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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of Vibrio cholerae enterotoxin on steroidogenesis and on formation of adenosine 3':5'-cyclic phosphate (cyclic AMP) in two adrenal tumor cell lines were compared. Steroidogenesis was half-maximal at concentrations of 1 ng of cholera toxin/ml in the mutant OS-3 cells and 3 ng of cholera toxin/ml in the parent Y-1 cells. At the end of an 8-hr incubation, toxin-induced formation of cyclic AMP in the mutant cell line was reduced by 90%. A molar ratio of GM1 ganglioside (galactosyl-N-acetylgalactosaminyl [sialosyl] lactosyl ceramide; GGnSLC) to cholera toxin of 3:1 caused half-maximal inhibition of steroidogenesis in both cell lines. When equine antiserum to choleragenoid was added to adrenal cells 15 min after cholera toxin, there was marked inhibition of cyclic AMP formation and of steroidogenesis. Pretreatment of Y-1 cells with adrenocorticotropin rendered them unresponsive to hormonal induction of cyclic AMP formation, but these cells had an unimpaired response to cholera toxin. These studies, utilizing two adrenal cell lines, suggest important differences between the mode of action of cholera toxin and that of adrenocorticotropin in cultured adrenal tumor cells.
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PMID:Mode of action of Vibrio cholerae enterotoxin in cultured adrenal tumor cells. 17 80

Treatment of cultured human HO melanoma cells with the mouse skin tumor promoter phorbol-12-myristate-13-acetate (PMA) at 5 x 10(-10) to 5 x 10(-7) M resulted in a dose-related inhibition of growth and a stimulation of differentiated functions. These included melanin synthesis and formation of dendrite-like structures. Higher doses of phorbol dibutyrate, a less potent tumor promoter, were required to produce an effect comparable to that of PMA for dendrite induction. Phorbol and two other phorbol esters, which lack tumor-promoting activity, were either inactive or elicited a poor response. In addition to morphological changes, treatment with PMA altered glucosamine incorporation into membrane gangliosides. After PMA treatment, glucosamine incorporation increased 8- to 10-fold in the GM3 ganglioside and decreased 2-fold in the GM1 ganglioside, as compared to phorbol or untreated control. Inhibition of cell growth and stimulation of melanin synthesis were also observed after treatment of the HO cells with dimethyl sulfoxide. Unlike the tumor-promoting agents, dimethyl sulfoxide did not induce the formation of dendrite-like structures in the cells. These findings indicate that HO melanoma cells can be stimulated into terminally differentiated cells after treatment with tumor-promoting agents such as phorbol diesters.
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PMID:Stimulation of differentiated functions in human melanoma cells by tumor-promoting agents and dimethyl sulfoxide. 44 63

The heat-labile enterotoxins of Vibrio cholerae and Escherichia coli induce morphologic changes and steroidogenesis in clonal lines of adrenal tumor cells in tissue culture; these effects are preventable by prior incubation of either toxin with GM1 ganglioside (galactosyl-N-acetylgalactosaminyl [sialosyl] lactosyl ceramide; GGnSLC) but are not preventable by prior incubation of adrenal cells with choleragenoid. Choleragenoid, however, is capable of interfering with the ability of GM1 ganglioside to neutralize the effects of either toxin. These results suggest that the GM1 ganglioside may not be the true receptor for the toxins on adrenal cells, but that it is acting as a pseudoreceptor. The ability of a subunit (A) of the cholera enterotoxin molecule to induce in adrenal cells morphologic changes and steroidogenesis similar to those effects inducible by the whole toxin indicates the possibility that separate receptor sites on these adrenal cells may exist for the binding and active fragments of the molecule.
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PMID:Interactions of choleragenoid and GM1 ganglioside with enterotoxins of Vibrio cholerae and Escherichia coli in cultured adrenal cells. 76 85

A partially purified enterotoxin was obtained from the growth medium of Escherichia coli strain 711 (P307), a derivative of E. coli K-12, by ultrafiltration, precipitation with ammonium sulfate, molecular sieving, and anion exchange column chromatography. The active moiety, which is heat-labile, behaved like a protein particle of 180,000 to 200,000 daltons during molecular sieving and ultracentrifugation. During polyacrylamide gel electrophoresis in sodium dodecyl sulfate (SDS-PAGE), it dissociated into two subunits with apparent molecular weights of 68,000 to 70,000 and 14,000 to 15,000. SDS-PAGE after heating in SDS changed the larger subunit to an apparent molecular weight of about 40,000; the smaller subunit did not change. The intact particle induced rounding of the cells in Y-1 mouse adrenal tumor cells used for assay. The detergent-dissociated molecules were not active. Proteolysis of the purified toxin by tolylsulfonyl phenylalanyl chloromethyl ketone-trypsin appeared to enhance its activity. The addition of serum to the assay medium resulted in partial depression of the activity. Activity was also abolished by preincubation of the toxin with either a rabbit antiserum to it or solutions containing GM1 ganglioside. The length of time needed to evoke a response in the assay system by fractions from different stages in the purification of the enterotoxin was a useful parameter in the evaluation of specific activity.
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PMID:Partial purification and characterization of a heat-labile enterotoxin of Escherichia coli. 78 81

