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

Contemporary clinical research is actively engaged at the conquest of residual neoplastic disease. The preliminary results of combined treatment modalities for osteogenic sarcoma, Ewing's sarcoma, rhabdomyosarcoma, breast cancer, malignant melanoma and Hodgkin's disease have shown a significant decrease in the incidence of distant metastases. In some neoplasias the decreased relapse rate was associated to improved survival. Since the problem of long-term carcinogenesis does exist, the use of prolonged adjuvant chemotherapy, at present moment, is best limited to patients at high risk of early relapse when treated only with local or local-regional modalities.
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PMID:Treatment of residual neoplastic disease in solid tumours. 106 17

Amplification and rearrangement of cellular proto-oncogenes are two of the several possible genetic alterations implicated in carcinogenesis and tumor progression. Although morphologically similar tumors may be heterogeneous at the level of the genome, some tumor types have shown relatively frequent and consistent abnormalities of specific oncogenes. In order to determine the frequency of oncogene amplification and rearrangement in several types of human sarcomas and to determine if histologically similar tumors have common genetic alterations, we analyzed 26 primary sarcomas by Southern hybridization. The oncogene probes utilized were N- and H-ras, sis, EGF-R (erb-B-1), neu (erb-B-2), fos, N- and c-myc, mos, and yes. The tumors studied included: five rhabdomyosarcomas (one alveolar, four embryonal), six malignant fibrous histiocytomas, six leiomyosarcomas, four liposarcomas, two Ewing's sarcomas, one osteosarcoma, and two fibrosarcomas. Oncogene abnormalities were identified in three tumors. One rhabdomyosarcoma showed 12-fold amplification and concurrent rearrangement of sis. This particular tumor also revealed rearrangement of H-ras and 15-fold amplification of c-myc. A second rhabdomyosarcoma revealed rearrangement of neu. A liposarcoma had a sis rearrangement. These findings suggest that many sarcomas show no common structural oncogene abnormalities. The presence of differing oncogene alterations within the rhabdomyosarcoma group indicates genetic heterogeneity among histologically similar sarcomas. The finding of a sis rearrangement in both a liposarcoma and a rhabdomyosarcoma, however, may suggest common oncogenesis among different tumor types.
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PMID:Genomic alterations in sarcomas: a histologic correlative study with use of oncogene panels. 149 46

Renal hyaline droplets were defined by histochemical and ultrastructural methods in eight female Wistar rats in a carcinogenesis bioassay. All eight rats had neoplasms of varied type (five histiocytic sarcoma, one phaeochromocytoma, one rhabdomyosarcoma, one leiomyosarcoma). Renal hyaline droplets were not seen in female rats without tumours and, although in this study, rats with tumours did not all have hyaline droplets, the source of the protein is likely to be the neoplasm. Presence of hyaline droplets may be useful as a confirmatory criterion in tumour diagnosis.
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PMID:Renal hyaline droplets in tumour-bearing female Wistar rats. 172 13

The effects of carcinogenic nickel [(Ni) CAS: 7440-02-0] and Ni compounds on the natural killer (NK) cell activity of rat peripheral blood mononuclear cells (PBMCs) were studied. Rhabdomyosarcomas were locally induced by one im injection of Ni or Ni subsulfide [(Ni3S2) CAS: 12035-72-2] dust in the hind leg of WAG rats. A weakly tumorigenic dose of 5 mg Ni3S2 (tumor incidence, 2%) induced a transient decrease of PBMC NK activity against YAC-1 cells in vitro (from the 17th to the 23d wk after Ni3S2 inoculation), which could be restored by in vivo injections of partially purified rat fibroblastic interferon (IFN). Injection of 20 mg Ni (tumor incidence, 47.5%) produced a long-lasting depression of NK cell activity (from the 8th to the 23d wk). In vivo chronic IFN treatment of the Ni-injected rats neither restored NK cell activity nor affected the tumor incidence. However, NK cells of Ni-treated animals responded normally to IFN in vitro. Prospective analysis of individual NK cell responses showed that a persistent depression of basal NK cell activity was restricted to rats that subsequently developed a tumor. In these animals the time between carcinogen treatment and clinical detection of the primary tumor was positively correlated with the mean level of NK cell activity (3-4 determinations/rat). Admixture of manganese to Ni inhibited the development of tumors and also prevented the depression of NK cell activity produced by Ni alone. Noncarcinogenic Ni oxide stimulated NK cell activity. These results point out the possible involvement of NK cells in resistance to Ni-induced carcinogenesis.
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PMID:Inhibition of rat natural killer cell function by carcinogenic nickel compounds: preventive action of manganese. 243 44

