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

A 57-year-old female presented with general fatigue. She had neither lymphadenopathy nor hepatosplenomegaly. Laboratory data revealed anemia and leukopenia (1,500/microliters) with a differential count of 4.5% leukemic cells. The myelogram revealed 34.4% leukemic cells, of which diameter ranged from 20 to 28 microns. The diagnosis was acute myelogenous leukemia (FAB: M2) with myelodysplasia. Cytogenetic analysis revealed that the leukemic cells had chromosome abnormalities involving both diploidy and tetraploidy with structural rearrangement. Structural rearrangement included del(5) (q22q33), del(15) (q22q24), and t(3; 12) (q25;p13). Small dose aclacinomycin-A treatment was effective in reducing the number of leukemic cells in bone marrow, and both anemia and leukocytopenia were improved.
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PMID:[Acute myelogenous leukemia transformed from myelodysplastic syndrome with tetraploid chromosome constitution]. 160 14

Relapse continues to be a problem after bone marrow transplantation (BMT) for hematologic malignancies, particularly in recipients of autologous or T-cell-depleted allogeneic grafts and in patients with advanced disease. Interferon (IFN) has shown antiproliferative activity in several malignant hematologic diseases and potentially may be of benefit when administered early after BMT when the number of residual cells is minimal. We tested in a phase I study the maximum tolerated daily dose of recombinant IFN alpha-2b in patients who had received a transplant for a disease at high risk for relapse (acute myeloid leukemia or non-Hodgkin's lymphoma beyond first remission, advanced myelodysplastic syndrome, acute lymphoblastic leukemia at any stage, chronic myeloid leukemia in accelerated or blast phase. Recombinant IFN alpha-2b was started at a dose of 0.5 x 10(6) IU/m2 and escalated by 0.5 x 10(6) IU/m2 in groups of three or four patients. The intention was to administer IFN as soon as stable engraftment after BMT was achieved (defined as an absolute neutrophil count of greater than 2.0 x 10(9)/L and platelet count greater than 100 x 10(9)/L for 5 consecutive days) and continued for 2 months. A total of 14 patients were enrolled after autologous (n = 3) or allogeneic (n = 11) BMT. Dose-limiting toxicity was myelosuppression. Significant (grade 2 to 4) neutropenia and thrombocytopenia led to discontinuation or dose reduction in five of eight patients receiving 1.5 x 10(6) or 2 x 10(6) IU/m2 IFN. Mild to moderate (grade 1 or 2) anorexia, weight loss, and fatigue occurred in the majority of patients independent of the IFN dose. De novo acute GVHD responsive to steroid treatment developed in 3 of 11 allograft recipients. Natural killer (NK) cell function was low before IFN treatment and was not improved with the cytokine. Conversely, interleukin-2-activated NK cells showed normal function even before starting IFN and no change was seen during IFN treatment. Clonogenic hematopoietic progenitor studies showed depression of all progenitor lines (colony-forming unit [CFU]-granulocyte, erythroid, monocyte, megakaryocyte, CFU granulocyte-macrophage, burst-forming unit-erythroid) by IFN at all dose levels except at 0.5 x 10(6) IU/m2. Considering this result and the incidence and severity of marrow depression seen at doses greater than 1.0 x 10(6) IU/m2, we would consider this the maximum dose safely tolerated if IFN alpha-2b is administered in this setting for a prolonged course on a daily basis.
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PMID:Treatment with recombinant interferon (alpha-2b) early after bone marrow transplantation in patients at high risk for relapse [corrected]. 174 91

Low-dose aclarubicin (LDACR) therapy is one of the differentiation induction therapy, such as low-dose cytosine arabinoside therapy, 1 alpha, 25 dihydroxy-vitamin D3 or retinoic acid therapy, for myelodysplastic syndrome and atypical leukemias. A 36-year-old female with hypoplastic acute myelogenous leukemia was treated with this atypical leukemias. A 36-year-old female with hypoplastic acute myelogenous leukemia was treated with this LDACR therapy. On admission, she was suffered from general fatigue and her peripheral blood smear showed pancytopenia with 23% of myeloblasts. Bone marrow examination revealed a moderately hypoplastic marrow with 35.4% of myeloblasts. She was diagnosed as having hypoplastic acute myelogenous leukemia. Thereafter, 20 mg of aclarubicin was given daily by one-shot intravenous injection for 10 days. After this LDACR therapy, myeloblasts disappeared from her peripheral blood and pancytopenia improved. Bone marrow examination showed increase in nuclear cell counts and she achieved complete remission. In this article, we report the clinical course of this patient and discuss the effect of LDACR therapy as useful chemotherapy for this patient.
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PMID:[Hypoplastic leukemia successfully treated with low-dose aclarubicin: a case report]. 194 47

