Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We treated a patient with chronic granulocytic leukemia (CGL), in the accelerated phase by intensive chemotherapy followed by the infusion of cryopreserved peripheral blood buffy-coat cells. The cells had been stored for 32 months. The chemotherapy consisted of daunorubicin 40 mg X 2 days, vincristine 2 mg X 1 day, cytosine arabinoside (Ara-C) 200 mg X 6 days and prednisolone 30 mg X 7 days in the first week, then Ara-C 3 g/m2 X 3 days and cyclophosphamide 60 mg/kg X 2 days in the second week, but reversion to the chronic phase was not achieved. Therefore, total body irradiation (TBI) was added to repeated intensive chemotherapy followed by infusion of the remaining cells. Marrow recovery was good. The patient is currently alive and has been in the chronic phase for 22 months. This preliminary result indicates that this therapy may be tried soon after transformation in CGL and that TBI is an important part of therapy in BMT in the accelerated or blastic phase of CGL.
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PMID:Treatment of chronic granulocytic leukemia in the accelerated phase by transfusion of autologous buffy-coat cells--a case report. 233 Aug 6

The serum concentrations of Ara-C are in the range from 10(-6) to 10(-8) M in LD-Ara-C treated patients. The growth of CFU-GM from bone marrow of healthy volunteers was depressed depending on Ara-C-concentration applied in vitro. The growth of CFU-L from peripheral blood of two patients with AML (M 2) and one patient with CML in blast crisis was differently influenced by Ara-C-application in vitro. An elevated proportion of mature cells was observed in smears of cultured cells with Ara-C from two patients. The usefulness of Ara-C for a differentiation inducing therapy is discussed.
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PMID:[Effect of cytosine arabinoside on the differentiation of granulocyte-monocyte progenitors (CFU-GM) and myeloid leukemia blasts (CFU-L) in vitro]. 246 64

The therapeutic potential of recombinant interferon gamma (IFN gamma) alone or in combination with two cytotoxic drugs - 5-fluorouracil (5-FU) and cytosine arabinoside (Ara-C) - was studied in vitro on two myeloid leukemia systems: HL60 promyelocytic cell line and chronic granulocytic leukemia (CGL) progenitor cells. When applied individually, IFN gamma and the drugs inhibited in a dose-dependent manner HL60 cell colony formation in semisolid culture. Moreover, IFN gamma or the cytotoxic drugs dose-dependently reduced the colony formation of CGL progenitor cell in agar. When added in combination, IFN gamma potentiated synergistically the inhibitory action of 5-FU in both systems. The most pronounced potentiation was detected at concentrations of 0.5 microgram/ml 5-FU and 50 U/ml IFN gamma. On the contrary, the antiproliferative effect of Ara-C was enhanced only subadditively when combined with IFN gamma. In view of the present findings, which are supported by new evidence from the literature, the use of 5-FU in leukemia should be reconsidered. The results further imply the potential value of combined treatment of 5-FU and IFN gamma in leukemia.
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PMID:New combination of 5-fluorouracil and interferon-gamma effective against human myeloid leukemia in vitro. 251 May 79

Ara-C sensitivity test and suicide tests of L-CFU using [3H] deoxycytidine (dCyd) and [3H] thymidine (TdR) were performed in patients with acute nonlymphocytic leukemia (ANLL) and with chronic myeloid leukemia in blastic crisis (CML-BC). We found a correlation between ara-C sensitivity and the [3H] dCyd suicide test of L-CFU (p less than 0.001); and between ara-C sensitivity and the [3H] TdR suicide test (p less than 0.05). These results suggest that the [3H] dCyd suicide test reflects the degree of activity of ara-C metabolism in L-CFUs.
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PMID:[Relationship between Ara-C sensitivity of leukemic-colony forming units (L-CFU) and [3H] deoxycytidine suicide test of L-CFU]. 261 40

Ph1-positive chronic myelocytic leukemia (CML) developing in a treated case of acute promyelocytic leukemia (APL) is reported. The patient was a 62-year-old male who was diagnosed as having APL in December 1978. He was treated with daunorubicin, Ara-C and 6MP and a complete remission was obtained 4 months later. But APL recurred in February 1981. He was treated with BHAC, aclarubicin, 6MP and prednisolone. He remained in continuous complete remission for 5 years, when all therapy was discontinued. After then, the leukocytes count continued to rise and a diagnosis of Ph1-positive CML was made in September 1986. His leukocytes count has been well controlled with the use of busulfan. The event in this case suggests a possibility of the Ph1-positive CML being a secondary disease related to prior long term chemotherapy.
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PMID:[Chronic myelocytic leukemia following chemotherapy of acute promyelocytic leukemia]. 269 21

Knowing the good penetration of systemic HDara-C into the CNS, we treated with this approach overt meningeal leukemia, either isolated or with bone marrow (BM) disease, in 31 adults: 18 ALL, 4 ANLL, 1 lymphoid blast crisis of CGL (LBC-CGL), and 8 non-Hodgkin's lymphoma (NHL). Treatment consisted of Ara-C, 3 g/m2 i.v. q 12 h, by 3 h infusion for 8 doses, followed by 4 doses at day 21. Complete remitters received consolidation with four monthly 4-dose courses of HDara-C. Additional multidrug consolidation and direct CNS therapy with intrathecal (i.t.) methotrexate (MTX) or Ara-C +/- cranial RT was administered to the 11 remitters last treated. Twenty of 31 patients (64%) achieved CR: 10/10 with isolated meningeal leukemia and 10/21 with concurrent CNS and BM disease. Of the remaining 11 patients, 8 had cerebrospinal fluid (CSF) clearing with persistent BM disease. In all cases but one CNS symptoms resolved promptly. CR median duration was 6 months (range 2 to 20). The main toxicity was myelosuppression requiring intensive support. There was no neurologic toxicity. These results show that systemic HDara-C is highly effective in acute leukemias and NHL with CNS involvement, and suggest the utility of this regimen for sanctuary chemoprophylaxis in patients at high risk for CNS disease.
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PMID:Central nervous system (CNS) leukemia: the role of high dose cytarabine (HDAra-C). 271 52

