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)

Basic fibroblast growth factor (bFGF) is a mitogen that is thought to play a important role in myocyte growth. In previous work, we found the increase of immunoreactivity of bFGF in cardiac myocyte of young SHR and pressure over loaded rat heart, and it suggested that endogenous bFGF which contained high molecular form of bFGF contributes to myocardial hypertrophy. To examine this hypothesis, rhabdomyosarcoma (A 204 cells) derived bFGF was used as wild type bFGF. Extracted bFGF from A 204 cells and nonserum conditioned medium of A 204 cells included high molecular form (22, 24 kd), as well as low molecular (18 kd) bFGF by western blotting, and showed hypertrophic effect in cultured myocardial cells. The hypertrophic effects were indicated in remarkable enlargement of cell size and significant increase in phenylalanine incorporation (x 2.2). The maximum expression of c-myc mRNA by A 204 conditioned medium was observed 30 min after stimulation, and it was also accompanied by an increase of accumulation of alpha skeletal actin mRNA by primer extension. After absorption of heparin binding growth factor from A 204 conditioned medium, it indicated no hypertrophic effects. In conclusion, it is likely that wild type bFGF including high molecular weight form plays a important role in cardiac myocyte growth and hypertrophy.
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PMID:[Cultured myocardial cell growth and hypertrophy by basic fibroblast growth factor]. 835 38

Cytotoxic agents used in cancer therapy may induce differentiation in tumour cells with no proliferative potential. However, chemotherapy can also induce multidrug resistance, a formidable obstacle to the successful treatment of tumours. Both events were recently shown to occur in a rhabdomyosarcoma cell line (RD-DAC) resistant to actinomycin D, a drug of choice in the treatment of these tumours. To analyse this connection, cell line RD cultures were investigated with progressive concentrations of actinomycin D and it was shown that a minimum dose (1.2 x 10(-6) mM) of the drug was necessary to increase mdr 1 mRNA in RD-DAC. The mechanism of mdr 1 overexpression was an increase in the number of copies of the mdr 1 gene, although the mRNA levels were not correlated with mdr 1 amplification. Drug resistance mediated by mdr 1 overexpression coincided with the development of myogenic differentiation in RD-DAC and with a decrease in c-myc mRNA levels, whereas levels of N-myc mRNA showed no modulation. These findings suggest that factors implicated in cell proliferation and differentiation, such as c-myc, may be responsible for the control of genes related to the development of multidrug resistance in rhabdomyosarcomas. Modulation of these factors may determine the sensitivity of rhabdomyosarcoma cells to drugs and may play an important role in triggering the differentiation programme found in these resistant rhabdomyosarcoma cells.
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PMID:Inverse expression of mdr 1 and c-myc genes in a rhabdomyosarcoma cell line resistant to actinomycin d. 894 21