Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035412 (rhabdomyosarcoma)
 6,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rhabdomyosarcomas were induced in mice by intramuscular injections of crystalline nickel sulfide and 3-methylcholanthrene. At early passage, karyotypes were performed by G-banding for four nickel sulfide cell lines and for three 3-methylcholanthrene cell lines. Six cell lines were near-diploid and one nickel sulfide line was near-tetraploid. Three of the nickel sulfide cell lines were characterized by a rearranged marker chromosome which was present in a majority of the cells of each line. The rearrangements leading to the formation of marker chromosomes were different in each nickel sulfide cell line but involved chromosome 4 in two of the nickel sulfide cell lines. Extra copies of chromosome 15 were present in two nickel sulfide cell lines. Possible rearrangement and/or gene activation was examined for the c-mos oncogene on chromosome 4 and the c-myc oncogene on chromosome 15, but no alteration or activation was observed. None of the 3-methylcholanthrene cell lines contained rearranged marker chromosomes; however, one MCA cell line did contain large numbers of double minutes. In all cell lines, minichromosomes (small atypical acrocentric chromosomes) were observed that contained distinct centromeric regions but no other G-positive bands.
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PMID:Chromosomal changes in cell lines from mouse tumors induced by nickel sulfide and methylcholanthrene. 322 11

We have used 5'-deoxy-5'-S isobutyl-thioadenosine (SIBA), an analog of S-adenosylhomocysteine, alone or in association with a methionine-depleted diet in order to obtain an antitumoral effect in two different tumor models: a transplantable rat rhabdomyosarcoma (RMS-J1) induced by i.m. injection of nickel and the well-known Lewis lung carcinoma (3LL) of C57BL/6 mice. Since SIBA has been reported to inhibit the methyl group transfer from methionine to S-adenosylhomocysteine, among other activities, its association with a reduction of methyl donors, achieved by methionine depletion of the diet (in vivo) or the culture medium (in vitro), should logically lead to an additive effect. In vitro, 3LL and RMS-J1 were sensitive to the cytotoxic effect of SIBA and were methionine-dependent for their proliferation. Fibroblast proliferation was not affected by these two treatments alone or in association. In vivo, either SIBA treatment or a low methionine diet led to a significant decrease in the metastatic character of these two tumors; however, local tumor growth was not significantly affected. The median number of 3LL metastases counted in the lungs was reduced from 100 to 18 by SIBA treatment, and to 27 by the low methionine diet. No additive effect could be detected when the treatments were given simultaneously. RMS-J1-bearing rats treated with SIBA and fed a low Met diet underwent primary tumor excision. The median numbers of lung metastatic nodules were 27, 26, 14 and 8 for the control, SIBA-treated rats, methionine-deprived rats and rats receiving the combined therapy. Expressed as percentages 20 per cent were cured, 23 per cent showed a low number of lung metastases (P less than 10), whereas all the rats in the control group developed more than 10 pulmonary nodules. No cytotoxic effect could be observed on the treated rats. The role of SIBA and methionine depletion, as agents interfering with transmethylation processes, in regard to the control of tumor development, namely metastatic invasiveness, is discussed.
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PMID:Association of SIBA treatment and a Met-depleted diet inhibits in vitro growth and in vivo metastatic spread of experimental tumor cell lines. 325 80

A series of 11 cloned cell lines derived from a primary, nickel-induced rat rhabdomyosarcoma was evaluated for their metastatic capacity (number of lung colonies following i.v. injection) and attachment kinetics to confluent pig endothelial cell monolayers grown in vitro. The morphology of the adhering cells was also studied by optical and scanning electron microscopy. Cells from all lines tested began to attach to the endothelial monolayers within 15 min of incubation at 37 degrees C, with 64% to 93% of the cells adhering after 2 h. Attachment rates at 30 min ranged from 29 to 48% for four lines classed as "weakly adhesive" (attachment, less than 50%) and from 53 to 78% for seven lines classed as "highly adhesive" (attachment, greater than 50%). Four clones of five displaying low lung-colonizing capacities also showed low attachment rates to endothelial monolayers in vitro. All of six highly colonizing lines studied had high attachment rates. A degree of positive correlation was observed between the amount of cell surface fibronectin as evaluated by immunofluorescence and the early phase attachment rates (and lung-colonizing capabilities) of the different cloned cell lines. Early (15 min) attachment of tumor cells to isolated extracellular matrix preparations proceeded at higher rates than to endothelial monolayers, and previously detected differences between high- and low-colonizing clones were less evident with these matrix substrates. Our results suggest possible interrelationships between specific cell adhesion properties and the metastatic potential of blood-borne tumor cells.
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PMID:Differential adhesiveness of rhabdomyosarcoma-derived cloned metastatic cell lines to vascular endothelial monolayers. 370 93

