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Chemical Compound Review

SureCN331331     4-amino-1-[3,4-dihydroxy-5...

Synonyms: NSC-63878, NSC-143922, NSC-526786, NSC63878, CTK9A2616, ...
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Disease relevance of Aracytidine


Psychiatry related information on Aracytidine


High impact information on Aracytidine

  • Preincubation of bone marrow cells with Ara-C produced significant megaloblastic changes by the end of the 2-d incubation and increased the proportion of Hb F-positive erythroblasts, CFUe colonies, and e-clusters, but BFUe-derived progeny was unaffected [10].
  • The rationale is based on a) evidence that, following drug-induced aplasia, resultant bone marrow proliferation in vivo corresponds temporally with induced humoral stimulatory activity, and on b) models that demonstrate increased cytotoxicity of beta-cytosine arabinoside (Ara-C) to myeloblasts cultured in humoral stimulatory activity (HSA) [5].
  • CD2F1 mice bearing L-1210 leukemia received a course of 60 mg Ara-C/kg every 8th hour (q.8 h) three times on day 0 and on another day in sequence (0,1 through 0,7) [5].
  • Free Ara-C (5 mg/kg) administered into the trachea effectively suppressed macromolecular incorporation of [14C]thymidine ([14C]dThd) in the bone marrow and gut as well as in the lung [11].
  • The results indicate that Ara-C facilitates GS accumulation largely by preventing degradation of the enzyme [12].

Chemical compound and disease context of Aracytidine


Biological context of Aracytidine


Anatomical context of Aracytidine

  • This selective improvement of Ara-C metabolism in AML blasts was associated with an enhanced Ara-C-mediated leukemia colony-forming unit (CFU) growth inhibition [23].
  • Two-dimensional flow cytometry of topo IIalpha or IIbeta staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling assay showed that one topo IIbeta epitope situated at the C-terminal end decreased specifically in apoptotic HL-60 cells treated with Ara-C, etoposide, and vincristine [24].
  • Importantly, cotreatment with CGP57148B significantly increased Ara-C- or doxorubicin-induced apoptosis of HL-60/Bcr-Abl and K562 cells [25].
  • Logistic regression analysis of factors associated with complete response indicated that treatment with IDR/Ara-C offered a significant advantage to patients who presented with a high initial white blood cell count compared with treatment with DNR/Ara-C [26].
  • Stromal cell coculture was shown to sustain the proliferation of B-lineage leukemic cells and to reduce leukemic cell apoptosis when exposed to Ara-C or VP-16 [27].

Associations of Aracytidine with other chemical compounds


Gene context of Aracytidine

  • Ara-C treatment of cells that express wild type or a dominant negative, kinase-inactive c-Abl(K-R) was associated with formation of c-Abl-p53 complexes and increased expression of the cyclin-dependent kinase (Cdk) inhibitor p21 [31].
  • However, enhancement of Ara-C cytotoxicity to AML progenitors by IL-3 or GM-CSF stimulation was significantly less in the cell specimens from AML recurrence patients as compared with the original diagnosis samples [32].
  • IL-3 stimulation enhanced Ara-C incorporation in all samples tested [32].
  • Therefore, we conclude that Ara-C is not a substrate for BCRP and that MDR proteins do not play a significant role in drug resistance in infant ALL [33].
  • The UA cells resist apoptosis induced by TNF-alpha and anti-Fas antibody but not by anticancer drugs, such as VP-16 and Ara-C [34].

Analytical, diagnostic and therapeutic context of Aracytidine

  • To predict the results of induction chemotherapy, it could be useful to detect leukemic cells that are resistant to Ara-C in patients with AML [35].
  • As univariate parameters, self-renewal and Ara-C sensitivity contributed to remission induction, but only self-renewal was related to survival [36].
  • Using a bromodeoxyuridine/DNA (BrdUrd/DNA) staining method in flow cytometry (FCM), we have developed a cell resistance index to Ara-C (RI) [35].
  • Eighteen patients were primarily resistant to conventional daunorubicin and Ara-C induction treatment; eight patients had relapsed within 6 months from initial remission; six patients had relapsed after a bone marrow transplantation (BMT) procedure [37].
  • Following another period of hydration, 500 mg/m2 of Ara-C was administered by continuous intravenous infusion daily for 4 days [38].


