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)

In the first clinical study on GM-CSF in acute leukemias continuous infusion of the growth factor is given to patients in aplasia and at high risk of early death due to age over 65 years and/or intensive chemotherapy for resistance or relapse. Among 6 patients (4 AML, 2 ALL) receiving a total of 7 courses two died too early to contributing adequate data. Three patients and 4 courses showed earlier neutrophil recovery than related control groups and a fourth patient with secondary AML showed a neutrophil recovery time in the normal range, but much shorter than her platelet and reticulocyte recovery. No evidence was obtained so far for leukemic regrowth in these patients including blood and bone marrow cytology, monitoring of DNA aneuploidy by flow cytometry and clonogenic cells by colony assays. Thus, GM-CSF may be useful for rescue after intensive chemotherapy of AML and ALL and may not necessarily increase the risk of leukemia progression.
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PMID:Human recombinant granulocyte macrophage colony stimulating factor (GM-CSF) treatment of patients with acute leukemias in aplasia and at high risk of early death. 307 45

Patients with secondary acute myeloid leukaemia (AML) following treatment with alkylating agents and/or radiation show a poor response to standard induction therapy. Between 1983-1987 8 consecutive patients were treated with high-dose cytosine arabinoside (HD-ARA C; 3 g/sqm twice daily for 6 days) or intermediate-dose cytosine arabinoside (ID-ARA C; 0.5 g/sqm twice daily for 6 days). Complete remission was achieved in 3 patients (HD-ARA C: 2/3l; ID-ARA C: 1/5) and partial remission in 3 patients (ID-ARA C: 3/5). One patient (HD-ARA C) died during prolonged aplasia, one patient (ID-ARA C) proved refractory to treatment. The respective duration of remission in the 3 responsive patients was 3, 7 and 8 months. The probability of survival of the whole group was 50% after 12 months and 25% after 24 months. Our results confirm the efficacy of monotherapy with ARA C in the treatment of secondary AML. Consolidation therapy with ID-ARA C for 4 days seems to prolong remission.
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PMID:[High dosage and intermediate dosage cytosine arabinoside in the treatment of secondary leukemias]. 317 3

We analyzed clinical trials of low dose cytosine arabinoside (LDARA-C) in 324 patients with acute myelogenous leukemia (AML) and 129 patients with myelodysplasia (MDS). Complete and partial remission rates were 31% and 18%, respectively, in patients with AML, and 24% and 27% in patients with MDS. Toxicity was primarily hematologic. Although in vitro data suggested that LDARA-C acts as a differentiating agent, clinical data generally indicate a cytotoxic mechanism. Given the lack of effective therapeutic options in MDS and high risk AML (patients greater than 65 years old, secondary AML), these data are encouraging. LDARA-C warrants further study, comparing continuous infusion with intermittent subcutaneous administration and comparing LDARA-C to conventional dose therapy.
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PMID:Low dose cytosine arabinoside in myelodysplasia and acute myelogenous leukemia: a review. 331 46

Both mitoxantrone and etoposide have been shown to be active in monotherapy trials of relapsed and refractory acute myelogenous leukemia (AML). This phase II study was undertaken to assess the antitumor activity and toxicity of the combination in refractory and poor-risk AML. The regimen consisted of mitoxantrone, 10 mg/m2/d intravenously (IV), and etoposide, 100 mg/m2/d as short infusion, both on days 1 to 5. Sixty-one patients are evaluable for response and toxicity. Twenty-one were primarily refractory to conventional courses of cytarabine, daunorubicin, and thioguanine; 20 patients had poor-risk first relapse (relapse within 6 months of first complete remission [CR] or relapse under continuous maintenance therapy); 11 had second or subsequent relapses; and nine developed secondary AML after myelodysplastic phase or myelofibrosis. Twenty-six patients (42.6%) attained a CR and seven (11.5%) a partial remission (PR). The median duration of continuous CR was 4.7 months, with a range of 21 days to 14 months, excluding four patients who underwent autologous bone marrow transplantation. Severe myelosuppression was observed in all patients, with a median time to CR of 49 days. Nonhematologic toxicity included stomatitis (mainly grade 1 and 2) in 41 patients, nausea (mainly grade 1 and 2) in 44, infections (mainly grade 3) in 33, and fever of unidentified origin in 11. Other than transient, mild cardiac failure in nine patients, in some of them combined with grade 1 to 2 tachyarrhythmia, no other drug-related cardiac events were observed. Two cases of early death within the first 6 weeks of treatment were registered. Thus, the combination of mitoxantrone and etoposide is a highly active and well-tolerated regimen for refractory and poor-risk AML.
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PMID:Combination of mitoxantrone and etoposide in refractory acute myelogenous leukemia--an active and well-tolerated regimen. 342 60

A comparison of chromosome abnormalities between 31 cases of de novo acute nonlymphocytic leukemia (ANLL) with complex karyotypes and 30 cases of secondary ANLL or dysmyelopoietic syndromes (DMS) revealed significant differences. Hyperdiploidy and partial or complete monosomy 5 were more frequent in complex de novo ANLL, whereas, hypo or pseudodiploidy and partial or complete monosomy of chromosome #7 were more frequent in secondary ANLL/DMS. Monosomy 17 and partial deletion of the short arm of chromosome #12 (12p-) occurred more commonly in de novo ANLL and secondary ANLL/DMS, respectively, but were not statistically significant. Therefore, although the abnormalities found in the two groups were of the same basic type, the frequencies of occurrence differed. These findings suggest the role of as yet unknown agents in the etiology of some so called de novo ANLL, and that different mutagenic or carcinogenic agents may produce different chromosomal abnormalities.
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PMID:Complex chromosomal abnormalities in acute nonlymphocytic leukemia. 370 47

