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)

Cell loss patterns of five tumors and their histological findings were investigated in WHT/Ht strain mice. The tumors investigated were squamous cell carcinoma H, squamous cell carcinoma NOS, squamous cell carcinoma TAK, rhabdomyosarcoma KAS, and fibrosarcoma YAS. The present study revealed that histological findings of tumor tissues are not necessarily corded structure presented by Thomlinson and Gray. The five were divided into two groups according to their histological findings, i.e. a corded structure (squamous carcinoma H and NOS) and a non-corded structure (squamous cell carcinoma TAK, rhabdomyosarcoma KAS and fibrosarcoma YAS). The cell loss patterns (125I-iododeoxyuridine retention curves) were also divided into two groups which corresponded to the histological structures. Two tumors with the corded structure (squamous cell carcinoma H and NOS) have a cell loss pattern with a constant shoulder portion (a migration time of tumor cells through a tumor cord from capillary to necrotic region). In these tumors, the cell loss occurred in the necrotic regions. In the other tumors with the non-corded structure, cell loss curves have no constant shoulder portion and cell loss might occur throughout the tumor. The origin of hypoxic cells in these two types of histology are presumably different. The diffusion-limited hypoxia, i.e. chronically hypoxic cells, may be the main cause for the tumors with corded structure. On the other hand, hypoxia as a result of temporary cessation of blood flow within the tumor vasculature, i.e. acutely hypoxic cells, may mainly occur in the tumor with non-corded structure.
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PMID:Two different types of cell loss patterns of murine tumors and their corresponding histological findings and possible mechanisms of production of hypoxic cells. 850 92

TAK-475 is a squalene synthase inhibitor, rapidly metabolized to T-91485 in vivo. We investigated the myotoxicities of T-91485 and 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors in a human rhabdomyosarcoma cell line, RD, and in human skeletal myocytes. In differentiated RD cells, T-91485, atorvastatin (ATV) and simvastatin acid (SIM) inhibited cholesterol biosynthesis, with IC(50) values of 36, 2.8 and 3.8 nM, respectively. ATV and SIM decreased the intracellular ATP content, with IC(25) values (concentrations giving a 25% decrease in intracellular ATP content) of 0.61 and 0.44 microM, respectively. Although T-91485 potently inhibited cholesterol synthesis in RD cells, the IC(25) value exceeded 100 microM. In human skeletal myocytes, T-91485, ATV and SIM concentration-dependently inhibited cholesterol biosynthesis, with IC(50) values of 45, 8.6 and 8.4 nM, respectively. ATV and SIM decreased intracellular ATP content, with IC(25) values of 2.1 and 0.72 microM, respectively. Although T-91485 potently inhibited cholesterol synthesis, the IC(25) value exceeded 100 microM. Myotoxicity induced by ATV was prevented by mevalonate or geranylgeranyl-PP, but not by squalene in skeletal cells. Furthermore, T-91485 attenuated the myotoxicity of ATV. These findings suggest that TAK-475 and T-91485 may not only be far from myotoxic, they may also decrease statin-induced myotoxicity in lipid-lowering therapy.
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PMID:Comparing myotoxic effects of squalene synthase inhibitor, T-91485, and 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors in human myocytes. 1460 38