Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 44-year-old house-wife was admitted to the hematological clinic of our hospital on December 21, 1981 for the treatment of acute myeloid leukemia. Hematological examination showed severe anemia, leukocytosis and thrombocytopenia. She was soon started on DCMP therapy (Daunomycin, Cytosine arabinoside, 6-MP and prednisolone). After several repeats of remission and aggravation, she suffered from vertigo, nausea and vomiting in early August of 1982. The CT scan and angiography showed a mass lesion in the middle of the posterior cranial fossa. On August 26, surgical extirpation of the tumor locating in the vermis of the cerebellum was performed successfully. On gross examination the tumor revealed smooth yellowish-red surface, elastic in consistency and measured 40 X 40 X 30 mm in size. Histologically it comprised the leukemic cells. The pathology of the central nervous system due to leukemic cells was discussed in relation to the pertinent literature, including the CT findings and the indication of the surgical treatment.
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PMID:[Acute myeloid leukemia with intracranial tumor formation--case report]. 386 29

Nine patients with acute myelogenous leukaemia were treated with low-dose ARA-C (10 mg/m2, q 12h) for a planned 21 d. Complete remission was attained in only one patient (11.1%). Definite cytoreductive effect was seen in four additional patients. There was one treatment-related death. Haematologic toxicity occurred in all nine patients with sever thrombocytopenia most prominent. Severe hepatotoxicity precluded further ARA-C treatment in one patient. Because of toxicity only two patients were able to complete their scheduled 3 week courses of low-dose ARA-C. No evidence of ARA-C induced differentiation of leukaemic cells was noted on follow-up bone marrow examination during or shortly after the treatment course. The utility and indication for low-dose ARA-C therapy of AML remains to be determined.
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PMID:Low-dose ARA-C fails to enhance differentiation of leukaemic cells. 388 2

Diaziquone given as a bolus has not been effective in patients with relapsed or refractory leukemia. Because of in vitro data suggesting enhancement of diaziquone-induced cytotoxicity for human and murine leukemia cells with increased duration of drug exposure and the relatively short terminal plasma half-life of diaziquone, 49 patients (34 acute nonlymphocytic leukemia [ANLL], six chronic myelogenous leukemia in blast crisis [CML-B], five acute lymphocytic leukemia [ALL], four 2 degrees ANLL) with leukemia were given diaziquone as a continuous infusion for seven days. The maximum tolerated dose was 28 mg/m2/d for seven days. The dose-limiting toxicity was the duration of bone marrow aplasia (median, 49 days to greater than 500 PMNs in responders; range, 28 to 101 days). Nonhematologic toxicity was minimal. Responses occurred only in patients with relapsed ANLL, of whom 26 were treated at effective doses. There were six complete responses (CR) (23%) and two partial responses (PR) (8%), although five of eight responders never achieved platelet counts greater than 100,000/microL. Thrombocytopenia in these patients was felt to be a manifestation of diaziquone effect, not persistence of leukemia. The median duration of CR was 195 days (range, 88 to 860+). One patient had active CNS leukemia at the start of treatment and has had a durable (28+ month) CR in both sites of disease. Diaziquone produced prolonged aplasia in patients with secondary ANLL and CML-B (five of ten patients died aplastic), whereas patients with ALL all had regrowth of leukemia and two failed to become aplastic. The lack of significant nonhematologic toxicity and the activity in patients with relapsed ANLL render diaziquone of interest as second-line therapy or consolidation therapy in first remission for patients with ANLL.
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PMID:Diaziquone given as a continuous infusion is an active agent for relapsed adult acute nonlymphocytic leukemia. 394 May 46