Cytogenetic studies, using improved short-term culture techniques, were performed on 64 patients with acute leukemia to determine the incidence and kinds of clonal karyotypic changes detectable with this newer methodology. An adequate number of analyzable mitoses was obtained from 59 patients. Clonal chromosomal alterations were found in 88% (52 of 59) of patients, as compared to approximately 50% in previous studies of acute leukemia in which conventional techniques were used. From our series, abnormal karyotypes were detected in 37 of 44 (84%) cases with primary acute nonlymphocytic leukemia, all 5 with secondary acute nonlymphocytic leukemia, and all 10 with acute lymphoblastic leukemia. Among the entire group of patients, several recurrent abnormalities were observed, e.g., -7 in eight cases, +8 in seven cases, t(15;17) in four cases, and t(8;21) or a variant of this translocation in four cases. In five patients, the only abnormality was a rather subtle structural rearrangement (e.g., tiny deletion). Five other patients had clonal changes which were found in less than 10% of the mitoses examined in each case. Our results indicate that most patients with acute leukemia, both acute nonlymphocytic leukemia and acute lymphoblastic leukemia, have clonal chromosome abnormalities associated with their disease.
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PMID:Chromosomal alterations in acute leukemia patients studied with improved culture methods. 385 85

A deletion of the long arm of chromosome #5 (5q-) occurs nonrandomly in human malignancies. As a rule, the deletion is interstitial; the distal breakpoint by conventional techniques is usually in band q32, the proximal breakpoints in q12 or q14. Variant breakpoints occur in less than 10% of all cases. As the sole anomaly, 5q- is characteristically found in refractory anemia with or without excess of blasts. It can occur as the sole anomaly in de novo or secondary acute nonlymphocytic leukemia, but is usually accompanied in those disorders by other chromosome changes that are also nonrandomly distributed. In addition, it can be found in lymphoproliferative disorders, and occasionally, also in solid tumors. The 5q- myelodysplastic syndrome typically occurs in older age groups, particularly in females. Characteristic features are macrocytic anemia, normal or elevated platelets in the presence of megakaryocytic anomalies, and a mild clinical course. In cases with 5q- only, transformation into ANLL occurs rarely. Additional chromosome anomalies and male sex are prognostically unfavorable signs. Sex ratio is also at the disadvantage of females in de novo 5q- ANLL, and the latter disorder can occur without being preceded by a myelodysplastic phase. A myelodysplastic phase usually precedes 5q- secondary leukemia, in males as well as in females, and additional chromosome anomalies, especially of chromosome #7, are almost invariably present in those cases. We conclude that 5q- is the most frequently occurring single chromosome anomaly in secondary leukemia. Furthermore, the resemblance between de novo and secondary 5q- MDS and ANLL is striking; clinically, as well as cytogenetically, they are indistinguishable, suggesting that all de novo cases may be due to environmental (chemical) carcinogens. Response to treatment and prognosis are very poor with current therapeutic regimens in de novo as well as in secondary 5q- ANLL. Morphologically, these ANLLs fall into all FAB categories. There is considerable evidence to show that the 5q- anomaly occurs in a myeloid precursor stem cell. The occasional occurrence in lymphoid malignancies, of B cell as well as T cell type, suggests that, as in Ph-positive disorders, a common progenitor stem cell may be affected in 5q- also. The 5q- lymphoid malignancies, however, are much more rare; it is not clear at the present time whether or not a 5q- counterpart of Ph-positive ALL exists, and mixed lymphoid-myeloid 5q- disorders have not yet been documented.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The 5q-anomaly. 389 Oct 74

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

A register of 746 cases of secondary acute leukemias has been established by reviewing the literature from 1930-1980. Out of these 680 belong to acute nonlymphocytic leukemias, FAB M1-M6. Data have been subjected to a multiparameter analysis in term of previous therapy and subtype characteristics of acute nonlymphocytic leukemia (ANLL). There are indications that secondary ANLL are characterized by the preponderance of early acute myeloblastic leukemias if compared to de novo ones. Furthermore it has been shown that alkylating agents induced decidedly more acute myelomonocytic leukemias whereas irradiation tended to induce more acute myeloblastic leukemia. Since secondary acute leukemias represent a serious late consequence of alkylating agent and irradiation therapy it is high time to find new therapeutical modalities for lymphomas and to consider the withdrawal of alkylating agents from the therapy of autoimmune disorders.
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PMID:Characteristics of secondary acute nonlymphocytic leukemias. Cytological aspects (a review). 620

Two cases of secondary acute nonlymphocytic leukemia developing after combined chemo-radiotherapy for Hodgkin's disease (HD) are reported. The first case was a 28-year-old woman with PSIIIsA HD, treated with total lymphoid irradiation followed by combination chemotherapy that was almost entirely ABVD (Adriamycin, bleomycin, vinblastine, dacarbazine), who developed acute monoblastic leukemia three years after the diagnosis of Hodgkin's disease. We believe this to be the first reported case of secondary leukemia associated with the combination of radiotherapy and ABVD chemotherapy. The second case was a 37-year-old man with Stage IVB Hodgkin's disease, treated with radiotherapy and MOPP (nitrogen mustard, vincristine, procarbazine, prednisone) who developed acute myeloblastic leukemia five years after the diagnosis of Hodgkin's disease. Both cases showed typical changes of panmyelosis demonstrated by cytochemical and ultrastructural studies. In both cases, bone marrow cells had a dominant clone with a markedly abnormal karyotype. The nature of therapy-related secondary leukemia after Hodgkin's disease and its relationship to current modes of treatment are discussed.
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PMID:Secondary leukemia following treatment of Hodgkin's disease: ultrastructural and cytogenetic data in two cases with a review of the literature. 634 27


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