Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neocarzinostatin (NCS) used for the chemotherapy of leukemia and cancers such as stomach, pancreas and bladder, has been pointed out to have the side effects mainly causing leukopenia. In order to prevent these side effects of NCS by systemic administration, we have attempted to inject NCS directly into the tumor tissues and to inactivate NCS leaked from the tissues by the treatment of antidotes for NCS. The present report deals with the influence of some antidotes on the toxicity of NCS in vitro and in vivo. The results demonstrated that; Four SH-compounds, such as thiopronin, glutathione (reduced form), sodium thioglycolate and L-cysteine monohydrochloride monohydrate were effective to inactivate antibacterial activity of NCS against M. luteus ATCC 9341 in vitro. It was recognized that acute toxicity of NCS was reduced by pretreatment of these SH-compounds and its action was dose related. The LD50 values of NCS intravenous administration in mice increased 5.8- to 24-fold when 150, 300, 500 and 1,000 mg/kg of thiopronin were administered intravenously 2 minutes prior to NCS. And 2.3- to 4.2-fold by 500 and 1,000 mg/kg of glutathione (reduced form), 1.6- to 4.2-fold by 50, 100 and 200 mg/kg of sodium thioglycolate, 1.9- to 4.2-fold by 100, 200 and 400 mg/kg of L-cysteine monohydrochloride monohydrate respectively. On the other hand, pretreatment of NCS didn't affect the acute toxicity of thiopronin.
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PMID:[Screening for the antagonizing agents against lethal toxicity of neocarzinostatin. I. Inhibitory effects of various drugs on the toxicity of neocarzinostatin in vitro and in vivo]. 315 7

Patients with follicular non-Hodgkin's lymphoma (NHL) respond well to chemotherapy but frequently relapse and progress with conversion to more aggressive histology lymphomas. In a prior Cancer and Leukemia Group B (CALGB) trial, oral cyclophosphamide, given as a single agent, was found to be equivalent to a five-drug regimen in remission induction in patients with follicular NHL who had not received prior chemotherapy. Recently, interferon alfa-2b (Intron A; Schering Plough) has been demonstrated to elicit complete or partial responses in up to 50% of patients with nodular NHL who had received prior chemotherapy. In the current CALGB pilot trial, oral cyclophosphamide (100 mg/m2 daily) combined with interferon alfa-2b (2 X 10(6) IU/m2 s.c. on alternate days) is being evaluated, both in previously treated and untreated patients with stage III or IV follicular NHL, for toxicity, safety and efficacy in remission induction. A total of 68 patients have been entered into this study. Four patients are ineligible on pathology review, and 60 have on-study data currently available. Forty-one (60%) had not received prior chemotherapy and 19 (32%) had previously received some form of chemotherapy. Leukopenia was found to be the single, most common toxicity experienced by all patients. Previously untreated patients experienced leukopenia of less than 2,000 WBC/microliter at a significantly higher rate (53% versus 14%) than a similar patient population receiving oral cyclophosphamide as a single agent in the prior CALGB trial. Leukopenia was found to be promptly reversible, however, by dose suspension or adjustment, and other toxicities were demonstrated to be mild and tolerable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Combination trial of subcutaneous interferon alfa-2b and oral cyclophosphamide in favorable histology, non-Hodgkin's lymphoma. 329 31

Cisplatin and melphalan given ip exert a synergistic therapeutic effect against ascitic P388 leukemia in mice and have different dose-limiting toxic effects as well as favorable pharmacokinetic characteristics in ip phase I studies. We gave a total of 98 courses of cisplatin (escalated from 40 to 120 mg/m2) and melphalan (escalated from 12 to 30 mg/m2) to 30 patients with ip tumors, most of whom had residual ovarian cancer following iv cisplatin-containing regimens. Treatment was delivered in 2 L of 0.9% NaCl through a Tenckhoff catheter with or without a Port-a-Cath system every 28 days for one to nine cycles. Myelosuppression was dose-related and leukopenia was dose-limiting. The maximum tolerated dose was 120 mg of cisplatin/m2 and 20 mg of melphalan/m2. With the exception of treatment-induced nausea and vomiting, nonhematologic toxic effects were mild and no (or very little) local toxicity occurred. Pharmacokinetic analyses showed that the areas under the peritoneal concentration versus time curve averaged 16-fold and 17-fold more than the area under the plasma curve for cisplatin and melphalan, respectively. Objective responses were documented by third-look laparotomy in ovarian cancer patients with minimal (less than 2 cm) residual disease.
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PMID:Intraperitoneal chemotherapy with cisplatin and melphalan. 341 24