The Gastrointestinal Tumor Study Group's (GITSG) adjuvant rectal carcinoma study compared four postoperative treatment regimens: (1) control (no adjuvant therapy); (2) chemotherapy alone consisting of pulses of 5-fluorouracil and methyl CCNU for 18 months; (3) pelvic and perineal radiotherapy using parallel opposed fields with 4000 rad in 4.5 to 5 weeks or 4800 rad in 5 to 5.5 weeks; and (4) a combination of both modalities. The results of this study are published elsewhere and show a significantly reduced recurrence rate and prolonged disease-free survival time for the combined modality arm compared with the no therapy arm. Severe toxicity in the combined therapy arm was significantly worse (P less than 0.001) than in either single modality arm. Most of the differences in toxicity experienced between the three regimens involved diarrhea, thrombocytopenia, and leukopenia. Analysis of all parameters of radiotherapy quality assurance data was not significantly associated with toxicity. Radiation enteritis was noted in 5 patients of 96 (5.2%) in the two arms containing irradiation. All five required laparotomy. The two enteritis fatalities occurred late at 605 and 1000 days after start of combined modality treatment, respectively. One other patient on the chemotherapy arm died of acute nonlymphocytic leukemia. The authors conclude that combined radiotherapy and chemotherapy, although significantly more effective in reducing recurrence than no therapy, is significantly more toxic than single-modality therapy in many parameters, although most of the toxicity is transient and therefore not limiting. Late complications, which are less reversible and therefore much more important than early reactions, and radiation enteritis in this study were relatively uncommon. This schedule of combined modality therapy is not only effective but appears to have tolerable toxicity, because of the relative lack of late effects.
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PMID:Toxicity associated with adjuvant postoperative therapy for adenocarcinoma of the rectum. 394 37

A Phase II study of a new anthracycline, (2''R)-4'-0-tetrahydropyranyladriamycin (THP), was conducted in 162 patients with various hematological malignancies in a multi-institutional cooperative study. THP was given intravenously at a dose of either 10-30 mg/body for 3-5 consecutive days or 40-60 mg/body at 3-week intervals. Of 22 patients with AML, complete remission (CR) was observed in 2 patients and partial remission (PR) in 2. Of 18 patients with ALL, CR was observed in 5 and PR in 3. Of 68 patients with NHL, CR was observed in 11 and PR in 22. Of 8 patients with HD, CR was observed in 4 and PR in 2. One CML case showed CR and one ATL case showed PR. PR was noted in one of 2 patients with mycosis fungoides. Overall remission rate was 43.1% (CR 23 cases and PR 33 cases). The predominant toxicity was myelosuppression. Leukopenia (less than 4,000/mm3) was noted in 67 (77.6%) and thrombocytopenia (less than 10 X 10(4)/mm3) in 24 (27.0%). Nausea/vomiting and anorexia were common, and were observed in 61 (43.3%) and 65 (46.1%) cases, respectively. Hair loss and cardiotoxicity were mild and recovered quickly on discontinuation of THP. Thus, THP was found to be effective for various hematological malignancies including acute leukemia and malignant lymphoma.
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PMID:[A phase II study of (2''R)-4'-0-tetrahydropyranyladriamycin (THP) in patients with hematological malignancies. THP Study Group]. 394 12

A Phase II clinical trial of NK 171 (Etoposide), a semisynthetic podophyllotoxin, was undertaken in 56 patients with advanced malignant lymphoma and 36 patients with acute leukemia. The dosage of NK 171 was 110-130 mg/m2 day p.o. or 80-100 mg/m2 day i.v. for 5 consecutive days. Of the 92 patients, 23.9% obtained a complete or partial remission. By tumor type, good responses were obtained in non-Hodgkin's lymphoma (34%, 17/50), Hodgkin's disease (25%, 1/4), AML (21.4%, 3/14), and CML-BC (25%, 1/4). Side effects included leukopenia (78.4%), alopecia (62.0%), anorexia (40.2%), nausea (30.4%) thrombocytopenia (25.6%) and fever (16.3%). These results demonstrated NK 171 to be an effective agent against malignant lymphoma and acute myeloblastic leukemia.
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PMID:[Phase II study of NK 171 (etoposide) on malignant lymphomas and acute leukemia. A cooperative study group on NK 171 in hematological malignancies]. 395 73