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  8. Dose- and stage-related sex difference in the incidence of cytosine arabinoside induced digit anomalies in the mouse fetus. Goto, T., Endo, A. Teratology (1987) [Pubmed]
  9. Conversion disorder with convulsion and motor deficit mimicking the adverse effects of high-dose Ara-C treatment in a posttransplant acute myeloid leukemia patient: a case report and review of the literature. Onishi, H., Kamijo, A., Onose, M., Yamada, T., Mizuno, Y., Ito, M., Saito, H., Maruta, I. Palliative & supportive care. (2004) [Pubmed]
  10. Mechanism of Hb F stimulation by S-stage compounds. In vitro studies with bone marrow cells exposed to 5-azacytidine, Ara-C, or hydroxyurea. Galanello, R., Stamatoyannopoulos, G., Papayannopoulou, T. J. Clin. Invest. (1988) [Pubmed]
  11. Organ-selective action of an antitumor drug: pharmacologic studies of liposome-encapsulated beta-cytosine arabinoside administered via the respiratory system of the rat. McCullough, H.N., Juliano, R.L. J. Natl. Cancer Inst. (1979) [Pubmed]
  12. Effects of cytosine arabinoside on differential gene expression in embryonic neural retina. II. Immunochemical studies on the accumulation of glutamine synthetase. Jones, R.E., Moscona, A.A. J. Cell Biol. (1977) [Pubmed]
  13. Differential protection of normal and malignant human myeloid progenitors (CFU-GM) from Ara-C toxicity using cycloheximide. Slapak, C.A., Fine, R.L., Richman, C.M. Blood (1985) [Pubmed]
  14. Activation of lymphocytes induced by recombinant human granulocyte-macrophage colony-stimulating factor in patients with malignant lymphoma. Ho, A.D., Haas, R., Wulf, G., Knauf, W., Ehrhardt, R., Heilig, B., Körbling, M., Schulz, G., Hunstein, W. Blood (1990) [Pubmed]
  15. Feasibility of using quinine, a potential multidrug resistance-reversing agent, in combination with mitoxantrone and cytarabine for the treatment of acute leukemia. Solary, E., Caillot, D., Chauffert, B., Casasnovas, R.O., Dumas, M., Maynadie, M., Guy, H. J. Clin. Oncol. (1992) [Pubmed]
  16. A prospective randomized trial of single-agent versus combination chemotherapy in meningeal carcinomatosis. Hitchins, R.N., Bell, D.R., Woods, R.L., Levi, J.A. J. Clin. Oncol. (1987) [Pubmed]
  17. Neuro-Oncology Working Group 01 trial of nimustine plus teniposide versus nimustine plus cytarabine chemotherapy in addition to involved-field radiotherapy in the first-line treatment of malignant glioma. Weller, M., Müller, B., Koch, R., Bamberg, M., Krauseneck, P. J. Clin. Oncol. (2003) [Pubmed]
  18. Activation of the CPP32 protease in apoptosis induced by 1-beta-D-arabinofuranosylcytosine and other DNA-damaging agents. Datta, R., Banach, D., Kojima, H., Talanian, R.V., Alnemri, E.S., Wong, W.W., Kufe, D.W. Blood (1996) [Pubmed]
  19. Survival advantage from imatinib compared with the combination interferon-alpha plus cytarabine in chronic-phase chronic myelogenous leukemia: historical comparison between two phase 3 trials. Roy, L., Guilhot, J., Krahnke, T., Guerci-Bresler, A., Druker, B.J., Larson, R.A., O'Brien, S., So, C., Massimini, G., Guilhot, F. Blood (2006) [Pubmed]
  20. Deoxycytidine kinase: properties of the enzyme from human leukemic granulocytes. Coleman, C.N., Stoller, R.G., Drake, J.C., Chabner, B.A. Blood (1975) [Pubmed]
  21. Granulocyte-macrophage colony-stimulating factor/interleukin-3 fusion protein (pIXY 321) enhances high-dose Ara-C-induced programmed cell death or apoptosis in human myeloid leukemia cells. Bhalla, K., Tang, C., Ibrado, A.M., Grant, S., Tourkina, E., Holladay, C., Hughes, M., Mahoney, M.E., Huang, Y. Blood (1992) [Pubmed]
  22. Prolongation of drug exposure in cerebrospinal fluid by encapsulation into DepoFoam. Kim, S., Khatibi, S., Howell, S.B., McCully, C., Balis, F.M., Poplack, D.G. Cancer Res. (1993) [Pubmed]