By using the combination of alpha-naphthyl butyrate esterase and chloroacetate esterase for cytochemical detection of monocytes and granulocytes, respectively, we examined and identified five adult patients with acute myeloid leukemia whose leukemic cells often (20 to 30%) had the characteristics of both monocytes and granulocytes. All five patients were men, 23 to 82 years of age. Two patients had manifestations of preleukemia. One of these two patients had received treatment for lymphoma for 12 months before acute myelomonocytic leukemia was diagnosed. One patient had gum hypertrophy, and two had leukemia cutis. At the time of initial examination, four patients had blood leukocyte counts higher than 80,000/mm3 and one had leukopenia. Four patients received chemotherapy; three responded temporarily but died within 1 year after the myelomonocytic leukemia had been diagnosed. The patient with leukopenia has remained in complete remission for 2 years. With more frequent use of double esterase stains for classification of acute myeloid leukemias, this variant of acute myelomonocytic leukemia should be detected more often and its clinical behavior should be better understood.
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PMID:Acute myelomonocytic leukemia: an unusual variant with both granulocytic and monocytic esterases in the leukemic cells. 345 74

A 7-year-old Quarter Horse stallion with a myeloproliferative disorder was examined because of colic, and an enterolith was removed surgically. The horse experienced secondary complications after abdominal surgery, and leukopenia and thrombocytopenia were detected. Five months later, the horse was examined for recurrent peripheral edema and for repair of an abdominal incisional hernia. Acute myelomonocytic leukemia was diagnosed, and treatment with low-dose (noncytocidal) cytosine arabinoside was unsuccessful. Necropsy revealed neoplastic infiltrate in the spleen, liver, lung, adrenal gland, testes, and eye. The persistent hematologic abnormalities before the onset of overt leukemia may represent hematopoietic dysplasia or preleukemia.
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PMID:Acute myelomonocytic leukemia in a horse. 345 90

Aclarubicin, a new anthracycline antibiotic, was used to treat 24 adult patients with refractory adult leukemia, using a total dose of 300 mg/m2 (75 mg/m2/day X 4). There were 20 patients with acute myelogenous and four with acute lymphoblastic leukemia. Approximately two-thirds of the patients had a Karnofsky score of less than or equal to 2, and two-thirds had received two or more previous induction programs. Interim bone marrow evaluation was obtained in 18 of 30 remission induction courses and revealed marked hypocellularity in 14, inadequate specimens in three, and persistent disease in one. Seven patients received more than one course. Two patients refused further therapy. In patients with myelogenous leukemia, there were two complete remissions lasting 10 and 16 months and one partial remission lasting 4 1/2 months. There were no responders in patients with lymphoblastic leukemia. Toxicity included profound leukopenia and thrombocytopenia, moderate nausea and vomiting, diarrhea, and mucositis. There were no cardiac symptoms associated with the drug infusion, but there were three late events possibly associated with anthracycline cardiotoxicity. Used in this dosage schedule, aclarubicin is an active, but toxic, agent in the acute myelogenous leukemias.
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PMID:Phase II evaluation of aclarubicin in refractory adult acute leukemia: a Southwest Oncology Group Study. 346 Jul

The effect of chloramphenicol on the toxic and therapeutic action of cyclophosphamide was studied on CBA and DBA male mice. The animals were intact or infected with L1210 leukemia. It was found that the use of chloramphenicol prolonged the life-span of the mice and/or increased the number of the survivals after exposure to the lethal doses of cyclophosphamide. It reduced leukopenia and almost completely protected the animals from macular canities developing after administration of cyclophosphamide. The therapeutic effect of cyclophosphamide did not change after the use of chloramphenicol. The mechanisms of the above diverse effects of chloramphenicol on the toxic and therapeutic action of cyclophosphamide and the possibility of the use of chloramphenicol for lowering the cyclophosphamide toxicity in treatment of oncological patients are discussed.
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PMID:[Effect of chloramphenicol on the toxic and therapeutic actions of cyclophosphane]. 371 19

