Protective effect of ß-glucan and glutamine on intestinal and immunological damage in mice induced by cytarabine (Ara-C) / Efeito protetor do ß-glucano e glutamina em lesões intestinais e imunológicas induzidas por ciratabina (Ara-C) em camundongos

Recently, glutamine and ß-glucan have been demonstrated to play an important role in modulation of the immune system and in promoting intestinal health benefits. The aim of this study was to investigate the effect of this intervention on inflammatory responses and intestinal health in mice orally pretreated with soluble Saccharomyces cerevisiae derived 1,3/1,6-ß-glucan (80mg/kg) with or without glutamine (150mg/kg) and then challenged with cytarabine (Ara-C) (15mg/kg). Improvements in villi and crypts were not observed in the ß-glucan group. The intestinal morphometry in the glutamine group showed the best results. ß-glucan in combination with glutamine presented the highest values of IL-1ß and IL-10 and lowest values for leukocytes and INF-γ. Based on these results, combined ß-glucan and glutamine pretreatment reduced intestinal inflammation and improved the immune response after Ara-C challenge.(AU)

Recentemente, glutamina e ß-glucano têm demonstrado desempenhar um papel importante na modulação do sistema imune e na promoção de benefícios para a saúde intestinal. O objetivo deste estudo foi investigar o efeito dessa intervenção sobre as respostas inflamatórias e saúde intestinal de camundongos pré- tratados por via oral com 1,3/1,6-ß-glucano (80mg/kg) derivado de Saccharomyces cerevisiae com ou sem glutamina (150mg/kg) e posteriormente desafiados com citarabina (Ara-C) (15mg/kg). Melhoras em vilosidades e criptas não foram observadas no grupo de tratamento com ß-glucano. A morfometria intestinal no grupo de tratamento com glutamina apresentou os melhores resultados. O grupo em que foi utilizado ß-glucano em combinação com glutamina apresentou os maiores valores de IL-1ß e IL -10 e valores mais baixos para os leucócitos e INF-γ. Com base nestes resultados, o pré-tratamento de ß-glucano combinado com glutamina reduziu a inflamação intestinal e melhorou a resposta imune após o desafio com Ara-C.(AU)

Mecanismos de resitência as antraciclinas e a citarabina em leucemia mielóide aguda / [Mechanisms of resistance to anthracyclines and cytarabine in leukemia acute myeloid]

A leucemia mielóide aguda (LMA) é uma doença heterogênea em relação às características citogenéticas, moleculares, resposta ao tratamento, sobrevida global e livre de doença. A maioria dos pacientes apresenta recidiva precoce e evolui para o óbito devido à resistência à quimioterapia. O tratamento atual, baseado na associação das antraciclinas Idarrubicina (IDA) ou Daunorrubicina (DNR) com a Citarabina (Ara-c), se mantém por mais de 40 anos apesar dos resultados insatisfatórios. Objetivos: Avaliar os mecanismos de resistência aos quimioterápicos IDA, DNR e Ara-c, em linhagens celulares e em amostras de pacientes com LMA. Metodologia e Resultados: O perfil de resistência das linhagens HL60, Kasumi e U937 foi comparado por imunofenotipagem, citogenética, expressão e atividade das proteínas transportadoras de efluxo: glicoproteína P (Pgp), MRP1 e BCRP e expressão de proteínas envolvidas com a evasão da apoptose. Para avaliar a sensibilidade aos quimioterápicos foram utilizados o ensaio de viabilidade celular (MTT), fragmentação do DNA e ativação de caspase 3. As linhagens celulares foram comparadas, entre si em relação à sensibilidade e resistência aos fármacos. A IDA foi mais eficiente em reduzir a viabilidade celular na linhagem HL60, a IDA e a DNR na linhagem Kasumi, sendo o Ara-c o mais eficiente em reduzir a viabilidade na linhagem U937. O perfil de resistência da linhagem HL60R foi analisado através de um array de proteínas fosforiladas, onde encontramos diversas vias de sinalização inibidas na linhagem resistente como a via de sinalização das MAPKs JNK e p38, importantes para o processo de indução de apoptose pelos quimioterápicos. Foi verificado que a ativação de tais vias de sinalização pelos quimioterápicos esta diminuída nas linhagens de LMA resistentes em comparação com as linhagens sensíveis. As vias de sinalização de JNK e p38 nas linhagens de LMA foram inibidas com RNA de interferência. Tal inibição resultou na redução da sensibilidade aos quimioterápicos na linhagem Kasumi e U937, aumento da expressão da Pgp e do miR-27a. A análise das amostras de pacientes com LMA mostrou alta expressão do miR-27a quando comparadas com as amostras dos doadores saudáveis. No entanto, a expressão do miR-27a apresentou baixa correlação com a Ppg e diferenças na sobrevida global apenas em 12 meses após o tratamento. A técnica do CRISPR foi utilizada para editar/silenciar os genes JNK e p38 a fim de corroborar os resultados com o silenciamento. Nossos dados sugerem que alterações na fosforilação das MAPKs JNK e p38, envolvidas no processo de indução de apoptose, estão associadas à resistência aos quimioterápicos na LMA.

