Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-seven children and adolescents with acute leukemia in relapse were treated with cyclocytidine in a cooperative group setting. Only one of the 27 evaluable patients achieved complete remission. A significant decrease (greater than or equal to 20%) in circulating and/or bone marrow leukemia cells occurred in an additional five patients. Drug toxicity was evaluated in 35 patients and included ten cases of jaw pain, two cases of hypotension, one case of fever, and one case of severe vomiting.
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PMID:Cyclocytidine in the treatment of refractory acute childhood leukemia: a Southwest Oncology Group Phase I-II study. 9 13

Neocarzinostatin is a new anticancer drug developed by Japanese investigators. In order to delineate the potential usefulness of this drug, we have reviewed the preclinical data and summarized the Japanese clinical data on 462 patients. The bulk of these patients had carcinoma of the stomach or pancreas and acute leukemia. Neocarzinostatin was administered intravenously in a daily dose of 2-3 mg for five to 15 day periods. Significant antitumor activity was observed in acute leukemia. A few responses were also reported in pancreatic adenocarcinoma, but the drug was inactive against gastric carcinoma. The side effects observed included nausea, vomiting, myelosuppression, fever, and occasional hypersensitivity reactions. The Investigational Drug Branch of the National Cancer Institute has recently sponsored an investigational new drug application with the Food and Drug Administration, and phase I studies are expected to begin soon in the United States.
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PMID:Neocarzinostatin (NSC 157365) a new cancerostatic compound. 14 Oct 12

Neocarzinostatin (NCS) is an antibiotic from streptomyces carzinostaticus which inhibits DNA synthesis. Clinical trials in Japan began in 1971. NCS is active against S-180, Ehrlich tumor, L1210, Yoshida sarcoma, and a range of ascitic hepatomas. In rabbit NCS is distributed at high concentrations in the kidney, skin, stomach, pancreas, lung, and muscles. The high distribution in the pancreas and the stomach suggested possible effectiveness in human tumors at these sites. In clinical studies NCS has been shown to be active against acute leukemia. As a single agent 9 out of 51 obtained a CR with 9 more achieving a PR. Anorexia, nausea, and vomiting were the most frequent side effects. NCS has been tried in combination with Ara-C, daunorubicin and prednisolone and CR was ssen in 11 out of 14. In stomach cancer responses of some kind were observed in 12 out of 141 cases, while in the case of pancreatic tumors there were 10 out of 68.
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PMID:Clinical investigations of neocarzinostatin in Japan. 15 99

Twenty-three children with advanced cancer refractory to conventional therapy received weekly iv doses of neocarzinostatin for 5 weeks. Doses were escalated from 500 to 6750 units/m2/week. Four types of toxic manifestations occurred: acute reactions consisting of shaking chills with or without fever and cyanosis (rigor), hypersensitivity, vomiting, and marrow depression. Evidence of oncolytic activity was limited to patients with acute leukemia in whom phase II trials at doses between 3000 and 4500 units/m2 appear warranted.
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PMID:Phase I study of neocarzinostatin in children with cancer. 15 67

In an ongoing cooperative study of the Cancer and Acute Leukemia Group B, 21 evaluable patients with advanced malignant lymphomas were treated with 70 mg/m2 of cis-dichlorodiammineplatinum(II) (cis-platinum) once every 3 weeks. All patients had received extensive prior therapy. Partial remission was obtained in two of seven patients with Hodgkin's disease, for 1+ and 7 months, and in three of 14 patients with non-Hodgkin's lymphoma, for 2, 2+, and 2.5 months. In another ongoing trial, 11 patients with advanced, pretreated small cell cancer of the lung received 80 mg/m2 of cis-platinum once every 3 weeks. Four patients achieved partial remissions. These lasted 2+ and 2.5 months in the two patients evaluable for duration of response. Two further clear-cut tumor regressions were noted. The major toxic effects were myelosuppression and vomiting. In the second trial, one case of probable drug-related fatal nephrotoxicity was encountered despite optimal forced diuresis with mannitol and furosemide. cis-Platinum definitely warrants further evaluation in these diseases because of significant effectiveness even after extensive prior treatment.
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PMID:Phase II trial of cis-dichlorodiammineplatinum(II) in advanced malignant lymphoma and small cell lung cancer: preliminary results. 22 99

Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.
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PMID:Electrolyte and acid-base disturbances in the management of leukemia. 26 90

The carcinogenic potential of procarbazine is under investigation in three species (Macaca mulatta, Macaca fascicularis, and Cercopithecus aethiops) of nonhuman primates. A total of 55 monkeys have received procarbazine s.c., p.o., or i.p. for periods of up to 12 years. Eleven of the 42 monkeys (26%) necropsied thus far have had malignant neoplasms, 6 of which were acute leukemia. Two monkeys developed osteogenic sarcomas, two monkeys developed hemangiosarcomas, and a single case of lymphocytic lymphoma was found. The average total dose of procarbazine received by the monkeys developing cancers was 36.0 g; the average duration of procarbazine treatment was 75 months. A number of the toxic effects of procarbazine seen in humans were also noted in this series of monkeys, including vomiting and myelosuppression. Another striking toxic effect was on the reproductive system of the males. The majority of the adult males necropsied to date have had testicular atrophy with complete aplasia of the germinal epithelium.
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PMID:Carcinogenic and other adverse effects of procarbazine in nonhuman primates. 41 74

