vivo. YIGSR, a synthetic laminin pentapeptide, inhibited the enhancement of lung colonization by CPA when it was co-injected intravenously with tumor cells. This inhibitory effect of YIGSR may be due to a reduction in the adhesion of HT1080 cells to injured blood vessel walls since YIGSR inhibited both the adhesion of HT1080 cells to CPA-treated endothelial cell monolayers and the invasion through basement membranes in vitro.
Clin Exp Metastasis 1992 May
PMID:YIGSR, a synthetic laminin peptide, inhibits the enhancement by cyclophosphamide of experimental lung metastasis of human fibrosarcoma cells. 158 88

Tricyclic antidepressants, such as amitriptyline (Elavil), and the nontricyclic agent, fluoxetine (Prozac), bind to growth-regulatory intracellular histamine receptors, associated with anti-estrogen binding sites in microsomes and nuclei. The prototype anti-estrogen binding site/intracellular histamine receptor ligand, N,N-diethyl-2-[4-(phenylmethyl)phenoxy]ethanamine HCl, inhibits normal cell proliferation in vitro but stimulates tumor growth in vivo. Because of their structural similarity to N,N-diethyl-2-[4-(phenylmethyl)phenoxy]ethanamine HCl, we carried out studies to determine whether amitriptyline and fluoxetine stimulate tumor growth and/or development in rodents at concentrations relevant to the treatment of human depression (equivalent human dose range, approximately 100-150 mg/day for amitriptyline and approximately 20-80 mg/day for fluoxetine). All experiments were performed blinded. In studies of growth stimulation of transplantable syngeneic tumors, groups of mice were inoculated s.c. with C-3 fibrosarcoma cells or given i.v. or s.c. injections of B16f10 melanoma cells, followed 24 h later by daily i.p. injections of saline, amitriptyline, or fluoxetine. Tumor latency (fibrosarcoma), aggregate tumor weight (s.c. injected melanoma), or time to death from pulmonary metastasis (i.v. injected melanoma) was determined; drug-induced stimulation of DNA synthesis in C-3 fibrosarcoma cells in vitro was correlated with tumor growth acceleration in vivo. In a mammary carcinogenesis model, the effects of chronic saline, amitriptyline, or fluoxetine administration on the rate and frequency of development of mammary tumors in rats fed dimethylbenzanthracene (DMBA) were compared. Eight of 20 amitriptyline- or fluoxetine-treated mice developed fibrosarcoma tumors by day 5, as compared to none of 20 saline controls (P less than 0.002). Similarly, 20 of 21 DMBA-treated rats receiving the antidepressant drugs developed 33 mammary tumors by week 15 as compared to 5 tumors in 4 of 7 DMBA-treated rats receiving saline (P less than 0.001). For both models, tumor latency decreased 30-40% and, in the DMBA model, tumor frequency increased greater than 2-fold in the antidepressant-treated rats as compared to controls. Stimulation of fibrosarcoma growth in vivo correlated with a corresponding bell-shaped drug-induced increase in DNA synthesis in vitro. While the median time to death from pulmonary metastases did not differ among groups given i.v. injections of melanoma cells, a significant (P less than 0.01) stimulation of growth of s.c. injected melanoma was observed in mice receiving the antidepressants.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Stimulation of malignant growth in rodents by antidepressant drugs at clinically relevant doses. 161 49

The injection of B16F10 melanoma cells with recombinant human tumor necrosis factor alpha (TNF-alpha) into the tail vein of C57BL/6 mice resulted in 2- to 25-fold more metastatic foci in the lungs than the injection of tumor cells alone. Clearly, TNF-alpha significantly enhanced experimental tumor metastasis. Furthermore, it enhanced the metastasis of Lewis lung carcinoma cells. In contrast, a mutein of TNF-alpha, designated as F4236, having the cell-adhesive sequence (Tyr-Ile-Gly-Ser-Arg) at the N-terminus of the TNF molecule did not enhance metastasis, but rather exhibited similar antitumor activity to wild-type TNF-alpha in fibrosarcoma-bearing mice.
Clin Exp Metastasis 1992 Jul
PMID:A YIGSR-containing novel mutein without the detrimental effect of human TNF-alpha of enhancing experimental pulmonary metastasis. 161 34

