1. Kidd, J.G., Regression of transplanted lymphomas induced in vivo by means of normal guinea pig serum. I. Course of transplanted cancers of various kinds in mice and rats given guinea pig serum, horse serum or rabbit serum, J. Exp. Med., 97, 565, 1953.

2. Kidd, J.G., Regression of transplanted lymphomas induced in vivo by means of normal guinea pig serum. II. Studies on the nature of the active serum constituent: Histological mechanism of the regression: Tests for effects of guinea pig serum on lymphoma cells in vitro, J. Exp. Med., 9S, 5S3, 1953.

3. Broome, J.J.D., Evidence that the L-Asparaginase activity of guinea pig serum is responsible for its antilymphoma effects, Nature, 191, 1114, 1961.

4. Clementi, A., La désamidation enzymatique de L-asparagine chez les differentes espèces animales et la signification physiologique de sa présence dans l'organisme, Arch. Int. Physiol., 19, 369, 1922.

5. Yellin, T.O. and Wriston, J.C., Jr., Purification and properties of guinea pig serum asparaginase, Biochemistry, 5, 1605-1612, 1966.

6. Dolowy, W.C., et al., Toxic and antineoplastic effects of L-asparaginase. Study of mice with lymphoma and normal monkeys and report on a child with leukemia, Cancer, 19, 1S13-1S19, 1966.

7. Asslin, B.L., The three asparaginases. Comparative pharmacology and optimal use in childhood leukemia, Adv. Exp. Med. Biol., 457, 621, 1999.

S. Irion, E. and Arens, A., Biochemical characterization of L-asparaginase from E. coli, in Experimental and Clinical Effects of L-Asparaginases, Grundmann, E. and Oettgen, H.F., Eds., RRCR, Springer, Heidelberg, 1979, p. 39.

9. Campbell, H.A. and Mashburn, L.T., L-Asparaginase EC-2 from Escherichia coli. Some substrate specificity characteristics, Biochemistry, S, 3766-3775, 1969.

10. Swain, A.L., et al., Crystal structure of Escherichia coli L-asparaginase, an enzyme used in cancer therapy, Proc. Natl. Acad. Sci, USA, 90, 1474-147S, 1993.

11. Müller, H.J. and Boos, J., Use of L-asparaginase in childhood ALL, Crit. Rev. Oncol. Hematol., 2S, 97-113, 199S.

12. Abuchowski, A., et al., Treatment of L517SY tumor-bearing BDF1 mice with a nonimmunogenic L-glutaminase-L-asparaginase, Cancer Treat. Rep., 63, 1127-1132, 1979.

13. Davis, F.F., et al., Reduction of immunogenicity and extension of circulating half-life of peptides and proteins, in Peptide and Protein Drug Delivery, Lee, V.H.L., Ed., Marcel Dekker, Inc., New York, 1991, p. S31.

14. Uren, J.R. and Ragin, R.C., Improvement in the therapeutic, immunological and clearance properties of Escherichia coli and Erwinia carotovora L-asparaginases by attachment of poly-DL-alanyl peptides, Cancer Res., 39, 1927-1933, 1979.

15. Park, Y.K., et al., Pharmacology of Escherichia coli-L-asparaginase polyethylene glycol adduct, Anticancer Res., 1, 373-376, 19S1.

16. Abuchowski, A., et al., Cancer therapy with chemically modified enzymes. I. Antitumor properties of polyethylene glycol-asparaginase conjugates, Cancer Biochem. Biophys., 7, 175-186, 1984.

17. Avramis, V.I., et al., A randomized comparison of native Escherichia coli asparaginase and polyethylene glycol conjugated asparaginase for treatment of children with newly diagnosed standard-risk acute lymphoblastic leukemia: A Children's Cancer Group study, Blood, 99, 1986-1994, 2002.

18. Holcenberg, J.S. and Roberts, J., Enzymes as drugs, Ann. Rev. Pharmacol. Toxicol., 17, 97-116, 1977.

19. Riccardi, R., et al., L-asparaginase pharmacokinetics and asparagine levels in cerebrospinal fluid of rhesus monkeys and humans, Cancer Res., 41, 4554-4558, 1981.

20. Boos, J., et al., Monitoring of asparaginase activity and asparagine levels in children on different asparaginase preparations, Eur. J. Cancer, 32A, 1544-1550, 1996.

21. Albersten, B.K., et al., Comparison of intramuscular therapy with Erwinia asparaginase and asparaginase Medac: Pharmacokinetics, pharmacodynamics, formation of antibodies and influence on the coagulation system, Br. J. Haematol., 115, 983-990, 2001.