Experimental study on influence of cytarabine on K562 cells proliferation and apoptosis by autophagy pathway / 重庆医学

Objective To investigate the effect of cytarabine (Ara-C) on proliferation and apoptosis of human erythroleukemia K562 cell linethrough autophagy pathway and its possible mechanism.Methods The cellular proliferation inhibiting rate after different concentrations of Ara-C acting for 24,48 h was detected by CCK-8;the cell cycle and apoptosis were detected by flow cy tometry(FCM);the chromatin morphological changes in nucleus were observed by Hoechst staining;the cell acidic autophagy vesicles were detected by acridine orange staining;the expression changes of p38 and p-p38 proteins were detected by Western blot.The expressions of autophagy apoptosis related gene and protein were examined by RT-PCR and immunofluorescence.Results The CCK-8 results found that different concentrations of Ara-C could inhibit the proliferation of K562 cells with dose-and time-dependent manners.FCM detecting indicated that Ara-C could increase apoptosis and could arrest the cell cycle at S phase;Hoechest staining showed that K562cells had typical apoptotic morphological changes after Ara-C treating;the Acridine orange staining revealed that Ara-C caused the inclease of the green fluorescene in cells of the Ara-C group,and the cells appeared a great number of acidic autophagy vesicles;RT-PCR results showed that Ara-C up-regulated the expression of autophagy key genes Beclin-1,LC3A and LC3B;Western blot results showed that Ara-C increased the expression of phosphorylated p-p38.Immunofluorescence results showed the expression of LC3B was significantly enhanced.Conclusion Ara-C canactivate p-p38 mediated K562 cells to generate autophagy,then inhibit the cell proliferation and promotes apoptosis.

Docosahexaenoic Acid Reduces Cyto-Genotoxicity of Cytosine Arabinoside in Normal Mouse Bone Marrow.

Aims: This paper evaluates the use of percentage of micronucleus (MN), polychromatic erythrocytes (PCEs), chromosomal aberration (CA) and mitotic index (MI) frequencies in mice bone marrow smears as a method for assessing the ability of docosahexaenoic acid (DHA, is an omega-3 fatty acid) to reduce cyto-genotoxicity damage of cytosine arabinoside (ara-C). Ara-C is widely prescribed antineoplastic drug, especially for the treatment of acute myeloid leukemia. It is a pyrimidine analog, in which the ribose sugar of cytidine is replaced by arabinose moiety. Methodology: Positive control group of mice was only given intraperitoneal dose of ara- C of 75 mg/kg (every 12 h for 5 days); this dose was selected in accordance with its human therapeutic values. Negative control group of mice group only received 0.1 ml sterile distilled water every 12 hours for 5 days. Three treatment groups of mice were given same dose of ara-C in addition to three different doses of DHA (125, 250 and 500 mg/kg of mice). Experimental data were analyzed using (Mann–Whitney U-test) to compare values of positive and negative controls. However, Kruskal–Wallis test followed by Dunn’s multiple comparisons test were used to compare values of treatments with positive control. All values were accepted at p = 0.05. Results: When 75 mg/kg ara-C was applied, positive control group showed a significant increase in MN and CA, a high decrease in PCE, and a significant decrease in MI. When DHA was used with ara-C, the picture is changed, particularly at a medium dose of DHA of 250 mg/kg where a decrease MN and CA and an increase in PCEs in addition to an increase in MI were observed. Conclusion: DHA at 250 mg/kg was able to reduce cytogenotoxicity of ara-C, and lead to protecting the normal proliferating cells in bone marrow from the damaging effect of ara-C and hence improving therapy by ara-C.