Interleukin 2 (IL-2) mediates the regression of metastatic cancer but clinical use has been limited due to associated toxicities. Tumor necrosis factor (TNF) is an important mediator of IL-2 toxicity and may have a limited role in IL-2 antitumor efficacy. Because pentoxifylline (PTXF) inhibits TNF production, we hypothesized that PTXF would ameliorate IL-2 toxicity without compromising antitumor efficacy. Four groups of female C57BL/6 mice with pulmonary metastases from a 3-methylcholanthrene-induced fibrosarcoma (MCA-105) and four groups of nontumored mice were treated every 6 h for 4 d by intraperitoneal injections of either IL-2 alone, IL-2 and PTXF, PTXF alone, or equal volumes of saline. Upon completion of therapy, we found that PTXF suppressed many of the IL-2-induced effects including TNF production, lymphocytic infiltration of multiple organs, multiple organ edema, hepatic dysfunction, leukopenia, and thrombocytopenia. Tumor response was determined 21 d after cessation of therapy by quantitating the number and surface area of pulmonary metastases. PTXF preserved antitumor efficacy while reducing the morbidity and mortality caused by IL-2 treatment. These data strongly support the use of PTXF in extending the therapeutic index of IL-2 in the treatment of cancer.
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PMID:Pentoxifylline inhibits interleukin-2-induced toxicity in C57BL/6 mice but preserves antitumor efficacy. 164 28

We have examined the binding and functional activity of monoclonal antibody (MAb) SG-1 that was raised by immunization against embryonal carcinoma cells and screened using KHT fibrosarcoma cells. Quantitative absorption, binding and in situ immunochemical staining assays indicate that the MAb SG-1-defined epitopes are expressed preferentially by the highly metastatic KHT35-L1 cells relative to the weakly metastatic, parental KHTp cells. Furthermore, there was a significant correlation (p less than 0.05) between the expression of MAb SG-1-defined antigen on the cells, following trypsin treatment, and their metastatic ability. Binding of MAb SG-1 to antigen was inhibited by specific sulfated polysaccharides including cerebroside sulfate (brain sulfatide), fucoidan, and dextran sulfate (500 kD) but not by heparan, chondroitin, keratan or dextran (5 kD) sulfates. Initial characterization of antigen from KHT cells indicates that the epitope of MAb SG-1 is defined by sulfated glycoconjugates containing galactose and sulfate but not N-acetylglucosamine. In the total lipid extracts of KHT35-L1 cells the antigen was detected in the delipidated protein fraction as well as in the chloroform/methanol fraction. These results suggest that the sulfated glycoconjugate determinants identified by MAb SG-1 may be relevant to the metastatic process of KHT fibrosarcoma cells.
Clin Exp Metastasis
PMID:Sulfated glycoconjugate determinants recognized by monoclonal antibody, SG-1, correlate with the experimental metastatic ability of KHT fibrosarcoma cells. 169 55

We report 38 cases of inflammatory fibrosarcoma occurring in 23 females and 15 males, 2 months to 74 years of age (median, 8.5 years; mean, 15 years) with symptoms of abdominal pain (17 cases), anemia (21 cases), fever (14 cases), mass (16 cases), and gastrointestinal obstruction (7 cases). Primary tumor sites included mesentery and retroperitoneum (31 cases), omentum (two cases), mediastinum (two cases), liver (one case), diaphragm (one case), and abdominal wall (one case). Sizes ranged from 2.4 cm to 20 cm (mean, 9.6 cm). Follow-up data in 27 cases revealed local recurrences in 10 patients, with multiple local recurrences in three and histologically proven distant metastases to lung (two cases) and brain (one case). Five patients died from their disease (median, 20 months). All tumors, including metastases, consisted of fibroblasts, myofibroblasts, and plasma cells, with variable degrees of fibrosis and calcification. Immunostains indicate myofibroblastic differentiation; 18 of 20 (90%) stained for actin, 15 of 18 (83%) for vimentin, and 10 of 13 (77%) for keratin (primarily in a submesothelial location). Ultrastructural studies also disclosed myofibroblastic features. The locally aggressive, recurrent nature of these neoplasms, as well as the occurrence of metastases and tumor deaths, indicate that they are potentially malignant neoplasms that we believe are better classified as inflammatory fibrosarcomas, not as cellular inflammatory pseudotumors.
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PMID:Inflammatory fibrosarcoma of the mesentery and retroperitoneum. A tumor closely simulating inflammatory pseudotumor. 174 82


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