Acute promyelocytic leukemia: Recent advances in therapy and molecular basis of response to arsenic therapies

Current Opinion in Hematology

Volumn 12, Issue 1, 2005, Pages 1-6

  Chou, Wen Chien ^a   Dang, Chi V ^b,c  

^a NATIONAL TAIWAN UNIVERSITY HOSPITAL   (Taiwan)

^b JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE   (United States)

^c Ross Research Building ^*  (United States)

Author keywords

Acute promyelocytic leukemia; All trans retinoic acid; Arsenic; Reactive oxygen species

Indexed keywords

ACETYLCYSTEINE; ADENINE NUCLEOTIDE TRANSLOCASE; ARSENIC TRIOXIDE; ARSENOSOBENZENE; BRYOSTATIN 1; CATALASE; DITHIOL DERIVATIVE; GLUTATHIONE; GLUTATHIONE TRANSFERASE; MITOGEN ACTIVATED PROTEIN KINASE; PROMYELOCYTIC LEUKEMIA PROTEIN; REACTIVE OXYGEN METABOLITE; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE OXIDASE; RETINOIC ACID; RETINOIC ACID RECEPTOR ALPHA; STRESS ACTIVATED PROTEIN KINASE;

ACUTE GRANULOCYTIC LEUKEMIA; APOPTOSIS; BIOACCUMULATION; BLOOD LEVEL; CALCIUM CURRENT; CANCER CELL; CARDIOTOXICITY; CELL DIFFERENTIATION; CELL NUCLEUS INCLUSION BODY; CELL SURFACE; CYTOTOXICITY; DIGESTIVE SYSTEM FUNCTION DISORDER; DRUG EFFICACY; FATIGUE; FLUID RETENTION; HEADACHE; HEART ARRHYTHMIA; HUMAN; HYPERGLYCEMIA; HYPOKALEMIA; LEUKEMIA CELL; LEUKOCYTOSIS; LIVER DYSFUNCTION; MEMBRANE POTENTIAL; MITOCHONDRIAL MEMBRANE; MITOCHONDRION; MONOTHERAPY; NEUROPATHY; NONHUMAN; PRIORITY JOURNAL; PROMYELOCYTIC LEUKEMIA; PROTEIN DEGRADATION; PROTEIN PHOSPHORYLATION; QT PROLONGATION; REMISSION; REVIEW; RHEUMATIC DISEASE; SIDE EFFECT; SKIN; T LYMPHOCYTE; XEROSTOMIA;

ANTINEOPLASTIC AGENTS; ARSENICALS; CELL DIFFERENTIATION; HUMANS; LEUKEMIA, PROMYELOCYTIC, ACUTE; MODELS, BIOLOGICAL; ONCOGENE PROTEINS, FUSION; OXIDES; REACTIVE OXYGEN SPECIES;

EID: 13244267274     PISSN: 10656251     EISSN: None     Source Type: Journal    
DOI: 10.1097/01.moh.0000148552.93303.45     Document Type: Review

References (63)