The effects of three different ganglioside preparations on cholera enterotoxin (CT) and heat-labile Escherichia coli enterotoxin (ECT)-induced steroidogenesis in Y1 and OS3 adrenal tumor cells in tissue culture were examined. Only with GM1 ganglioside was any inhibition of the toxins' effects noted. Concentrations of the crude ECT preparation that gave similar morphogenic and steroidogenic effects as CT were inhibited by the same amount or less of GM1 as that required to inhibit the effects of CT. The results of competition experiments also demonstrated that previous incubation of GM1 with one toxin could inhibit the ganglioside's ability to inactivate the other toxin. These findings indicate that at least for Y1 and OS3 adrenal tumor cells, GM1 may resemble or be the receptor for both CT and ECT.
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PMID:Inhibition of the steroidogenic effects of cholera and heat-labile Escherichia coli enterotoxins by GM1 ganglioside: evidence for a similar receptor site for the two toxins. 109 65

A 61-year-old male visited us with chief complaints of macroscopic hematuria and bladder irritation symptoms. Cystoscope, U/S, MRI, and CT showed an extensive non-papillary, wide-based tumor centering around the anterior wall of the bladder. Transabdominal U/S-guided full-thickness biopsy indicated a pT3a (Biopsy) primary small cell carcinoma of the bladder containing neuroendocrine granules. Immunohistochemical studies revealed Fuc GM1, an antigen related to small cell carcinoma of the lung. Neoadjuvant therapy consisted of preoperative irradiation at 50 Gy and intra-arterial infusion chemotherapy with CDDP and THP. Since a follow-up full thickness biopsy indicated pT0 (Biopsy), total cystectomy was performed. Examination of the resected specimen also indicated pathological CR.
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PMID:[Small cell carcinoma of the bladder. Small cell lung cancer-associated ganglioside (Fuc GM1) expression]. 133 26

With the aid of specific monoclonal antibodies, tumor tissues from 68 patients with lung cancer were examined for their expression of two small cell lung carcinoma (SCLC) antigens, Fuc-GM1 (fucosyl GM1; IV2FucII3NeuAc GgOse4) and neural-cell adhesion molecule (NCAM), and two broader tumor antigens, carcinoembryonic antigen (CEA) and carbohydrate cancer-associated antigen CA 50. Expression of Fuc-GM1 was seen in 75% and NCAM in 78% of the SCLC specimens, but also in 12 and 20% of non-SCLC. Either or both of these antigens were expressed in more than 90% of SCLC and in 25% of non-SCLC. CEA was found in more than 80% of SCLC and non-SCLC. Expression of CA 50 was seen in 65-68% of non-SCLC and SCLC, showing preference for SCLC and lung adenocarcinoma. In SCLC, cellular expression of Fuc-GM1 was generally seen together with NCAM and CA 50, but rarely with CEA. There was considerable inter- and intratumor heterogeneity in the expression of all four antigens. The results suggest that CEA is the antigen of choice for the detection of lung cancer regardless of histotype. In combined analysis of CEA, CA 50, Fuc-GM1 and NCAM, two patterns of antigen expression were recognized that appear to discriminate between SCLC and non-SCLC tumors, respectively. A considerable fraction of SCLC and non-SCLC tumors, however, exhibited similar patterns of antigen expression. The biological and clinical significance of these observations remains to be investigated.
Tumour Biol 1992
PMID:Coexpression of ganglioside antigen Fuc-GM1, neural-cell adhesion molecule, carcinoembryonic antigen, and carbohydrate tumor-associated antigen CA 50 in lung cancer. 133 98

The aim of this study was to investigate the influence of oral administration of OK-432 on the tumor growth of tumor-bearing mice. In addition, the changing pattern of the splenic lymphocyte subsets of tumor-bearing mice was evaluated by flow cytometry. OK-432 at a dose of 0.1, 1 or 10 KE was administered orally every 3 days or every other day for 30 days to subcutaneously Meth A tumor-inoculated mice. The tumor growth was significantly inhibited in the 1 KE every 3 days group, in the 1 KE every other day group and in the 10 KE every 3 days group. In the 10 KE every other day group, OK-432 inhibited the tumor growth on days 10 and 20, while the agent did not show a marked inhibitory effect on day 30. The percentages of splenic L3T4-positive cells and splenic asialo GM1-positive cells were significantly increased in the 1 KE every other day group, while the Lyt2+/Thy1.2+ ratio was decreased. On the other hand, in the 10 KE every other day group, OK-432 showed no effect on the percentages of splenic L3T4-positive cells and Lyt2+/Thy1.2+ ratio on days 20 and 30. Our results suggest that the antitumor effect of oral administration of OK-432 may be correlated with the changing pattern of L3T4-positive cells and Lyt2+/Thy1.2+ ratio.
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PMID:The changing pattern of the splenic lymphocyte subsets in tumor-bearing mice after oral treatment with OK-432. 135 56

