Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.1.1 (asparaginase)
 2,695 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A number of therapeutic agents including L-asparaginase, Actinomycin-D, CCNU, Hydroxyurea, 5-FU, Cis-platinum, Cyclophosphamide, orchiectomy, Adriamycin and DES alone and in various combinations has been applied against the Dunning R-3327 rat prostatic adenocarcinoma subline G. We have found a parallel between the results of this study and those of similar therapeutic application to the human tumor. We conclude that this animal model may prove to be a useful screening system for agents against human prostatic cancer.
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PMID:Chemotherapy of the transplantable adenocarcinoma (R-3327) of the Copenhagen rat. 91 40

Increasingly vigorous chemotherapy of cancer including primary and metastatic central nervous system disease has resulted in prolonged good-quality survival. However, there has been an associated increase in neurotoxicity from both radiation therapy and chemotherapy. All classes of chemotherapeutic agents contain drugs that are potentially neurotoxic, often only at high doses. Mechlorethamine, the first nitrogen mustard, is not neurotoxic at conventional dosage, but at high doses, it may produce both an acute and a delayed encephalopathy. Methotrexate administered intrathecally often induces reversible aseptic meningitis, but chronic administration, either intrathecally or high-dose intravenously, may produce fatal leukoencephalopathy. 5-Fluorouracil at high dosage may cause cerebellar ataxia, but may also do so at low dosage when combined with thymidine infusions. Cytosine arabinoside at high dosage may also produce cerebellar ataxia. Vincristine produces a peripheral neuropathy, and less commonly causes both autonomic and cranial neuropathy. The enzyme L-asparaginase can produce a dose-related reversible encephalopathy. BCNU, now the mainstay of glioma chemotherapy, may combine with radiation to produce long-term cerebral atrophy. Both intracarotid and high-dose intravenous BCNU administration may cause encephalopathy. Several other chemotherapeutic agents have also been reported to cause neurotoxicity under certain circumstances.
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PMID:Neurological complications of antineoplastic therapy. 638 4

We tested the effectiveness of dihydroxyanthracenedione (DHAD) on cell growth of two human pancreatic carcinoma cell lines MIA PaCa-2 and PANC-1. At the level of ID50, the drug was almost equally effective against both cell lines. When the time exposure of MIA PaCa-2 cells to the drug was increased from 1 h to continuous exposure for 5 days, the ID50 was decreased about three-fold only (1.4 X 10(-8)M and 4 X 10(-9)M respectively). At the level of ID50 also the difference between 6 h exposure and continuous exposure for 5 days was minimal. In equimolar concentrations and with 1 h exposure, DHAD was more effective against MIA PaCa-2 cells than other chemotherapeutic agents including adriamycin, mitomycin-C, 5-FU, vincristine, vindesine, vinblastine, VP-16-213, bleomycin, cis-platinum, asparaginase and acivicin. In concentrations of 5 X 10(-7)M, DHAD caused about 40% inhibition of 14C-thymidine incorporation of MIA PaCa-2 cells. Treatment of MIA PaCa-2 cells with the ID50 of DHAD for 1 h caused retardation of cellular traverse, with the major effect appearing to be in G2 + M phase of the cycle. From these data DHAD appears to be a potent drug against human pancreatic carcinoma in vitro.
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PMID:Sensitivity of cultured human pancreatic carcinoma cells to dihydroxyanthracenedione. 669 38

The emetic effects of five anticancer drugs, cyclophosphamide, nitrogen mustard-N-oxide, actinomycin D, 5-fluorouracil and L-asparaginase, and the effects of bilateral abdominal vagotomy and bilateral greater splanchnic nerve section or a 5-HT3 receptor antagonist on the emesis induced by these drugs were investigated in dogs. Cyclophosphamide (20 mg/kg, i.v.), nitrogen mustard-N-oxide (5 mg/kg, i.v.) and actinomycin D (50 micrograms/kg, i.v.) caused vomiting in dogs with a long latency period. 5-Fluorouracil (5 mg/kg, i.v.) and L-asparaginase (2000 K.U./kg, i.v.) failed to induce vomiting. Bilateral abdominal vagotomy and bilateral greater splanchnic nerve section completely inhibited the vomiting induced by the former three anticancer drugs. Furthermore, the vomiting was inhibited completely by intravenous administration of ICS205930 (2 x 0.1 mg/kg), a 5-HT3 receptor antagonist. These results suggest that activation of visceral afferents through 5-HT3 receptors mediates the vomiting induced by cyclophosphamide, nitrogen mustard-N-oxide and actinomycin D.
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PMID:Emetic effects of anticancer drugs and involvement of visceral afferent fibers and 5-HT3 receptors in dogs. 811 85