The cell line TE671 has been widely used as a model of human medulloblastoma. In the present study we have demonstrated that transfection of DNA from this cell line into NIH 3T3 cells reveals the presence of an activated N-ras gene. Using oligonucleotide probes we have shown that the N-ras gene is activated by a point mutation at the third base of codon 61 resulting in the substitution of histidine for glutamine in the p21 ras gene product. We noted that this relatively uncommon activating mutation is also present in the human rhabdomyosarcoma cell line RD. Based on this finding and on the observation that several of the phenotypic characteristics of TE671, such as the presence of muscle-type nicotinic acetylcholine receptors and the intermediate filament protein desmin, are suggestive of myoid origin we investigated the possible identity of these two cell lines. Cytogenetic analysis revealed the presence of marker chromosomes common to both TE671 and RD. DNA fingerprinting using both locus specific and multilocus core probes showed indistinguishable band patterns in the two cell lines. Taken together our data show that TE671 and RD are derivatives of the same cell line and we conclude that the properties of the TE671 line should be ascribed to rhabdomyosarcoma rather than medulloblastoma cells.
Carcinogenesis 1989 May
PMID:Characterization of the human cell line TE671. 265 Sep 8

Two dinitrofluoranthenes (DNFs) derived from 3-nitrofluoranthene were purified to over 99%, and tested for tumorigenicity in F344/DuCrj male rats. Rats were inoculated s.c. with 0.05 mg 3,7- or 3,9-DNF twice a week for 10 weeks. All 21 rats given 3,7-DNF and 10 of 11 rats (91%) given 3,9-DNF developed tumors at the injection site by 48 weeks after the first injection. Twenty of the 21 tumors induced by 3,7-DNF and seven of the 10 tumors induced by 3,9-DNF were classified as malignant fibrous histiocytoma, but one tumor in the 3,7-DNF-treated group and three tumors induced by 3,9-DNF showed typical features of rhabdomyosarcoma. The first tumors in 3,9-DNF-treated rats appeared on day 88 (on day average 117), 10 weeks earlier than in 3,7-DNF-treated ones (on day average 186).
Carcinogenesis 1987 Dec
PMID:Induction of subcutaneous tumors in rats by 3,7- and 3,9-dinitrofluoranthene. 282 85

N-homocysteine thiolactonyl retinamide was synthesized from trans retinoic acid and the free base of homocysteine thiolactone. In doses of 90-1800 mg/kg given i.p. in mixed lipid vehicle over nine weeks, the compound decreased to 60% of controls the number of lung tumors which was induced in A/J mice by 20 mg of ethyl carbamate. The highest dose also decreased the mean volume of lung tumors to 50% of controls, resulting in a total tumor volume of 30% of controls. Retinoic acid itself at 450 mg/kg was toxic, and no chemopreventive activity was observed. The free base and the lipophilic perchlorate salt of homocysteine thiolactone both increased the number of lung tumors to 114-117% of controls, indicating a co-carcinogenic effect. In C57BL/6N mice with transplanted MUO4 rhabdomyosarcoma, N-homocysteine thiolactonyl retinamide in a dose of 1000 mg/kg given over 11-21 days decreased the weight of the tumors to 30-70% of controls. These results show that N-homocysteine thiolactonyl retinamide has chemopreventive activity against chemical carcinogenesis and antineoplastic activity against a transplanted neoplasm.
Carcinogenesis 1987 Oct
PMID:Chemopreventive and antineoplastic activity of N-homocysteine thiolactonyl retinamide. 365 91