22. Haskell, C.M. and Canellos, G.P., L-asparaginase resistance in human leukemia — Asparagine synthetase, Biochem. Pharmacol., 18, 2578-2580, 1969.

23. Kiriyama, Y., et al., Biochemical characterisation of U937 cells resistant to L-asparaginase: The role of asparagine synthetase, Leukemia, 3, 294-297, 1989.

24. Hutson, R.G., et al., Amino acid control of asparagine synthetase: Relation to asparaginase resistance in human leukemia cells, Am. J. Physiol., 272, C1691-C1699, 1997.

25. Woo, M.H., et al., Hypersensitivity or development of antibodies to asparaginase does not impact treatment outcome of childhood acute lymphoblastic leukemia, J. Clin. Oncol., 18, 15251532, 2000.

26. Klug-Albertsen, B., et al., Anti-Erwinia asparaginase antibodies during treatment of childhood acute lymphoblastic leukemia and their relationship to outcome: A case-control study, Cancer Chemother. Pharmacol., 50, 117-120, 2002.

27. Müller, H.J., et al., Pharmacokinetics of native Escherichia coli asparginase and hypersensitivity reactions in ALL-BFM 95 reinduction treatment, Br. J. Haematol., 114, 794-799, 2001.

28. Friesen, C., et al., Involvement of the CD95 (APO-1/FAS) receptor/ligand system in drug induced apoptosis in leukemia cells, Nat. Med., 2, 574-577, 1996.

29. Green, D.R. and Reed, J.C., Mitochondria and apoptosis, Science, 281, 1309-1312, 1998.

30. Castedo, M., et al., Mitochondria perturbations define lymphocytes undergoing apoptotic depletion in vivo, Eur. J. Immunol., 25, 3277-3284, 1995.

31. Li, P., et al., Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade, Cell, 91, 479-489, 1997.

32. Holleman, A., et al., Resistance to different classes of drugs is associated with impaired apoptosis in childhood acute lymphoblastic leukemia, Blood, 102, 4541-4546, 2003.

33. Den Boer, M.L., et al., Patient stratification based on prednisolone-vincristine-asparaginase resistance profiles in children with acute lymphoblastic leukemia, J. Clin. Oncol., 21, 3262-3268, 2003.

34. Okada, S., et al., In vitro efficacy of L-asparaginase in childhood acute myeloid leukemia, Br. J. Haematol, 123, 802-809, 2003.

35. Clavell, L.A., et al., Four-agent induction and intensive asparaginase therapy for treatment of childhood acute lymphoblastic leukaemia, New Engl. J. Med., 315, 657-663, 1986.

36. Duval, M., et al., Comparison of Escherichia coli asparaginase with Erwinia asparaginase in the treatment of childhood lymphoid malignancies: Results of a randomized European Organisation for Research and Treatment of Cancer-Children"s Leukemia Group phase 3 trial, Blood, 99, 2734-2739, 2002.

37. Kurre, H.A., et al., A pharmacoceconomic analysis of Pegaspargase versus native Escherichia coli L-asparaginase for the treatment of children with standard-risk, acute lymphoblastic leukemia: The Children Cancer Group study (CCG-1962), J. Pediatr. Hematol. Oncol., 24, 175-181, 2002.

38. Khan, A. and Hill, J.M., Neutralizing precipitin in the serum of a patient treated with L-aspara-ginase, J. Lab. Clin. Med., 73, 846-852, 1969.

39. Peterson, R.G., Handschumacher, R.E., and Mitchell, M.S., Immunological responses to L-aspar-aginase, J. Clin. Invest., 50, 1080-1090, 1971.

40. Maral, R., et al., Studies on the immunosuppressive activity of L-asparaginase, in Experimental and Clinical Effects of L-Asparaginase Grundmann, E.E. and Oettgen, H.F., Eds., Springer, Berlin, 1970, p. 160.

41. Dellinger, C.T. and Miale T.D., Compariason of anaphylactic reaction to asparaginase derived from Escherichia coli and Erwinia cultures, Cancer, 38, 1843-1846, 1976.

42. Elhag, K.M., Bettelheim, K.A., and Huber, T.J., Antibodies to bacterial L-asparaginases, New Zealand Med. J., 86, 280-281, 1977.

43. Fabry, U., et al., Anaphylaxis to L-asparaginase during treatment of acute lymphoblastic leukemia in children — Evidence of a complement-mediated mechanism, Pediatr. Res., 19, 400-408, 1985.

44. Körholz, D., et al., Bildung spezifischer IgG-Antikörper unter L-Asparaginasebehandlung, Mschr. Kinderheilkd., 135, 325-328, 1987.