A toxic syndrome characterized by fever, headache, and vomiting, lasting 2-5 days, occurred in 61% of 39 children with acute leukemia in complete remission, receiving central nervous system prophylaxis with intrathecal methotrexate, and in 14% of 34 children receiving the same plus cranial radiation. The syndrome was accompanied by pleocytosis with lymphocytes, monocytoid cells, and neutrophils. There was evidence of cumulative Mtx toxicity, since the toxic syndrome occurred mostly after the third and fourth dose and did not recur with longer intervals between doses. The incidence of the syndrome was significantly reduced by the use of Elliott's B solution as Mtx diluent, rather than water or normal saline. The occurrence of pleocytosis and toxic clinical syndrome was also significantly reduced in patients receiving concomitant cranial radiation, probably due to the lympholytic action of radiotherapy and the depressed cellular response of irradiated tissues. The use of Elliott's B solution as diluent for IT Mtx and an appropriate interval between Mtx doses are suggested for prevention of this toxic syndrome.
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PMID:Adverse effects of intrathecal methotrexate in children with acute leukemia in remission. 109 8

We evaluated the responses of 39 children with cancer who, after failure to respond to conventional chemotherapeutic agents, received either or both of two epipodophyllotoxins: 4'-demethylepipodophyllotoxin 9-(4,6-o-2-thenylidene-beta-D-glucopyranoside) (NSC-122819) and 4'-demethylepipodophyllotoxin 9-(4,6-o-ethylidene-beta-D-glucopyranoside) (NSC-141540). Seventeen patients has acute lymphocytic leukemia (ALL). 12 had acute nonlymphocytic leukemia (ANLL), and ten had solid tumors. Initially, the patients in each disease category were randomized to receive 50 mg/m2/dose of NSC-122819 intravenously (iv) twice weekly or 75 mg/m2/dose iv of NSC-141540 twice weekly for 4 weeks. Drug dosages and schedules of administration were adjusted during the course of the study. Although objective responses were not detected in the heterogeneous group of solid tumor patients, definite clinical responses were obtained in nine of the 29 patients with acute leukemia. The responses to the two epipodophyllotoxins were noted in patients with ALL as well as in patients with ANLL. Toxic side-effects included nausea, vomiting, diarrhea, fever, alopecia, leukopenia, and thrombocytopenia. These results, the first reported with both NSC-122819 and NSC-141540 in childhood cancer, indicate that the epipodophyllotoxins are well tolerated and may be effective against acute leukemia.
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PMID:4'-demethylepipodophyllotoxin 9-(4,6-o-2-thenylidene-beta-D-glucopyranoside) (NSC-122819; VM-26) and 4'-demethylepipodophyllotoxin 9-(4.6-0-ethylidene-beta-D-glucopyranoside) (NSC-141540; VP-16-213) in childhood cancer: preliminary observations. 110 Feb 25

Because of the synergy seen in adult trials when 5-fluorouracil is combined with leucovorin, we initiated a Phase I trial of this combination in children's refractory cancer. Leucovorin, an equal mixture of the (6R,S)-diastereoisomers, was administered p.o. for 6 consecutive days as 4 equal doses at 0, 1, 2, and 3 h totaling 500 mg/m2/day. 5-Fluorouracil was given daily on days 2 to 6 as an i.v. bolus immediately following the last dose of leucovorin. The leucovorin dose was held constant while the 5-fluorouracil dose was escalated in cohorts of patients from 300 mg/m2/day to its maximally tolerated dose. Thirty-five patients (19 with acute leukemia and 16 with solid tumors) were evaluable for toxicity. The maximally tolerated dose of FUra was 450 mg/m2/day for 5 treatments for patients with solid tumors and 650 mg/m2/day for 5 treatments for the children with leukemia. The dose-limiting toxicities were myelosuppression and stomatitis. Other side effects included transient, mild elevations of serum transaminases, mild nausea, vomiting, and diarrhea. The pharmacokinetics of high-dose p.o. leucovorin was studied in 23 children. There was considerable interpatient variability in the plasma concentrations of total bioactive folates (TBAF), (6S)-leucovorin, and (6S)-5-methyltetrahydrofolic acid. The maximum plasma concentration (Cmax) of TBAF was 821 +/- 97 (SE) nM, occurring at a median of 8 h; the Cmax of (6S)-leucovorin was 77 +/- 11 nM, occurring at 4 h. The TBAF concentration fell to 146 +/- 42 nM by 24 h. (6S)-5-Methyltetrahydrofolic acid accounted for 90 +/- 7% of the TBAF at the Cmax. The plasma concentration of (6R)-leucovorin, the unnatural isomer, was equal to that of TBAF. Thus, p.o. leucovorin reduced the 5-fold excess of (6R)-leucovorin over TBAF seen after i.v. doses. The relative amounts of the three major plasma species were approximately the same as in adults, even though the Cmax of each compound was lower.
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PMID:Pharmacology and phase I trial of high-dose oral leucovorin plus 5-fluorouracil in children with refractory cancer: a report from the Children's Cancer Study Group. 189 77


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