The effect of chronic uremia on the development of subcutaneously injected malignant tumoral cells was evaluated in 213 male Wistar AG rats made chronically uremic by simultaneous right nephrectomy and partial ligation of the left renal artery. The tumoral cells injected were stemming from a parental rhabdomyosarcoma (9-4/0) induced by intramuscular injection of 20 mg of colloidal nickel suspended in oil to a male Wistar rat. 54 sham-operated rats and 43 nonoperated animals served as control-groups. Renal function and tumoral growth were checked weekly up to the 60th postoperative day, at which time the surviving rats were sacrificed and submitted to autopsy. At day 15 after cell grafting, a tumoral lump could be felt by finger touch in 68% of the uremic rats, but in only 11% of the sham-operated and 14% of the nonoperated controls (p less than 0.0001). Throughout the study, the tumoral lumps which developed in the uremic animals were of significantly larger size than in the nonuremic controls. Pulmonary tumoral metastases were evidenced at autopsy in 95% of the uremic rats, but in only 50% of the sham-operated and in 54% of the nonoperated controls (p less than 0.005). These results indicate an apparently accelerating and amplifying effect of uremia on the development of a malignant tumor in the rat, for which a decrease in cell-mediated immunity associated with the uremic state still remains a questionable hypothesis.
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PMID:Influence of the uremic state on the development of malignancy. An experimental study in the rat. 382 34

Glycosaminoglycans of cultured nickel-induced rat rhabdomyosarcoma cell lines with different metastatic potentials, grown in the presence or in the absence of hydrocortisone and of growth factor (EDF and EDGF) were investigated comparatively. The newly formed [35S]sulphate and [3H]glucosamine-labelled glycosaminoglycans were analysed in the extra-, peri- and intra-cellular compartments of the following cell lines: the strongly metastatic and colonizing 9-4/0 parental line, the very weakly metastatic and weakly colonizing subline 8 and the very weakly metastatic but colonizing subline 13a2. The cell surface of the weakly metastatic 8 and 13a2 lines was richer at least 5 and 2 times respectively in sulphated glycosaminoglycan label than the surface of the strongly metastatic 9-4/0 parental line. Hydrocortisone provoked an approximately four-fold increase in the label of the sulphated cell surface glycosaminoglycans of the 9-4/0 line. The pattern of the labelled cell surface glycosaminoglycans of these cells become similar to that of cells from the very weakly invading subline 8. Hydrocortisone induced only minor changes in the distribution of the glycosaminoglycans in the 8 and 13a2 lines, and at the same time, their proliferation rate and differentiation state was only slightly affected by this drug. Conversely to hydrocortisone, EGF increases the proliferation of the 9-4/0 line and also increases the label in sulphated cell surface glycosaminoglycans. This increase is about 50 per cent of that obtained by hydrocortisone. Thus, the accumulation of the glycosaminoglycan label on the cell surface is not directly related to the cell growth in the case of these cells. The results suggest that sulphated cell surface glycosaminoglycans, especially chondroitin sulphate, are involved in the inhibition of metastasis formation of the rhabdomyosarcoma cell lines studied.
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PMID:Modulation of proteoglycan metabolism by hydrocortisone and by growth factors in rhabdomyosarcoma cell lines of different metastatic potentials. 387 51

Putative human rhabdomyosarcoma (RMS) has been divided into two groups according to desmin content. Twenty-five tumors with histologic features consistent with but not necessarily sufficient to prove a diagnosis of RMS were desmin-positive. More than 95% of the tumor cells were desmin-positive, suggesting a muscle origin and supporting the diagnosis of RMS. Nine tumors for which the preferred first histologic diagnosis was also RMS were desmin-negative. Reexamination of the original histologic slides together with results from intermediate filament typing resulted in a diagnosis other than RMS for all tumors in this second group, and in several instances other tests were used to prove the correctness of the final diagnosis. The results on human material were extended to a rat model system in which RMS was induced by nickel sulfide. Again, all 24 tumors tested were desmin-positive. Vimentin was coexpressed in a varying percentage of tumor cells in RMS of human and rat origin. The results show that desmin is an excellent marker for rhabdomyosarcoma, yielding few if any false-positive or false-negative results in frozen or alcohol-fixed material.
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PMID:Desmin is a specific marker for rhabdomyosarcomas of human and rat origin. 388 Oct 39