45. Körholz, D., et al., Allergische Reaktionen unter der Behandlung mit L-Asparaginase — Bedeutung spezifischer IgE-Antikörper, Mschr. Kinderheilkd., 138, 23-25, 1990.

46. Wang, B., et al., Evaluaton of immunologic cross-reaction of antiasparaginase antibodies in acute lymphoblastic leukemia and lymphoma patients, Leukemia, 17, 1583-1588, 2003.

47. Wahn, V., L-Asparaginase: An essential antineoplastic drug, in Pharmaceutical Enzymes (Hrsg. Lauwers/Scharpe), Marcel Dekker, Inc., New York, 1997, pp. S223-S260.

48. Gugliotta, L., et al., Incidence of thrombotic complications in adult patients with acute lympho-blastic leukemia receiving L-asparaginase during induction therapy: A retrospective study, The GIMEMA group, Eur. J. Hematol., 49, 63-66, 1992.

49. Anderson, N., Lokich, J.J., and Tullis, J.L., L-Asparaginase effect on antithrombin-III levels, Med. Pediatr. Oncol., 7, 335-340, 1979.

50. Priest, J.R., et al., The effect of L-asparaginase on antithrombin, plasminogen and plasma coagulation during therapy for acute lymphoblastic leukemia, J. Pediatr., 100, 990-995, 1982.

51. Homans, A.C., et al., Effect of L-asparaginase administration on coagulation and platelet function in children with leukaemia, J. Clin. Oncol., 5, 811-817, 1987.

52. Gugliotta, L., et al., Hypercoagulability during L-asparaginase treatment: The effect of antithrombin III supplementation in vivo, Br. J. Haematol., 74, 465-470, 1990.

53. Barbui, T., et al., L-asparaginase lowers protein C antigen, Thromb. Haemostas., 52, 216, 1984.

54. Vigano D' Angelo, L., et al., L-asparaginase treatment reduces the anticoagulant potential of the protein C system without affecting vitamin K-dependent carboxylation, Thromb. Res., 59, 985-994, 1990.

55. Lee, J.H., Kim, S.W., and Kim, J.S., Sagittal sinus thrombosis associated with transient free protein S deficiency after L-asparaginase treatment: Case report and review of the literature, Clin. Neurol. Neurosurg, 102, 33-36, 2000.

56. Nowak-Göttl, U., et al., Prospective evaluation of the thrombotic risk in children with acute lymphoblastic leukemia carrying the MTHFR TT 677 genotype, the prothrombin G20210A variant and further prothrombotic risk factors, Blood, 93, 1595-1599, 1999.

57. Mauz-Körholz, C., et al., Low rate of severe venous thromboses in children with ALL treatment according to the CoALL-92 and -97 protocol, Klin. Pädiatr., 211, 215-217, 1999.

58. Mauz-Körholz, C., et al., Prothrombotic risk factors in children with acute lymphoblastic leukemia treated with delayed E. coli asparaginase (CoALL-92 and -97 protocols), Thromb. Haemostas., 83, 840-843, 2000.

59. Nowak-Göttl, U., et al., Thromboembolic events in children with acute lymphoblastic leukemia (BFM protocols): Prednisone versus dexamethasone administration, Blood, 101, 2529-2533, 2003.

60. Pui, C.H., et al., Risk factors for hyperglycemia in children with leukemia receiving L-asparagi-nase and prednisone, J. Pediatr., 99, 46-50, 1981.

61. Alvarez, O.A. and Zimmerman, G., Pegaspargase-induced pancreatitis, Med. Pediatr. Oncol., 34, 200-205, 2000.

62. McLean, R., Martin, S., and Lam-Po-Tang, P.R., Fatal case of L-asparaginase induced pancreatitis, Lancet, 2, 1401-1402, 1982.

63. Garnick, M.B. and Larsen, P.R., Acute deficiency of thyroxine-binding globulin during L-aspara-ginase therapy, New Engl. J. Med., 301, 252-253, 1979.

64. Heidemann, P.H., Stubbe, P., and Beck, W., Transient secondary hypothyroidism and thyrox-ine-binding globulin deficiency in leukemic children receiving polychemotherapy: An effect of L-asparaginase, Eur. J. Pediatr., 136, 291-295, 1981.

65. Ferster, A., et al., Thyroid function during L-asparaginase therapy in children with acute lymphoblastic leukemia: Difference between induction and late intensification, Am. J. Pediatr. Hematol. Oncol, 14, 192-196, 1992.

66. Graham, M.L., Pegaspargase: A review of clinical studies, Adv. Drug Deliv. Rev., 55, 1293-1302, 2003.

Was this article helpful?

0 0

Post a comment