Acute promyelocytic leukaemia (A.P.L.) is a rare but important type of acute myeloid leukaemia characterized by major bleeding in association with thrombocytopenia, a specific peripheral blood and bone marrow picture, low plasma fibrinogen, and the presence in the serum of fibrin degradation products. These last abnormalities are related to the disseminated intravascular consumption of coagulation factors with secondary fibrinolysis. A.P.L. requires early recognition and urgent treatment. With optimal management up to half of the patients may achieve complete remission of two years or more. Undoubtedly patients with A.P.L. do especially well when treated in special centres and some patients with A.P.L. now die before the nature of their disease is recognized. Increased familiarity with the problem, which has been known for nearly 20 years, should yield great dividends for those few patients who have this disease.
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PMID:Acute promyelocytic leukaemia. 452 93

The combination of pyrazofurin (PF) and 5-azacytidine (5-aza-CR) was evaluated in 12 patients with neoplastic diseases who had failed conventional therapies. They included 6 patients with acute myelocytic leukemia (AML) and 6 with various carcinomas. PF was given by i.v. bolus at doses ranging from 25 to 200 mg/m2 followed by 5-aza-CR given by continuous 24-hour infusion at doses ranging from 30 to 120 mg/m2/24 h during 40-ic diseases who had failed conventional therapies. They included 6 patients with acute myelocytic leukemia (AML) and 6 with various carcinomas. PF was given by i.v. bolus at doses ranging from 25 to 200 mg/m2 followed by 5-aza-CR given by continuous 24-hour infusion at doses ranging from 30 to 120 mg/m2/24 h during 40-ic diseases who had failed conventional therapies. They included 6 patients with acute myelocytic leukemia (AML) and 6 with various carcinomas. PF was given by i.v. bolus at doses ranging from 25 to 200 mg/m2 followed by 5-aza-CR given by continuous 24-hour infusion at doses ranging from 30 to 120 mg/m2/24 h during 40--120 h. Dose-limiting toxicity was mucocutaneous, which appeared in 11/17 courses. Skin rash was similar to that produced by PF alone, but was present after much lower doses of PF when followed by 5-aza-CR. Moderate and reversible thrombocytopenia and leukopenia occurred in 3/6 patients with carcinoma. No objective response was seen in patients with carcinoma, and no marrow remission occurred in patients with AML. 24-Hour urinary excretion of orotidine and oroticacid were measured during 11 courses in 8 patients, and were not much different than those obtained previously with PF alone. The occurrence of mucocutaneous toxicity precluded the use of higher doses of PF and 5-aza-CR, which might have been therapeutically more active.
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PMID:Sequential combination of pyrazofurin and 5-azacytidine in patients with acute myelocytic leukemia and carcinoma. 616 Apr 42

A combination therapy with 5 aza-cytidine (5 AZA-C), vincristine (VCR), and prednisone (PRED) was given to 53 children with acute nonlymphocytic leukemia resistant to conventional therapy. Of these, eight children obtained a complete remission and seven a partial remission. Maintenance therapy was initiated in 12 children. The remission duration varied between 19 and 176 days (median 69 days). The main toxicity was vomiting and myelosuppression manifested as severe neutropenia and thrombocytopenia. It is concluded that VCR and PRED do not increase the response rate to that of 5 AZA-C as a single agent.
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PMID:Low response rate to 5 aza-cytidine, vincristine, and prednisone therapy in previously treated childhood acute nonlymphocytic leukemia: a Southwest Oncology Group Study. 616 89

8 patients with acute myeloid leukaemia (AML), either at presentation or in remission, had normal T-cell subsets as defined by Fc receptors and monoclonal antisera. In contrast, a persistant excess of T lymphocytes staining with Leu 2a (defining suppressor cells) was noted in a case of AML in which persistant amegakaryocytic thrombocytopenia occurred after other haemopoietic lines had recovered from ablative chemotherapy. It is suggested that the 2a+ cells were involved in the suppression of megakaryocytopoiesis, and the phenotype of the lymphoid cells is compared and contrasted with previously described cases of other cytopenias associated with an excess of suppressor cells.
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PMID:A megakaryocytic thrombocytopenia associated with the excess of Leu 2a+ suppressor cells. 621 61


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