The new fluorinated adenine analog, fludarabine, has been tested for efficacy in many tumor types over the past ten years. Two other similar nucleoside analogs are currently available for commercial use. Cytarabine is used principally as an antileukemic agent, and vidarabine as an antiviral. Unlike vidarabine, fludarabine is resistant to deactivation by adenosine deaminase. Data from Phase I and II trials suggest that fludarabine is potentially effective in a number of leukemias, including acute lymphocytic leukemia, acute nonlymphocytic leukemia, and chronic lymphocytic leukemia (CLL). Unfortunately, the doses required to achieve adequate response in the acute leukemias (greater than 75 mg/m2) were above the maximum tolerated dose, resulting in intolerable granulocytopenia, thrombocytopenia, and a life-threatening neurotoxic syndrome. In CLL: however, the dose required to achieve a satisfactory response is well within tolerated limits. Long-term survival statistics are not yet available, but historical perspective strongly correlates response to other agents with increased survival times. Toxicities seen at dose regimens of 15-40 mg/m2/d for five consecutive days include somnolence, metabolic acidosis, confusion, fatigue, nausea, vomiting, increase in serum creatinine and aminotransferase concentrations, and pulmonary and hepatic abnormalities. Mild to severe hematologic toxicity has been observed at all dose levels.
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PMID:Fludarabine: a review. 206 37

As part of a multicenter trial 12 patients with myelodysplastic syndromes (MDS) were treated with 14-day-cycles of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF; 250 micrograms/m2 day s.c.). In addition, all patients received 20 mg/m2/day s.c. cytosine-arabinoside (Ara-C) 12 h after GM-CSF except for patients suffering from refractory anemia (RA) according to FAB classification. Courses were repeated after 4 weeks. In 11 evaluable patients, results according to FAB-classified MDS were as follows: RA, 1/2 response (R), 1/2 stable disease (SD); RAEB, 2/3 R, 1/3 SD; RAEB-T, 1/6 CR, 1/6 PR, 2/6 R, 2/6 progression; CMML, 1/2 SD. In 2 patients with RAEB-T, overt acute myeloid leukemia was observed 2 and 10 weeks after initiation of treatment. With few exceptions, treatment resulted in a prompt increase in granulocytes and eosinophiles. This was associated with improvement of infectious complications. Increases in red cells and platelets occurred variably and was apparently associated with responses of the underlying disease. Dose limiting side effects consisted of fever, severe fatigue and dolent local reactions at the site of GM-CSF injection. In addition, nausea and diarrhoea occurred frequently. Less often, respiratory and cardiovascular side effects were encountered. In summary, GM-CSF +/- Ara-C in MDS results in objective remission with manageable toxicity. Conceivably, this regimen will serve as a base for future treatment strategies against MDS.
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PMID:Recombinant human granulocyte-macrophage colony-stimulating factor and low-dose cytosine-arabinoside in the treatment of patients with myelodysplastic syndromes. A phase II study. 218 22

A 38-year-old male admitted to the Internal Medicine of Surugadai Nihon University Hospital, complaining of general fatigue and throat pain. The laboratory examinations revealed leukocytosis (83, 900/microliters) and an appearance of myeloblasts (90.2%) in the peripheral blood. The nucleated cell count was 56 x 10(4)/microliters with 85.5% myeloblasts in bone marrow. He was diagnosed as acute myeloblastic leukemia (AML). Though he received two courses of combination chemotherapy with daunorubicin, BH-AC, 6 MP and prednisone, one course of combination with mitoxantrone, etoposide and cytosine arabinoside and one course of combination with aclarubicin cytosine arabinoside and prednisone, he could not achieved remission. A chromosome analysis revealed 46, XY del(5)(q22). The amount of DNA fragments hybridized to 4.5 Kb v-fms probe in blastoid cells was approximately a half amount of normal persons. It is not defined the relationship between the decrease of fms and leukemia in this case. He was diagnosed de novo AML, since he had not been received the therapy with potential mutagenic and carcinogenic agents and had not been exposed the irradiation on his works.
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PMID:[Acute myeloblastic leukemia associated with 46, XY, del(5)(q22)]. 221 95