Seventeen nickel compounds were administered to Fischer-344 rats (N = 270) by intrarenal injection (7 mg Ni/rat); the compounds included nickel sulfides, selenides, arsenides, oxide, antimonide, telluride, titanate, ferronickel alloy and metallic nickel dust. Erythrocytosis, as defined by peak hematocrit values that averaged greater than 55% during 1-4 months post-injection, occurred in nine of 17 Ni-treated groups (NiS2, beta NiS, alpha Ni3S2, Ni4FeS4, NiSe, Ni3Se2, NiAsS, NiO, Ni dust). Renal cancers (N = 23) developed within 2 years post-injection in nine of 17 Ni-treated groups (NiS2, beta NiS, alpha Ni3S2, Ni4FeS4, NiSe, Ni3Se2, NiAsS, NiAs, NiFe alloy). The renal cancers included eight fibrosarcomas, five mesangial cell sarcomas, two renal cell carcinomas, two carcinosarcomas, two leiomyosarcomas, two undifferentiated sarcomas, one rhabdomyosarcoma and one nephroblastoma. No erythrocytosis or renal cancers occurred in control rats (N = 97) in three groups treated with the vehicles or metallic iron dust. Rank correlation (p less than 0.0001) was observed between the incidences of erythrocytosis and renal cancers in the 17 Ni-treated groups. Rank correlation (p less than 0.001) was observed between the present incidences of renal cancers and the sarcoma incidences previously reported following intramuscular administration of the 17 nickel compounds to Fischer-344 rats (14 mg Ni/rat). The incidences of renal cancer were not correlated with the mass-fractions of nickel in the 17 compounds, the dissolution half-times of the compounds in rat serum or renal cytosol, or the phagocytic indices of the compounds in rat peritoneal macrophages.
Carcinogenesis 1984 Nov
PMID:Association between erythrocytosis and renal cancers in rats following intrarenal injection of nickel compounds. 648 75

Metals have been evaluated as potential carcinogens by administering pure elements or compounds by a large variety of routes. These include mixing the agent in the food, dissolving the test compound in the drinking water, or administering the material by gavage. The respiratory tract routes tested include inhalation, intratracheal instillation, the direct injection of particulates into the pleural cavity, or the implantation of hooks by surgical intervention. The parenteral routes used were intravenous injection, intraperitoneal injection, subcutaneous implantation, as well as intrafemoral and intramuscular injection. This latter route is the most commonly used. There are major objections to the subcutaneous implantations route, and data generated from these experiments are difficult to interpret for the foreign body reaction may give rise also to fibrosarcomas. This then is a nonspecific reaction. Exotic routes tested include intrarenal, intratesticular, and intracranial injections. The endpoints of the carcinogenic reactions are, in the main, sarcomas of certain types with fibrosarcomas predominating. Rhabdomyosarcomas are the next most frequent cancer found, and squamous cell carcinoma may account for less than 2% of the cancers reported. Much more research is necessary to clarify the nature of metal carcinogenesis. Dose-response information is almost nonexistent; the divided dose problem has not been studied adequately, and very little information is available on interspecies reactions. More work is needed to help interpret the mechanism of action.
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PMID:Bioassay of metals for carcinogenesis: whole animals. 727 89

The s.c. infection of 10 mg benzo(a)pyrene dissolved in 1 ml tricaprylin induced in Wistar rats local malignant tumors, such as fibrosarcoma, rhabdomyosarcoma, and polymorph cell sarcoma. The growth of the tumors was relatively rapid, reaching weights of 140-155 g before rats died 142-168 days after the administration of the carcinogen. On the contrary, under the same experimental conditions, high doses of Vitamin C about 525 mg/day/rat administered orally in drinking water (total amount of Vitamin C 55 g/rat corresponding to 40% of their body weight ) inhibited to a great extent the benzo(a)pyrene carcinogenesis. Only one slowly growing rhabdomyosarcoma (13 g of weight) was developed showing characteristic damage of malignant cells and partial replacement of the neoplastic area with granuloma tissue. The significance ov Vitamin C for cancer prevention and treatment is discussed.
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PMID:Inhibition of benzo(a)pyrene carcinogenesis in rats with vitamin C. 740 Feb 11


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