MY-1, which consists of DNA and RNA extracted and purified from Mycobacterium bovis strain BCG, causes the regression of various experimental syngeneic tumors when injected intratumorally. In order to identify the host cells involved in the antitumor mechanism(s) of MY-1, we examined Meth A tumors inoculated intradermally to BALB/c mice, which were given multiple injections of MY-1 following tumor inoculation. Histological and immunohistochemical examinations were performed at several time points. On day 4 after inoculation, the MY-1-treated tumors were heavily infiltrated with a heterogeneous population of mononuclear cells with low density nuclei. The MY-1-injected tumors contained asialo-GM1-positive cells and Mac-1-positive cells, which indicated that the infiltrating mononuclear cells were natural killer cells and macrophages. On day 14 after inoculation, the tumors were infiltrated with a large number of L3T4-positive cells and fewer Lyt-2-positive cells, both of which were more abundant in the MY-1-treated tumors than in the control tumors. The observed sequence of host cell infiltration corresponded well with our previous studies which have indicated that the antitumor mechanism of MY-1 is divided into two phases, i.e. the early phase when natural killer cells and macrophages inhibit tumor growth, and the late phase when L3T4-positive cells act to induce tumor regression via a delayed-type hypersensitivity against tumor cells.
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PMID:Changes of host cell infiltration into Meth A fibrosarcoma tumor during the course of regression induced by injections of a BCG nucleic acid fraction. 138 Sep 50

Using light and electron microscopy, we investigated the in vivo distribution of liposomes sterically stabilized by specific lipids which prolong their circulation in blood. Tissue distribution of sterically stabilized liposomes composed of distearoyl phosphatidylcholine:cholesterol:monosialoganglioside GM1 (10:5:1)-encapsulated 67Ga-Desferal indicates that more than 30% of liposomes still remain in the blood at 24 h after tail vein injection. Moreover, such liposomes accumulated in tumors (C-26 colon carcinoma cells implanted s.c.), reaching almost the same level of uptake as liver (approximately 20% injected dose/g tissue). The microscopic localization of liposomes labeled with encapsulated colloidal gold or rhodamine-labeled dextran coincided well with the tissue distribution. To evaluate circulation parameters, two sizes of gold-containing egg phosphatidylcholine:cholesterol:distearoyl phosphatidylethanolamine (derivatized at its amino position with a 1900 molecular weight segment of polyethylene glycol) (10:5:0.8) liposomes were injected. The plasma was examined by electron microscopy of negative-stained preparations at 0.5, 4, and 24 h after liposome injection. It was found that the ratio of small (less than 100 nm diameter) to large (greater than 100 nm) liposomes increased with time, indicating a much faster clearance of the larger liposomes. To detect the localization of liposomes in various tissues, appropriate samples were fixed 24 h after the injection of gold-containing liposomes (between 80 and 100 nm in diameter) composed of egg phosphatidylcholine:cholesterol:monosialoganglioside GM1 (10:5:1) or egg phosphatidylcholine:cholesterol:derivatized distearoyl phosphatidylethanolamine. The tissues examined for this study included normal liver, bone marrow, and implanted neoplasms. Silver-enhanced colloidal gold was found predominantly within Kupffer cells in the normal liver and within macrophages in the bone marrow. Rarely were any silver-enhanced gold particles detected in hepatocytes. In all preparations, electron microscopy revealed the presence of gold in endosomes and lysosomes of fixed sinusoidal lining macrophages in the liver and bone marrow. Peripheral to the implanted tumors, silver enhancement revealed gold in small blood vessels and focally beyond the vessel boundaries in extracellular spaces around tumor cells. Gold particles were not observed within the tumor cell cytoplasm. At the tumor border, nonenhanced gold was occasionally seen by electron microscopy in cells of the mononuclear phagocyte system. We obtained the same localization pattern as with silver enhancement by using an alternative aqueous content marker, rhodamine B isothiocyanate-dextran. We conclude that liposomes of specific composition, which have the ability to remain in circulation with a half-life of 12-24 h, are also able to transverse the endothelium of small blood vessels, including those in tumors, and extravasate into extracellular spaces.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Microscopic localization of sterically stabilized liposomes in colon carcinoma-bearing mice. 139 21


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