A 57-year-old woman who suffered from acute myeloblastic leukemia during the course of chronic thyroiditis, is described. The patient was diagnosed as having chronic thyroiditis in 1984 when she was 53 year-old, and was treated with L-T4.Na. She admitted in July 1988 because of general fatigue, fever, cough and sore throat. On admission, hematological examination in the peripheral blood showed marked anemia and increased leukocytes with 20.5% leukemic cells positive for peroxidase staining. Bone marrow aspiration showed 38.8% leukemic cells. She was diagnosed acute myeloblastic leukemia. She reached complete remission after combination chemotherapy. The case of acute myeloblastic leukemia associated with chronic thyroiditis is rarely reported. We reviewed the literature and discussed acute myeloblastic leukemia associated with chronic thyroiditis including this case.
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PMID:[Acute myeloblastic leukemia associated with chronic thyroiditis]. 269 19

We report a patient with acute nonlymphocytic leukemia (FAB classification: M 2) with trisomy 4, which is the first case in our country. A 42-year-old man was admitted to our hospital because of fever and general fatigue in May, 1988. His WBC count was 8,100/microliters with 90% of leukemic cells and bone marrow smear showed 76.1% leukemic cells. The chromosomal analysis of marrow cells by G-banding revealed 47, XY, +4. In spite of administration of chemotherapy complete remission was not obtained, and he died of septic shock and severe liver damage 4 months after making the diagnosis. Chromosomal abnormality of trisomy 4 has been reported to be associated with predominantly either M 4 or M 2, and to be less than 0.1% of incidence in ANLL, according to the Second MIC Cooperative Study Group. It is suggested that trisomy 4 may be caused by exposure to some environmental factors such as toxic substances, since this chromosomal abnormality has been reported in the last 10 to 20 years.
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PMID:[Chromosomal abnormality of trisomy 4 in a patient with acute nonlymphocytic leukemia (FAB: M2)]. 269 22

A 23-year-old male who had suffered recurrent relapses of acute myelocytic leukemia was treated with a protocol including neocarzinostatin (NCS) and complete remission was obtained. At the age of 11 years, he had complained of general fatigue and anemia, and was diagnosed as having AML because of the presence of leukemic cell infiltration in the bone marrow as well as peripheral blood. Auer bodies and a positive reaction to peroxidase were found. The last episode of relapse occurred at the age of 15 years, when he achieved complete remission following a trial protocol which included NCS. NCS seemed to be effective after it had been used intravenously for a short time. The patient has maintained complete remission for the past 7 years and has had no consolidation therapy in the last 3 years. For the last 18 months, he has been working in a market as a clerk 8 hours a day. NCS with a rapid infusion time seems to have effects on leukemic cells when it used with proteolytic enzyme. Neither skull radiation nor testicular biopsy were attempted. Results of CSF examination were within normal limits, but EEG and CT scan revealed the probability of early-stage leukoencephalopathy, although no significant clinical signs were observed. He had suffered an asthmatic attack before the onset of AML, but no further attack occurred until several months ago. In order to establish any relationship between these two diseases, further detailed analysis will be necessary.
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PMID:[A case of complete remission following recurrent relapses 12 years after onset of acute myelocytic leukemia. Response to protocol including neocarzinostatin]. 296 38

A 76-year-old woman with acute myelogenous leukemia with approximately 65% myeloblasts on bone marrow examination was treated daily with a combination of 4 megaU of leukocyte interferon IM and 1,000 mg cimetidine PO. During therapy there was a gradual decrease of bone marrow myeloblasts down to 9% and a normalization of peripheral white blood cells. The treatment was discontinued after 6 weeks because of increasing fatigue and anorexia. The general condition improved greatly during the following weeks and the patient entered complete remission, which has continued for 6 months so far. In the course of therapy there was a gradual appearance of antibodies showing a selective binding capacity to autochthonous leukemic cells with no tendency to increased binding to remission cells. The aim of this report is to stimulate a further evaluation of this form of therapy in additional AML patients whenever this might be justified as an alternative to conventional chemotherapy.
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PMID:Complete remission in a patient with acute myelogenous leukemia treated with leukocyte alpha-interferon and cimetidine. 658 32


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