Sorting,identification and enrichment of side population cells in acute monocytic leukemia THP-1 Cells / 中华实用儿科临床杂志

Objective To assay and determine whether the human acute monocytic leukemia cell line THP-1 contains side populations (SP) cells,and to increase the proportion of SP cells using cytarabine (Ara-C).Methods Fluorescent microscope and flow cytometry (FCM) were employed for detecting the percentage of SP cells in THP-1 cells.Then,SP and non-SP (NSP) subpopulations were collected and identified.Finally,THP-1 cells were incubated with different concentrations of Ara-C for 24 hours and detected the proportion of SP cells,respectively.Results The results demonstrated that the percentage of SP cells was (1.81 ± 0.99) ％ in THP-1 cells.A majority of the SP cells remained in the G0/G1 phase,and the expressions of CD34 + and CD34 + CD38-and the proliferative ability of the SP cells were higher than those of NSP cells (P ＜ 0.05).The mRNA expression of multidrug resistance genes (ABCG2,ABCB1),apoptosis regulation genes (Bcl-2) and the Bcl-2/Bax ratio of SP cells were higher than those of NSP cells.SP cells have been shown to be more tumorigenic than NSP cells.After co-culture with Ara-C,the proportion of SP cells increased significantly and presented in a concentration-dependent manor.Conclusions All of these findings suggest that the THP-1 cell line contains SP cells and the SP cells possess some intrinsic stem cell properties.The proportion of SP cells can be increased when co-cultured with Ara C,and this technique is a useful and important application for the study of LSCs.

Effects of FLAG regimen and IA regimen for acute myeloblastic leukaemia cells on P-glycoprotein-positive and P-glycoprotein-negative / 白血病·淋巴瘤

Objective To explore in vitro effects and the mechanism for FLAG regimen compared with IA regimen in P-glycoprotein-positive and -negative acute myeloblastic leukemia(AML) cell lines. Methods The expression of P-glycoprotein in K562 and K562/A02 cells were analyzed by flow cytometry. The effects of FLAG and IA on the proliferation of K562 and K562/A02 cells were detected by MTT assay. The Ara-CTP and Ara-C levels in those cells were measured by HPLC,the gene expression of hENT1 in K562 and K562/A02 cells was detected by real-time PCR. Results The positive rates of P- glycoprotein were (1.32±0.24)% in K562 cell and (97.66±3.77)% in K562/A02 cell, respectively. The expression of P- glycoprotein had no change after treated with FLAG or IA. The cytotoxicity to K562 of IA was better than FLAG [(84.41±9.33) % v.s (73.17±13.20)%, P<0.05], and the cytotoxicity to K562/A02 of FLAG was better than IA [(70.55±11.32)% v.s (48.46±12.81)%, P<0.01]. Ara-C and Ara-CTP accumulation and hENT1 expression in AML cells treated with FLAG were higher than that treated with IA. Conclusion P-glycoprotein-positive AML cells are more sensitive to FLAG regimen than IA regimen. The biochemical modulation of Ara-CTP and Ara-C may be the major mechanism.

The changes of mRNA expression of telomerase subunits induced by Ara-C in HL-60 cells / 中国癌症杂志

Background and purpose:Ara-C is one of the most effective and common agents in the treatment of acute nonlyphocytic leukemia. Telomerase is a unique complex of ribonucleoprotein. It plays an important role in the pathogenesis and development of cancer. In this study, we investigate the changes of mRNA expression of telomerase subunits in HL-60 cells induced by Ara-c and try to come up with a theory that could help to assess the efficacy of Ara-C. Methods:The combinations of various Ara-C concentration and the incubation time were used to treat HL-60. The ratios of apoptotic cell to necrosis cell were determined by flow cytometry and the expressions of telomerase subunits mRNA were evaluated by RT-PCR.Results:① There was no influence on transcription of telomerase subunits gene after HL-60 cells was cultured with 0~0.2ug/ml Ara-C for 12 hours;② 2ug/ml and 10ug/ml of Ara-C could down regulate the expression of hTERT from 0.80+0.07 to 0.50+0.04 and 0.39+0.03, not hTR and hTP1;③ with longer incubation with 10ug/ml of Ara-C, the percentage of apoptosis could be increased. The maximal induction of apoptosis (18.16+4.25%) could be reached at 12hrs treatment of Ara-C, then gradually decreased later on. The rate of necrosis increased with time, the maximal percentage(57.94+12.03%) of necrosis was observed at 48hrs of incubation time with drug. The mRNA level of hTERT gene also decreased along with the cultured time , the lowest value (0.18+0.03) has been documented at 48hrs time point, but not hTR、TP1.Conclusions:① Ara-C could down-regulate the expression of hTERT mRNA in a dose-and time-dependent manner, but not hTR、hTP1;② There might be no relationship between the percentage of apoptosis induced by Ara-C apoptosis and the expression of telomerase hTERT gene mRNA, but a close relationship between necrosis and the expression of hTERT mRNA has been found.

