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)

Rubidazone was used as sole chemotherapy in 170 adults and children with acute leukemia and sarcoma. When rubidazone was employed to treat the first attack, complete remission was achieved in : 1) 40 out of 70 patients (57%) with AML; 2) two out of six patients with AML where previous chemotherapy had failed; 3) four out of five patients with ALL; 4) 12 out of 14 patients with acute monoblastic leukemia. When used to treat relapse, rubidazone produced complete remission in : 1) 14 out of 31 cases of AML; 2) 18 out of 39 cases of ALL; 3) 2 out of 3 cases of non-Hodgkin lymphoma. Treatment of a case of rhabdomyosarcoma was unsuccessful. In the treatment of acute myeloblastic and monoblastic leukemias, it may be concluded that rubidazone induces a higher rate of complete remission than any other previously reported drug which was used alone. It also achieves remission rates similar to those resulting from a combination of daunorubicin and Ara-C. Furthermore, when compared with daunorubicin, rubidazone allows better control of the induction of aplasia.
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PMID:Clinical study of rubidazone (22 050 R.P.), a new daunorubicin-derived compound, in 170 patients with acute leukemias and other malignancies. 106 26

Transient or permanent paraplegia after the use of intrathecal (IT) methotrexate (MTX) or cytosine arabinoside (Ara-C) for treatment or prophylaxis of patients with meningeal leukemia is an unusual complication, with an incidence of less than 3% among such patients. Only 15 cases involving IT MTX have been documented and even fewer with IT Ara-C. Three patients were studied who developed permanent or ascending myelopathy from treatment of their leukemia or rhabdomyosarcoma with IT chemotherapy. The patients' ages ranged from 7 to 62 years. Two of the three patients had electromyographic examinations. These revealed a primary motor neuron degeneration or a polyradiculopathy, superimposed on a mild axonal peripheral neuropathy associated with vincristine therapy. This is consistent with other electromyographic studies. Two of the patients showed an elevation of the cerebral spinal fluid (CSF) protein before development of paraplegia; one also showed a rise in myelin basic protein associated with his myelopathy. Neuropathologic findings suggest demyelination as the primary process leading to myelopathy. Increasing evidence has shown that total CSF protein, or more specifically, the myelin basic protein, may be elevated before development of paraplegia. Routine serial testing of the CSF for total protein could be used as a screening test during therapy.
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PMID:Paraplegia and quadriplegia after intrathecal chemotherapy. 321 64

Rhabdomyosarcoma (RMS) is an embryonal tumor of childhood that arises from primitive skeletal muscle-forming cells (rhabdomyoblasts) probably arrested and transformed along the normal myogenic pathway to maturation. Since Ara-C is an antitumor agent known to induce differentiation in human acute myelogenous leukemia, also presumably a disorder of cellular maturation, we treated RD, a human embryonal RMS cell line, with Ara-C and evaluated its effect on growth and differentiation. Ara-C treatment of RD cells in vitro caused a dose-dependent growth inhibition in the absence of cytotoxicity. Interestingly, RD cells treated with 5 x 10(-7) M Ara-C for 4 days were able to recover logarithmic growth after the removal of the drug from the media. A reexposure of these cells to Ara-C led to morphological and biochemical changes related to differentiation, including the appearance of an increased number of multinucleated cells that expressed muscle-specific actin and skeletal muscle myosin heavy chain (MHC) (fast). In vivo studies demonstrated that RD cells pretreated with 5 x 10(-7) M Ara-C lost their ability to form tumors in nude mice. We conclude that treatment of this human embryonal RMS cell line with Ara-C results in marked growth inhibition in vitro, loss of tumorigenicity in vivo, and the expression of biochemical markers present in a more differentiated phenotype. These data suggest a potential role for differentiation therapy as a therapeutic approach in RMS.
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PMID:Ara-C treatment leads to differentiation and reverses the transformed phenotype in a human rhabdomyosarcoma cell line. 844 Mar 18