Peripheral blood changes preceding therapy-related leukemia were studied in 105 patients who had received cytotoxic therapy, 53 for Hodgkin's disease and 52 for other cancers. Preleukemic anomalies were observed in 74.3% of the cases, appearing after a mean interval of 68.7 months after diagnosis of the initial cancer. This interval was only 57.5 months in patients aged 50 years or older and only 42.3 months in patients with Hodgkin's disease having received cytotoxic therapy for 6 months or less. The first changes most frequently observed were pancytopenia (24.8%) and isolated erythrocyte abnormalities such as anemia or macrocytosis (18.1%). Involvement of two cell lines, isolated thrombocytopenia or leukopenia, circulating immature cells, monocytosis, leukocytosis, or thrombocytosis were also observed. Therapy-related myelodysplastic syndrome was recognized in 19 patients and myelofibrosis in 3. Median duration of the preleukemic phase was 6 months; 9 months in cases of isolated erythrocyte involvement and 5 months in the other cases. Myelomonocytic or monoblastic leukemia appeared less frequently when the first sign involved erythrocytes only. Hematological surveillance thus appears necessary in all patients having received cytotoxic therapy. Bone marrow study with cytogenetic examination should be performed in cases of persistent peripheral blood abnormalities.
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PMID:Preleukemic changes in cases of nonlymphocytic leukemia secondary to cytotoxic therapy. Analysis of 105 cases. 373 Oct 20

It has been reported that L-histidinol, a structural analogue of the essential amino acid L-histidine, can transiently inhibit proliferative cycling in cells with normal phenotype while allowing continued cell cycle transit in tumor cells. Thus, in the presence of L-histidinol, the toxicity of a proliferation-dependent drug such as 5-fluorouracil (FUra) was found to be reduced in normal tissue cells of the DBA/2J mouse, but not in L1210 leukemia cells in the same mouse. Because of the potential clinical significance of this approach to reduce chemotherapy-associated host toxicity, we evaluated the L-histidinol-FUra combination in a nonleukemic, solid murine tumor model, the BALB/c X DBA/8 F1 (hereafter called CD8F1) breast tumor. The results of these studies indicate that the administration of L-histidinol can protect the CD8F1 mouse from FUra-associated leukopenia, body weight loss, and ultimately, from mortality. However, in contrast to results reported in the L1210 leukemic system, L-histidinol also reduced the cytotoxic activity of FUra against CD8F1 breast tumors. Therefore, although the dose of FUra that could be administered with safety was higher in mice receiving L-histidinol, the therapeutic results of the combination of FUra and L-histidinol were not superior to those obtained with FUra alone at a lower dose.
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PMID:Failure of L-histidinol to improve the therapeutic efficiency of 5-fluorouracil against murine breast tumors. 379 Dec 3

The literature as well as the author's data of this topic are reviewed. Lithium stimulates myelopoesis in vitro, especially via CSF-production. This effect is associated with a modulation of cyclic nucleotides. Lithium stimulates leukemic cell lines too. However, according to epidemiological data lithium does not play an etiological role in leukemia. Furthermore, lithium does not stimulate several tumor cell lines in culture. The effect of cytostatic drugs as well as remission rates are not lessened by lithium. In spite of increased production the functions of the granulocytes are not impaired. Because of the wide range of serum level variation serum level determinations are mandatory. To treat hematological disorders a serum level between 0.7 and 1.2 mmol/l should be achieved. Flame emission photometry and atomic absorption photometry are equivalent methods for determination of the serum level. CNS, thyroid gland, kidney, electrolyte balance, gastrointestinal tract have to be monitored for side effects. Lithium therapy has not be given in pregnancy and to breast feeding mothers. In neutropenia with increased susceptibility to infections lithium therapy including serum level monitoring can be given. Lithium reduces leukopenia and infections following cytotoxic chemotherapy for solid tumors. Current pediatric studies are investigating whether patients with chemotherapy induced neutropenia benefit from this effect in terms of increased and prolonged remission rates.
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PMID:[Lithium in the therapy of hematologic diseases in childhood]. 385 36


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