The most appropriate antimitotic treatment of Ara-C in schwann cell-enriched culture from dorsal root ganglia of new born rat

Schwann cell, one of important components of peripheral nervous system, interact with neurons to mutually support the growth and replication of embryonal nerves and to maintain the different functions of adult nerves. The Ara-C, known as an antimitotic agent, have been used to have high effectiveness in eliminating fibroblasts during Schwann cell culture period. This enrichment effect is also known to be cummulative with each successive pulse of Ara-C applied and is due to a progressive loss of fibroblasts. But the cytotoxicity by Ara-C is also cummulative and noticeable over the period. To determine the most effective application time and interval of Ara-C in the Schwann cell culture, we observed the Schwann cell purity and density with the Ara-C treatment in plain and three-dimensional culture from dorsal root ganglion of new born rat. By culturing dispersed dorsal root ganglia, we can repeatedly generate homogenous Schwann cells, and cellular morphology and cell count with mean percentages were evaluated in the plain culture dishes and in the immunostainings of S-100 and GFAP in the three-dimensional culture. The Ara-C treated cultures showed a higher Schwann cell percentage (31.0%+/-8.09% in P4 group to 65.5%+/-24.08% in P2 group), compared with that obtained in the abscence of Ara-C (17.6%+/-6.03%) in the plain culture after 2 weeks. And in the three-dimensional culture, S-100 positive cells increased to 56.22%+/-0.67% and GFAP positive cells to 66.46%+/-1.83% in G2 group (p<0.05), higher yield than other groups with Ara-C application. Therefore, we concluded that the Ara-C treatment is effective for the proliferation of Schwann cells contrast to the fibroblasts in vitro culture, and the first application after 24 hours from cell harvesting and subsequent 2 pulse treatment (P2 group in plain culture and G2 group in three-dimensional culture) was more effective than other application protocols.

The most appropriate antimitotic treatment of Ara-C in schwann cell-enriched culture from dorsal root ganglia of new born rat

Schwann cell, one of important components of peripheral nervous system, interact with neurons to mutually support the growth and replication of embryonal nerves and to maintain the different functions of adult nerves. The Ara-C, known as an antimitotic agent, have been used to have high effectiveness in eliminating fibroblasts during Schwann cell culture period. This enrichment effect is also known to be cummulative with each successive pulse of Ara-C applied and is due to a progressive loss of fibroblasts. But the cytotoxicity by Ara-C is also cummulative and noticeable over the period. To determine the most effective application time and interval of Ara-C in the Schwann cell culture, we observed the Schwann cell purity and density with the Ara-C treatment in plain and three-dimensional culture from dorsal root ganglion of new born rat. By culturing dispersed dorsal root ganglia, we can repeatedly generate homogenous Schwann cells, and cellular morphology and cell count with mean percentages were evaluated in the plain culture dishes and in the immunostainings of S-100 and GFAP in the three-dimensional culture. The Ara-C treated cultures showed a higher Schwann cell percentage (31.0%+/-8.09% in P4 group to 65.5%+/-24.08% in P2 group), compared with that obtained in the abscence of Ara-C (17.6%+/-6.03%) in the plain culture after 2 weeks. And in the three-dimensional culture, S-100 positive cells increased to 56.22%+/-0.67% and GFAP positive cells to 66.46%+/-1.83% in G2 group (p<0.05), higher yield than other groups with Ara-C application. Therefore, we concluded that the Ara-C treatment is effective for the proliferation of Schwann cells contrast to the fibroblasts in vitro culture, and the first application after 24 hours from cell harvesting and subsequent 2 pulse treatment (P2 group in plain culture and G2 group in three-dimensional culture) was more effective than other application protocols.