  23. Treatment with interleukin-3 plus granulocyte-macrophage colony-stimulating factors improves the selectivity of Ara-C in vitro against acute myeloid leukemia blasts. Bhalla, K., Holladay, C., Arlin, Z., Grant, S., Ibrado, A.M., Jasiok, M. Blood (1991) [Pubmed]
  24. Temporal and spatial distribution of DNA topoisomerase II alters during proliferation, differentiation, and apoptosis in HL-60 cells. Sugimoto, K., Yamada, K., Egashira, M., Yazaki, Y., Hirai, H., Kikuchi, A., Oshimi, K. Blood (1998) [Pubmed]
  25. CGP57148B (STI-571) induces differentiation and apoptosis and sensitizes Bcr-Abl-positive human leukemia cells to apoptosis due to antileukemic drugs. Fang, G., Kim, C.N., Perkins, C.L., Ramadevi, N., Winton, E., Wittmann, S., Bhalla, K.N. Blood (2000) [Pubmed]
  26. Results of a randomized trial comparing idarubicin and cytosine arabinoside with daunorubicin and cytosine arabinoside in adult patients with newly diagnosed acute myelogenous leukemia. Berman, E., Heller, G., Santorsa, J., McKenzie, S., Gee, T., Kempin, S., Gulati, S., Andreeff, M., Kolitz, J., Gabrilove, J. Blood (1991) [Pubmed]
  27. Stromal cells regulate survival of B-lineage leukemic cells during chemotherapy. Mudry, R.E., Fortney, J.E., York, T., Hall, B.M., Gibson, L.F. Blood (2000) [Pubmed]
  28. The sesquiterpene lactone parthenolide induces apoptosis of human acute myelogenous leukemia stem and progenitor cells. Guzman, M.L., Rossi, R.M., Karnischky, L., Li, X., Peterson, D.R., Howard, D.S., Jordan, C.T. Blood (2005) [Pubmed]
  29. Prognostic value of immunophenotyping in acute myeloid leukemia. Australian Leukaemia Study Group. Bradstock, K., Matthews, J., Benson, E., Page, F., Bishop, J. Blood (1994) [Pubmed]
  30. Double intensive consolidation chemotherapy in adult acute myeloid leukemia. Harousseau, J.L., Milpied, N., Briere, J., Desablens, B., Leprise, P.Y., Ifrah, N., Gandhour, B., Casassus, P. J. Clin. Oncol. (1991) [Pubmed]
  31. Genotoxic drugs induce interaction of the c-Abl tyrosine kinase and the tumor suppressor protein p53. Yuan, Z.M., Huang, Y., Fan, M.M., Sawyers, C., Kharbanda, S., Kufe, D. J. Biol. Chem. (1996) [Pubmed]
  32. Hematopoietic growth factor stimulation and cytarabine cytotoxicity in vitro: effects in untreated and relapsed or primary refractory acute myeloid leukemia cells. te Boekhorst, P.A., Löwenberg, B., Sonneveld, P. Leukemia (1994) [Pubmed]
  33. Multidrug resistance genes in infant acute lymphoblastic leukemia: Ara-C is not a substrate for the breast cancer resistance protein. Stam, R.W., van den Heuvel-Eibrink, M.M., den Boer, M.L., Ebus, M.E., Janka-Schaub, G.E., Allen, J.D., Pieters, R. Leukemia (2004) [Pubmed]
  34. Genetically recessive mutant of human monocytic leukemia U937 resistant to tumor necrosis factor-alpha-induced apoptosis. Dong, J., Naito, M., Mashima, T., Jang, W.H., Tsuruo, T. J. Cell. Physiol. (1998) [Pubmed]
  35. Detection of cytarabine resistance in patients with acute myelogenous leukemia using flow cytometry. Lacombe, F., Belloc, F., Dumain, P., Puntous, M., Makhoul, P.C., Saux, M.C., Bernard, P., Boisseau, M.R., Reiffers, J. Blood (1994) [Pubmed]
  36. The contribution of blast cell properties to outcome variation in acute myeloblastic leukemia (AML). McCulloch, E.A., Curtis, J.E., Messner, H.A., Senn, J.S., Germanson, T.P. Blood (1982) [Pubmed]
  37. Mitoxantrone, etoposide, and intermediate-dose cytarabine: an effective and tolerable regimen for the treatment of refractory acute myeloid leukemia. Amadori, S., Arcese, W., Isacchi, G., Meloni, G., Petti, M.C., Monarca, B., Testi, A.M., Mandelli, F. J. Clin. Oncol. (1991) [Pubmed]
  38. High-dose mercaptopurine followed by intermediate-dose cytarabine in relapsed acute leukemia. Lockhart, S., Plunkett, W., Jeha, S., Ramirez, I., Zipf, T., Cork, A., Pinkel, D. J. Clin. Oncol. (1994) [Pubmed]
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