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At least 1,225 records · Page 68Linked to original sources
PubMed1982

Characterization of anti-inflammatory factors produced by murine tumor cells in culture.

P-815 mastocytoma cells from DBA/2 mice and a 3-methylcholanthrene-induced fibrosarcoma from C57BL/6 mice produced in culture at least two soluble anti-inflammatory factors that inhibited macrophage accumulation in vivo when the factors were injected sc into syngeneic recipients. One factor was a low-molecular-weight peptide (less than 1,000), as judged by ultrafiltration, failure of extraction by lipid solvents, nonsusceptibility to DNase or RNase, partial inactivation by trypsin, and complete inactivation by carboxypeptidase B. The second anti-inflammatory factor had a molecular weight between 30,000 and 100,000 and was also not extractable with lipid solvents. Production of anti-inflammatory factors by P-815 mastocytoma cells was inhibited by cycloheximide and cell irradiation but not by colchicine pretreatment of the cells, suggesting a relationship to protein synthesis rather than cell growth. Soluble anti-inflammatory factors depressed granulocyte as well as macrophage responses. Anti-inflammatory factors were not found in supernatants from cultures of splenocytes, peritoneal exudate cells, or murine lung fibroblasts.

Animals↗
PubMed1995

Effect of endothelin-1 and sarafotoxin S6c on blood flow in a rat tumor.

The modification of tumor blood flow resulting from administration of endothelin-1 (ET-1) and sarafotoxin S6c (SX6c) was examined in female CBH rats. Blood flow in subcutaneous HSN tumors and normal tissues was measured by tissue uptake of 125I-labeled iodoantipyrine ([125I])IAP). A 75% increase in tumor blood flow was observed after 1 nM/kg ET-1, contrasting with flow in normal tissue, which was unaffected or reduced. The exception to this was the brain, in which blood flow was increased by 30%, resulting from a rise in mean arterial blood pressure (MABP) and the absence of vasoconstriction. Paradoxically, a significant drop in the tumor vascular resistance was observed after 1 nM/kg ET-1, whereas in all other tissues the vascular resistance was significantly increased. Vascular responses to SX6c differed from those observed with ET-1. At 1 nM/kg SX6c, blood flow in the tumor was increased to 175% of the control as a result of the increase in MABP, which was similar to ET-1. However, unlike ET-1, there was no associated vasodilatation. Vascular resistance was increased in all normal tissues with 1 nM/kg SX6c, corresponding to decreases in blood flow in the contralateral skin, skeletal muscle, and small intestine. This study therefore demonstrates that the vascular responses to ET-1 and SX6c are unique in the HSN tumor compared to normal tissues. This atypical response of the tumor vasculature may therefore be exploitable to improve the delivery of blood-borne anti-cancer agents in therapy.

Animals↗
PubMed1983

Hyperimmune human ABO blood-typing sera: reactivity with murine laminin and cytotoxicity for metastatic murine tumour cells.

Commercially prepared ABO blood-typing antisera have been tested for their ability to bind to murine laminin and their cytotoxic effects upon high and low metastatic variants of a murine fibrosarcoma. Previous studies have shown that alpha-D-galactopyranosyl end-groups comprise the major antigenic determinants on type B erythrocytes and that these same end-groups are present on murine laminin purified from the EHS sarcoma and on a laminin-like glycoprotein on the surface of the high, but not low, metastatic fibrosarcoma cells. In the present study we found that all sera containing anti-B activity were cytotoxic to the high, but not the low, metastatic cells and that all of these sera reacted strongly against immobilized murine laminin in an enzyme-linked immunosorbent assay. Sera lacking anti-B activity, i.e. anti-A antisera, were much less cytotoxic to either cell line and three of the four anti-A sera did not bind to murine laminin. The laminin reactivity and cytotoxic effect of the anti-B sera were specifically abrogated by preincubation of the sera with water-soluble blood group B substance or with murine laminin but not with water-soluble blood group A substance.

ABO Blood-Group System↗
PubMed1994

MDM2 gene amplification and transcript levels in human sarcomas: relationship to TP53 gene status.