1-beta-D-Arabinofuranosyl-cytosine Induces Chromosomal Breaks in vitro

PURPOSE: Fragile sites are points on chromosomes which tend to break non-randomly when exposed to specific chemical agents or conditions of tissue culture. The chromosomal break induced by the antineoplastic drug, 1-beta-D-arabinofuranosyl-cytosine(Ara-c), was investigated to study the laboratory conditions in which the incidence of chromosomal break could be enhanced. Besides, the fragile sites induced by Ara-C were investigated and compared to the already known locations of the specific chromosomal alterations observed in specific neoplasms. METHODS: T-lymphocytes from theree normal males and three females were cultured for 48 hours. Cells from each individual were exposed to the Ara-C for an additional 24 hours. After the caffeine was added during the last six hours culture, the metaphase chromosomes were prepared following the conventional method. A site was considered fragile if it was found to break two or more per 100 chromosomal breaks in more than four of six individuals tested. RESULTS: Ara-C induced 252.1 chromosomal breaks per 100 mitotic cells and this result was significantly higher than that of the control, which induced 25.2 breaks(P<0.05). The incidence of the chromosomal break by Ara-C was higher, if cultured in the MEM-FA, which has no folic acid, than in the RPMI 1640 which contains enough folic acid(P<0.05). The most common break site by Ara-C was 3p14.2(FRA3B). There were 20 fragile sites induced by Ara-C. Among these 20 fragile sites, seven coincided with the locations of the mapped oncogenes, JUN, SKI, REL, N-MYC, FHIT, MET, ETS-1, and FOS. CONCLUSIONS: S phase specific chemotherapeutic agent, Ara-C, induced the expression of the chromosomal fragile sites effectively using the T-lymphocyte in vitro. Some of the fragile sites by Ara-C highly coincided with the oncogenes and neoplasm specific chromosome breakpoints. In this regard, the fragile sites reported here could provide the unknown neoplasm related chromosomal alternation points.

The Treatment of Adult Acute Myelogenous Leukemia with AD Induction Therapy Followed by Consolidation Therapy with Intermediate Dose Ara-C; Long Term Follow-up Results / 대한혈액학회지

BACKGROUND: This study was to evaluate the therapeutic efficacy of consolidation therapy based on intermediate dose Ara-C in patients with newly diagnosed acute myelogenous leukemia (AML) in Seoul National University Hospital. And also, this study was to assess the toxicities of the treatment. METHODS: We have reviewed retrospectively our experience of patients with newly diagnosed non-M3 AML between January 1993 and July 1997. They were treated with induction chemotherapy with Ara-C 200mg/m2/d over 24 h for 7 days and daunorubicin 45mg/m2/d daily for 3 days. The patients achieving complete remission (CR) are to receive the 3 courses of consolidation chemotherapy based on intermediate dose of Ara-C 1,000mg/m2 given over 2h every 12 h for a total of eight to ten doses. Patients having HLA-matched sibling donors with informed consent could receive allogeneic bone marrow transplantation (BMT). RESULTS: One hundred and fifteen patients were reviewed. The median age was 41 years (range, 16-69) and median follow-up was 75 months. The CR rate was 72.2%. The median disease-free survival (DFS) of patients receiving consolidation therapy and allogeneic BMT was 21 months and 26.5 months, respectively. The overall survival (OS) was 13 months for patients not-receiving consolidation therapy, 21 months for consolidation therapy, and 31 months for allogeneic BMT, respectively. The rate of treatment-related mortality of consolidation therapy was 14% and cause of all deaths was infection. But in allogeneic BMT, that mortality rate was 42%; 2 infections, 2 veno-occlusive diseases and 1 cyclophosphamide-induced cardiomyopathy. CONCLUSION: Patients receiving consolidation therapy with intermediate dose Ara-C had longer DFS and OS. But their DFS and OS was not superior to that of patients receiving allogeneic BMT. In addition, that result was inferior to that of patients receiving high dose Ara-C based consolidation therapy, compared with other previous studies. However, this study was retrospective and so further prospective study will be required for comparing different doses of Ara-C consolidation therapy versus BMT.

