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)

N,N-Dimethylformamide treatment of cell cultures established from a transplantable murine rhabdomyosarcoma-induced morphological differentiation and a marked reduction in the tumorigenicity of the sarcoma cells. Fourteen of 17 CE/J mice receiving injections of inducer-treated cells did not develop tumors after 6 months, whereas all 21 mice receiving inocula of untreated sarcoma cells died of disease between 11 and 31 days. The drug-treated cells did not grow in soft agar; untreated tumor cells grew in the semisolid medium. The untreated tumor cells showed a reduced serum requirement and had a higher saturation density compared to drug-treated cells. Thus the reduction in tumorigenicity of N,N-dimethylformamide-treated cells correlated with certain in vitro growth properties that are more characteristic of normal, mesenchymally derived cells than of sarcoma cells.
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PMID:N,N-Dimethylformamide-induced morphological differentiation and reduction of tumorigenicity in cultured mouse rhabdomyosarcoma cells. 19 20

Differentiation-inducing ability of gamma-radiation, N,N-dimethylformamide and their combination has been tested on human rhabdomyosarcoma RMZ-RC2 clone cells. Ionising radiation at 2-5 Gy doses induced a more differentiated morphology, with the appearance of an increased proportion of multinuclear myotube-like cells, and a significant increase in myosin-positive and multinuclear cells. Radiation appeared to act by inducing de novo differentiated elements. N,N-dimethylformamide was able to induce an increased myosin expression, but did not affect multinuclear cell proportion. The combined treatment (ionising radiation and N,N-dimethylformamide) resulted in an additive increase in the proportion of myosin-positive cells, approaching 25-35%, but de novo differentiated elements were not increased above the levels obtained with irradiation alone.
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PMID:Induction of myogenic differentiation in human rhabdomyosarcoma cells by ionising radiation, N,N-dimethylformamide and their combination. 156 60

Three clonal subpopulations (A, B, C) isolated from the same rhabdomyosarcoma of the rat were tested and compared for their susceptibility to differentiation induction using retinoic acid (RA), dimethylformamide (DMF), and N-monomethylformamide (NMF). These subpopulations differ in that a block to spontaneous differentiation is imposed at different stages which are characteristic for each subpopulation. Whereas tumor cell proliferation was significantly inhibited (P less than 0.001) in all three subpopulations, the effects of RA, DMF, and NMF on tumor cell differentiation were strikingly heterogeneous. The response was most marked in subpopulation C, as evidenced by a significant increase in the number of terminally differentiated myotube-like giant cells (P less than 0.001) and in biochemical differentiation, as indicated by the creatine kinase activity (P less than 0.05). Between 5% (DMF and NMF) and 30% (RA) of the mononuclear cells in subpopulation C exhibited thick and thin myofilaments, which were never observed in the mononuclear cells of the control. In contrast, subpopulation A and B responded to RA, DMF, and NMF quite heterogeneously with an increase in biochemical differentiation, whereas terminally differentiated myotube-like giant cells were never observed. These results demonstrate that the therapeutic potential of differentiation induction in malignant tumors may be impaired by tumor heterogeneity.
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PMID:Heterogeneous response to differentiation induction in different clonal subpopulations of a rat rhabdomyosarcoma cell line (BA-HAN-1). 258 54

The aim of this investigation is to report the synthesis and fundamental photochemical properties of naphthalocyanines with potential interest for photodynamic therapy (PDT), as well as their pharmacokinetics and phototherapeutic effects in a tumor model. Four zinc naphthalocyanines (ZnNc), unsubstituted ZnNc 1, tetraacetylamido-substituted ZnNc 2, tetraamino-substituted ZnNc 3 and tetramethoxy-substituted ZnNc 4 absorbing around 760-770 nm, were synthesized. The dye-sensitized photo-oxidation of 1,3-diphenylisobenzofuran via 1O2 was studied in dimethylsulfoxide (DMSO). Quantum yields for this photoreaction are 0.135-0.164 and are relatively independent of the kind of substituent. In addition, the photoinduced electron transfer studied in N,N-dimethylformamide-water in the presence of methylviologen and mercaptoethanol is only slightly influenced by the kind of substituent. The pharmacokinetic properties of ZnNc 1 in hamsters bearing a transplanted rhabdomyosarcoma were studied using dipalmitoylphosphatidylcholine liposomes. Experimental PDT of rhabdomyosarcoma was carried out using liposome-delivered ZnNc 1-4. The phototherapeutic effect was evaluated by tumor photonecrosis, the mean tumor diameter during the observation period and the percentage of cured animals. The best effect was found after PDT with ZnNc 2 (50% of the treated animals were cured). A slightly lower effect was observed after application of ZnNc 4 (40% cured animals). No effect at all was noted after PDT with ZnNc 3 and a very low efficiency was found after treatment with ZnNc 1 as photosensitizer. Obviously, the photodynamic effect depends on the biological characteristics as well as on the nature of the substituents.
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PMID:Liposome-delivered Zn(II)-2,3-naphthalocyanines as potential sensitizers for PDT: synthesis, photochemical, pharmacokinetic and phototherapeutic studies. 830 12

The effects of dexamethasone, a synthetic glucocorticoid, and of N,N-dimethylformamide on in vitro growth and differentiation and on proto-oncogene expression of human rhabdomyosarcoma cells were studied. RD/18 clone cells (derived from the embryonal rhabdomyosarcoma cell line RD) treated with 100 nM dexamethasone showed an almost complete block of differentiation: about 5% myosin-positive cells were observed after 2 weeks of culture in dexamethasone-supplemented differentiation medium, compared to 20% of untreated cultures. Dexamethasone also induced a 20-30% growth inhibition and a more flattened morphology. The treatment with N,N-dimethylformamide induced a significantly increased proportion of myosin-positive cells (reaching about 30%) and a 40% growth inhibition. Induction of differentiation inversely correlated with the levels of c-myc proto-oncogene expression: after a 2 week culture dexamethasone-treated cells showed the highest c-myc expression and N,N-dimethylformamide-treated cells the lowest. Culture conditions per se down-modulated c-erbB1 and up-regulated c-jun expression, with no relationship to the differentiation pattern. Other proto-oncogenes were not expressed (c-sis, N-myc, c-mos, c-myb) or were not modulated (c-fos, c-raf). Therefore dexamethasone and N,N-dimethylformamide, both causing a decreased growth rate, showed opposing actions on myogenic differentiation and on c-myc proto-oncogene expression of human rhabdomyosarcoma cells.
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PMID:Uncoupling of growth inhibition and differentiation in dexamethasone-treated human rhabdomyosarcoma cells. 847 24