We report a 17-year-old female with chronic myeloid leukemia (CML) who developed monocytic crisis. She was diagnosed as chronic phase of Ph1-chromosome positive CML at 14 years old. Three years after the diagnosis of the disease, she was admitted to the hospital because of low grade fever, lethargy and marked splenomegaly. Small dose of Ara-C relieved her symptoms and splenomegaly. Six months later, however, a marked leukocytosis over 70,000/microliters were observed, and the peripheral blood smear disclosed that about 80% of the leukocytes were relatively mature monocytoid cells. Chromosomal analysis revealed additional abnormalities (double Ph1, +8, +9, +19). Lysozyme levels in serum and urine were high and NAP score was elevated. These monocytoid cells expressed receptors for IgG-Fc and C3, phagocytic activity, and monocytoid antigens which were determined by monoclonal antibodies (MY4, Mo2, OKM5). Cytochemically, almost all of monocytoid cells were positive for peroxidase and naphthol-ASD-chloroacetate esterase (CAE), but the monocytoid cells positive for non-specific esterase were limited. These data suggested that this case was monocytic crisis in CML with proliferation of CAE positive monocytoid cells. Among several types of blast crisis, monocytic crisis is extremely rare condition. The definite monocytic crisis demonstrated by this case may support the hypothesis that target cells of CML are pluripotent hematopoietic precursors.
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PMID:[Monocytic crisis in chronic myeloid leukemia: a case report]. 276 61

A high dose of cytosine arabinoside (ara-C) was given to 51 patients during consolidation therapy or with refractory or relapsed acute leukemia. Ara-C was administered as a 3-hour infusion at a dose ranging from 2 to 3 g/m2 every 12 hours, diluted in 500 ml of 5% dextrose in water for 2 to 6 days. Complete remission was attained in 3 (25%) of 12 evaluable patients. Two with blast crisis of chronic myelogenous leukemia of these did not obtain complete remission. Death due to marrow aplasia occurred in five patients, and two of these had relatively good performance status and were given a dose of 3.0 g/m2 x 8 or 12 of ara-C. At a dose of 3.0 g/m2 x 6, the mean duration of granulocytes of less than 100/mm3 was 6.7 days. This duration seemed to be manageable myelosuppression. Therefore, 3.0 g/m2 x 6 was thought to be an adequate dose. Seizure occurred in one patient, and conjunctivitis was seen in another. In conclusion, from the manageable myelosuppression observed, administration of 3.0 g/m2 x 6 of ara-C seemed to be an adequate dose.
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PMID:[High-dose cytosine arabinoside treatment of leukemia with special reference to the optimal number of doses]. 277 89

The effect of LD Ara-C (10(-8) mol/l) (Ara-C), TPA (1.6 x 10(-7) mol/l) and 13-cis-retinoic acid (RA) (10(-6) mol/l) on the differentiation in liquid culture of bone marrow cells from 5 patients with acute lymphoblastic, 17 patients with acute myelogenous leukemia, 1 patient in myeloid and 1 in lymphoid crisis of chronic granulocytic leukemia was studied. Ara-C induced morphological and cytochemical differentiation into monocytic cells in 2 cases (M1, M5 type). TPA induced convincing morphological and cytochemical features of maturation into monocytic cells in 4 cases (two M1, one M2, and one M5 type) and into differentiated myeloid cells in 2 cases (M1, M4 type). RA in one case (M2 type) out of three AML studied induced cytochemical and immunocytochemical features of maturation. The results of the study indicate that although TPA is a better inducer of blast cell differentiation than Ara-C, however, neither is a potent differentiation agent of leukemic blasts in liquid culture. The heterogeneity of leukemic blasts within the same type of leukemia was confirmed by their different response to differentiating agents.
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PMID:Study of differentiation of fresh human leukemic cells by low dose cytosine arabinoside (LD Ara-C) and 12-O-tetradecanoylphorbol-13-acetate (TPA). 281 52

High doses of cytosine arabinoside (ara-C) were administered by continuous infusion to 24 patients with acute leukemia in relapse or blast phase of chronic myelogenous leukemia (CML). Ara-C was infused at a dose rate of 250 mg/M2/hr for 36 to 72 hr. The major toxicities were myelosuppression, diarrhea, and abdominal pain. Other toxicities included pulmonary edema, neurotoxicity, and liver function abnormalities. The gastrointestinal toxicity was dose-limiting and a phase II dose was established at 250 mg/M2/hr for 60-72 hr. Four patients treated with this dose schedule had objective responses. Two patients with CML in blast phase returned to chronic phase and have remained stable without maintenance therapy for 12 and 18 months. Two patients with acute myelogenous leukemia in relapse entered complete remissions which continued unmaintained for 4 and 6 months. Steady-state plasma ara-C levels ranged between 7 and 24 x 10(-6) M, while ara-U levels were as high as 4.5 x 10(-4) M. There was no detectable accumulation of ara-C or ara-U during the infusion period. These findings would suggest that the continuous infusion of high dose ara-C may be useful in the treatment of acute leukemia and CML in blast crisis.
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PMID:Prolonged high dose ARA-C infusions in acute leukemia. 328 17


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