Some nickel compounds (Ni3S2,Ni) induce tumours in muscle, while others have no effect (NiO). It has been suggested that the carcinogenicity of nickel is related to its penetrating power (phagocytosis) in transformed cells. The penetration of various nickel salts into cultured rhabdomyosarcoma cells (RhC) was studied. Electron microscopy and microanalysis were used to study the ultrastructure and intracellular localization of nickel in ultra-thin sections. Nickel subsulfide (Ni3S2) and nickel oxide (NiO) penetrated into cells and were concentrated in vacuoles, exhibiting a particular affinity for membrane structure. They subsequently appeared to be eliminated in the extracellular medium. Colloidal nickel and iron carbonyl, on the other hand, did not penetrate these cells. Various tumoral and normal cells were compared for their ability to phagocytose Ni3S2; it was found that these compounds penetrated only RhC and macrophages. In vivo studies have demonstrated the various carcinogenic properties of nickel and two of its salts. Comparison with in vitro results suggests that the phagocytosis of nickel compounds is not directly related to eventual induction of a tumour. No nuclear localization could be detected, but a mechanism for concentration and elimination of these compounds, and especially for rhabdomyosarcoma tumour cells, was suggested.
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PMID:In vitro electron microprobe of carcinogenic nickel compound interaction with tumor cells. 399 86

The effect of various nickel salts on cultured rhabdomyosarcoma cells was studied. Certain of these compounds, e.g., nickel subsulfide (Ni3S2) and nickel itself, induce tumours in muscle, while others have no effect, e.g., nickel monoxide (NiO). It has been suggested that the carcinogenicity of nickel is related to its penetrating power (phagocytosis) in transformed cells. We have used electron microscopy and microanalysis to study the ultrastructure and intracellular localization of nickel in ultra-thin sections. Nickel subsulfide and nickel monoxide penetrate into cells and are concentrated in vacuoles, exhibiting a particular affinity for membrane structures. They subsequently appear to be eliminated in the extracellular medium. Colloidal nickel and iron carbonyl, on the other hand, do not penetrate cells. Various tumoral and normal cell lines were compared for their ability to phagocytose nickel subsulfide and it was found that the compound penetrated only macrophages and impregnated the membranes of polynuclear cells. These results suggest that the phagocytosis of nickel compounds is not directly related to the eventual induction of a tumour. No nuclear localization could be detected, but we did demonstrate a mechanism for the concentration and elimination of these compounds in certain tumour cells.
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PMID:Electron microprobe in vitro study of interaction of carcinogenic nickel compounds with tumour cells. 609 27

Rat, mouse, pig and chicken alphafoetoproteins (AFP), rat serum albumin and egg albumin, or their fluoresceinated conjugates were added to cultures of several cloned cell lines isolated from a nickel-induced rat rhabdomyosarcoma. The intracellular uptake of assayed proteins was revealed by the indirect immunoperoxidase technique and/or by direct fluorescence microscopy. All the clones examined bound AFP, and all but one internalized the protein. The protein localized in the membrane and the cytoplasm, as well as along straight processes interconnecting cells. Nuclei were always AFP negative. The protein uptake of fluoresceinated conjugates of AFP and serumalbumin was already visible 15 min after incubation and progressed with time to reach a plateau 4-5 h later. Ultrastructural radioautographs of cells incubated with [3H]-AFP (rat) showed protein accumulation in several organelles and particularly in lipid droplets. Parallel to these observations, the intracellular presence of AFP within myofibrillar structures was demonstrated in tongue sections of rat foetuses and neonates. The results presented here provide experimental evidence of the reappearance in cloned cell lines derived from a primary rhabdomyosarcoma of a property pertaining to foetal striated muscle.
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PMID:Alphafoetoprotein uptake by cloned cell lines derived from a nickel-induced rat rhabdomyosarcoma. 619 37

Studies were undertaken to ascertain the possible antitumorigenic effectiveness of sodium diethyldithiocarbamate (dithiocarb) on the development of tumors in rats following the muscular implantations of nickel subsulfide (Ni3S2). These tumors have histologic characteristics which suggest origin from striated muscle and have been classified as rhabdomyosarcoma. Most of the tumors metastasized. In two separate studies over a period of two years, a total of 100 four-month old Fischer rats received muscular implantations of Ni3S2. Of this total, 50 rats (25 males and 25 females) were treated with dithiocarb for a period of four to six weeks. Seventy-eight percent of the untreated rats developed sarcomas as compared to 32 percent of the treated rats. Analyses of the data revealed a striking difference in the sex responsiveness to dithiocarb. Of the 25 female rats with Ni3S2 implantations and treated with dithiocarb, only 12 percent developed sarcomas; of the male rats similarly treated, 52 percent developed sarcomas. The difference in sex response is statistically significant (p = 0.005). Therapeutic implications are suggested.
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PMID:Sodium diethyldithiocarbamate administration in nickel-induced malignant tumors. 619 53


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