A Case of Cerebral Syndrome Associated with High-Dose Cytosine Arabinoside Chemotherapy / 대한혈액학회지

Cytosine arabinoside (Ara-C) is a highly active agent in the treatment of acute leukemia and malignant lymphoma. The use of high-dose Ara-C therapy has been advanced as a possible means of overcoming resistance. High dose Ara-C regimens are occasionally associated with cerebellar and cerebral toxicities while toxicities in conventional dose regimens are mainly restricted to the bone marrow and gastrointestinal tract. A 21-year-old male patient with acute lymphoblastic leukemia in second relapse developed cerebral syndrome 10 days after high-dose Ara-C chemotherapy. We present a case of acute cerebral toxicity after high dose Ara-C chemotherapy with relevant literature review.

Effect of G-CSF on Myeloid Leukemic Cell Lines after Treatment with Ara-C / 대한임상병리학회지

BACKGROUND: G-CSF or GM-CSF was frequently used in treatment of acute myeloid leukemia patients. But it has been argued whether this increases the apoptosis of tumor cells in synergy with chemotherapeutic agent, or decreases apoptosis of leukemic cells. We attempted to determine the effect of granulocyte colony-stimulating factor (G-CSF) on leukemic cell line after cytosine arabinoside (Ara-C) treatment. METHODS: KG-1 and HL60 cell lines were incubated with Ara-C for 48 hours, and then washed with media, divided into two groups, one being with the addition of G-CSF and the other being without G-CSF and incubated for another 48 hours. The controls were the same cell lines incubated without Ara-C. The absolute cell counts and apoptotic percentage measured by flowcytometry after stained with 7-aminoactinomycin D (7-AAD) were compared among three groups at 0, 48, and 96 hours. RESULTS: KG-1 cell line showed decreased cell count and increased apoptotic percent in Ara-C/G-CSF and Ara-C group compared with the control group at 48 and 96 hours, and did not showed significant difference between G-CSF group and nonG-CSF group. In HL60, control group showed higher cell count at 48 hours, and G-CSF/Ara-C group showed lower cell count and higher apoptosis than Ara-C group in all trials. CONCLUSIONS: The treatment of G-CSF after Ara-C did not protect apoptosis nor increase the tumor cells in KG-1 and HL60 cell lines. We concluded it would be safe to use G-CSF after administration of chemotherapeutic drug.

GM-CSF and low-dose araC treatment of AML in prolonged hypoplasia with residual leukemic cells after induction chemotherapy

We describe a case with acute myelogenous leukemia (AML; M2) who developed prolonged marrow hypoplasia with residual leukemic blasts and recurrent infections after induction chemotherapy. He was treated successfully with a sequential treatment of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) and low-dose cytosine arabinoside (LD AraC). To the best of our knowledge this is the first reported case of a successful treatment of a patient with AML, who showed prolonged markedly hypocellular bone marrow with significant residual leukemic cells after induction chemotherapy, with a sequential treatment of GM-CSF and LD AraC.

Acute megakaryoblastic leukemia in children

We analyzed the clinical and laboratory features of ten children with acute megakaryoblastic lukemia (M7)and compared the findings with those reported in the literature. The diagnosis was supprted by ultrastructural examination of platelet peroxidase or immunophenotyping for glycoprotein IIb/IIIa. Of the ten children, five were girls and five were boys. The median age at diagnosis was 13 months. Two patients had prominent myelofibrosis and one patient had Down syndrome. Nine patients were treatd with low-dose cytosine arabinoside (10mg/m2)administered intravenously, or subcutaneously, or intramuscularly, twice daily in 21 day courses. Seven patients achieved hematologic response and three patients are alive without evidence of disease. The 4 year event free survival rate was30.0%. It is our impression that the prevalence of acute megakaryoblastic leukemia has been under-estimated, and low-dose cytosine arabinoside treatment may be of value in its management. This approach may be particularily useful in hospitals with scarce well-equipped facilities, since this protocol does not induce profound marrow hypoplasia and intensive supportive measures are not required as they would be with the use of more aggressive drug combination.

Clinical Analysis of Treating 11 Cases of Acute Nonlymphocytie Leukemia With Low Dose Ara-c / 昆明医科大学学报

In this paper, acute nonlyumphocytic leukemia that is not fit for strong chemotherapy treated with low dose cytosine arabinoside (Ara—c) in 11 cases is presented. One of the patients got a complete remission and another was partial remiss, the total remission rate being 18.2%. The therapeutic mechanism, side effect, and remission rate of low dose Ara-c have been discussed. The authors conclude that this treatment is still of choice to the patients who are not fit for strong chemotherapy.