BACKGROUND: Alterations of the TP53 tumor suppressor gene appear to be implicated in the tumorigenesis and progression of several types of human cancer, including different histologic subtypes of sarcomas. The MDM2 (murine double minute-2) gene encodes a nuclear phosphoprotein that may interact with both mutant and wild-type p53 proteins, thereby inhibiting p53-mediated transactivation in a dose-dependent manner. Recently it has been suggested that mdm2 and p53 proteins are components of an autoregulatory loop in which the MDM2 gene is transactivated by p53. PURPOSE: Our purpose was to examine the frequency of MDM2 amplifications in larger panels of sarcomas, determine if the mRNA level could be elevated in tumors without concomitant gene amplification, and relate MDM2 findings to the TP53 status of the tumors. METHODS: Sarcoma tissue of different histologic subtypes was obtained from 68 patients at the time of surgery and from 26 human xenografts in nude mice. In addition, two human sarcoma cell lines (OSA and U2OS) were studied. Genomic DNA from tumor tissue, in vitro cell lines, and peripheral blood cells were isolated by Southern-blot analysis methods to determine MDM2 gene amplification. Tumor DNA was analyzed for possible TP53 gene mutations in exons 5, 7, and 8 by constant denaturing gel electrophoresis. To determine the MDM2 and TP53 mRNA levels, Northern-blot analysis was performed. RESULTS: Amplification of the MDM2 gene was detected in 10 tumors (10.3%). Whereas MDM2 amplification and/or over-expression were found only in two (U2OS and OSA cell lines) of 18 osteosarcomas, one of 20 malignant fibrous histiocytomas (MFHs), and in none of 14 leiomyosarcomas, such alterations were observed in two of two fibrosarcomas, three of six malignant schwannomas, three of 19 liposarcomas, and in the one hemangiopericytoma examined. MDM2 overexpression was found in all nine examined cases with and in three tumors without amplification. TP53 mutations were detected in 12 cases (five osteosarcomas, four MFHs, and three leiomyosarcomas), of which none showed amplification, but one had increased levels of MDM2 mRNA. None of the fibrosarcomas, malignant schwannomas, and liposarcomas examined had mutated TP53. The six sarcomas that showed high TP53 mRNA expression in the absence of gene mutation also had elevated levels of MDM2 mRNA. CONCLUSIONS: The present data provide further indications that increased MDM2 expression level, caused by gene amplification or altered regulation of transcription, is involved in tumor progression of some, but not all, sarcoma subtypes.

Animals↗
PubMed2000

Serological analysis of BALB/C methylcholanthrene sarcoma Meth A by SEREX: identification of a cancer/testis antigen.

Antigens of BALB/c methylcholanthrene-induced fibrosarcoma Meth A recognized by the host humoral immune response were investigated by serological analysis of antigens by recombinant expression cloning (SEREX). Immunoscreening a cDNA library from Meth A (Kgamma) cells (Meth A retrovirally transfected with murine IFN-gamma cDNA) with sera from BALB/c mice growing parental Meth A transplants identified 10 antigens. One of them, OY-MS-4, showed characteristics of a cancer/testis (CT) antigen. Nucleotide sequence analysis revealed that OY-MS-4 was identical to a mouse placenta and embryonic expression gene (pem) known to be selectively expressed during embryogenesis and in transformed cell lines. In adult mice, expression of OY-MS-4 was restricted to testis and placenta. Four of 6 methylcholanthrene-induced fibrosarcomas in BALB/c mice showed strong expression of OY-MS-4. In 6 T-cell leukemias, only a dimethylbenzanthracene-induced leukemia, EL4 (C57BL), showed strong expression. Two other tumors, A20.2J and P815, induced by ethylnitrosourea and methylcholanthrene, respectively, also strongly expressed OY-MS-4. The other 9 gene products identified in Meth A by SEREX were expressed in all 15 tumors tested and in a range of normal tissues. Sequence analysis of cDNA inserts coding for the SEREX-defined antigens showed no evidence of mutation. Despite the expression of OY-MS-1-10 antigens in methylcholanthrene sarcomas other than Meth A, no antibody was detected in the sera of mice bearing these other sarcomas. The basis for the unique immunogenicity of OY-MS-1-10 presented by Meth A, but not by other syngeneic tumors expressing these gene products, is unknown.

Amino Acid Sequence↗
PubMed1994

[Increased incidence of sarcoma in patients treated for seminoma].

In a nationwide cancer registry analysis of second primary malignancies in 6187 men with testicular cancer in the period 1943-1987, 13 sarcomas were found, yielding a 4-fold increase of the relative risk (RR). The majority of sarcomas occurred in men with seminoma, and the increased incidence was seen irrespective of time since the diagnosis of testicular cancer. The interval between the testicular cancer and the sarcoma varied from five to 34 years. After investigation of the hospital records and re-examination of the histological specimens, three patients were excluded. In spite of this, the RR was still considerably increased (at least three-fold). Seven of the 10 sarcomas were found to be located within the field of the radiation treatment administered and three at the periphery. The histological type of sarcomas varied, with leiomyosarcoma as the most frequent (three cases), followed by malignant fibrous histiocytoma (two cases) and fibrosarcoma (two cases). Since none of these patients had received chemotherapy and did not harbour sarcomatous components within the primary testis cancer, the sarcomas were probably caused by the radiation treatment. The absolute number of these secondary sarcomas is low, but the risk of developing such neoplasms and other malignancies should, even so, be kept in mind in the follow-up of testicular cancer patients.

Adolescent↗