1. Weider B, Fournier JH: Activation analyses of authenticated hairs of Napoleon Bonaparte confirm arsenic poisoning. Am J Forensic Med Pathol 1999, 20:378-382.
2. Westveer AE, Trestrail JH 3rd, Pinizzotto AJ: Homicidal poisoning in the United States: an analysis of the Uniform Crime Reports from 1980 through 1989. Am J Forensic Med Pathol 1996, 17:282-288.
3. Zhu J, Chen Z, Lallemand-Breitenbach V, et al.: How acute promyelocytic leukaemia revived arsenic. Nat Rev Cancer 2002, 2:705-713.
4. Waxman S, Anderson KC: History of the development of arsenic derivatives in cancer therapy. Oncologist 2001, 6(suppl 2):3-10.
5. Warrell RP Jr, de The H, Wang ZY, Degos L: Acute promyelocytic leukemia. N Engl J Med 1993, 329:177-189.
6. Piazza F, Gurrieri C, Pandolfi PP: The theory of APL. Oncogene 2001, 20:7216-7222.
7. Wang ZY: Ham-Wasserman lecture: treatment of acute leukemia by inducing differentiation and apoptosis. Hematology (American Society Hematology Education Program), 2003:1-13.
8. 3) in the treatment of acute promyelocytic leukemia (APL): II: clinical efficacy and pharmacokinetics in relapsed patients. Blood 1997, 89:3354-3360.
9. Soignet SL, Maslak P, Wang ZG, et al.: Complete remission after treatment of acute promyelocytic leukemia with arsenic trioxide. N Engl J Med 1998, 339:1341-1348.
10. Soignet SL, Frankel SR, Douer D, et al.: United States multicenter study of arsenic trioxide in relapsed acute promyelocytic leukemia. J Clin Oncol 2001, 19:3852-3860.
11. Lu DP, Qiu JY, Jiang B, et al.: Tetra-arsenic tetra-sulfide for the treatment of acute promyelocytic leukemia: a pilot report. Blood 2002, 99:3136-3143.
12. Au WY, Kumana CR, Kou M, et al.: Oral arsenic trioxide in the treatment of relapsed acute promyelocytic leukemia. Blood 2003, 102:407-408.
13. Murgo AJ: Clinical trials of arsenic trioxide in hematologic and solid tumors: overview of the National Cancer Institute Cooperative Research and Development Studies. Oncologist 2001, 6(suppl 2):22-28.
14. Chen Z, Chen GQ, Shen ZX, et al.: Expanding the use of arsenic trioxide: leukemias and beyond. Semin Hematol 2002, 39:22-26.
15. Slack JL, Waxman S, Tricot G, et al.: Advances in the management of acute promyelocytic leukemia and other hematologic malignancies with arsenic trioxide. Oncologist 2002, 7(suppl 1):1-13.
16. Niu C, Yan H, Yu T, et al.: Studies on treatment of acute promyelocytic leukemia with arsenic trioxide: remission induction, follow-up, and molecular monitoring in 11 newly diagnosed and 47 relapsed acute promyelocytic leukemia patients. Blood 1999, 94:3315-3324.
17. Huang SY, Chang CS, Tang JL, et al.: Acute and chronic arsenic poisoning associated with treatment of acute promyelocytic leukaemia. Br J Haematol 1998, 103:1092-1095.
18. Barbey JT, Pezzullo JC, Soignet SL: Effect of arsenic trioxide on QT interval in patients with advanced malignancies. J Clin Oncol 2003, 21:3609-3615.
19. Ficker E, Kuryshev YA, Dennis AT, et al.: Mechanisms of arsenic-induced prolongation of cardiac repolarization. Mol Pharmacol 2004, 66:33-44.
20. 3) in the treatment of patients with acute promyelocytic leukemia: the M. D. Anderson experience. Cancer 2003, 97:2218-2224.
21. Raffoux E, Rousselot P, Poupon J, et al.: Combined treatment with arsenic trioxide and all-trans-retinoic acid in patients with relapsed acute promyelocytic leukemia. J Clin Oncol 2003, 21:2326-2334.
22. 3 combination yields a high quality remission and survival in newly diagnosed acute promyelocytic leukemia. Proc Natl Acad Sci USA 2004, 101:5328-5335. This article showed that the combination of arsenic and retinoic acid in patients with newly diagnosed APL yielded a higher percentage of remission and survival than in those receiving monotherapy.
23. Lin CJ, Wu MH, Hsueh YM, et al.: Tissue distribution of arsenic species in rabbits after single and multiple parenteral administration of arsenic trioxide: tissue accumulation and the reversibility after washout are tissue-selective. Cancer Chemother Pharmacol 2004. Epub ahead of print. This paper presented a thorough animal study of arsenic metabolism in vivo.
24. Hei TK, Liu SX, Waldren C: Mutagenicity of arsenic in mammalian cells: role of reactive oxygen species. Proc Natl Acad Sci USA 1998, 95:8103-8107.
25. Hei TK, Filipic M: Role of oxidative damage in the genotoxicity of arsenic. Free Radic Biol Med 2004, 37:574-581.
26. Jing Y, Dai J, Chalmers-Redman RM, et al.: Arsenic trioxide selectively induces acute promyelocytic leukemia cell apoptosis via a hydrogen peroxide-dependent pathway. Blood 1999, 94:2102-2111.
27. Chou WC, Jie C, Kenedy AA, et al.: Role of NADPH oxidase in arsenic-induced reactive oxygen species formation and cytotoxicity in myeloid leukemia cells. Proc Natl Acad Sci USA 2004, 101:4578-4583. This paper demonstrates that the source of superoxide induced by arsenic in leukemia cells is NADPH oxidase, and through this mechanism bryostatin 1 and arsenic are synergistically cytotoxic.
28. 3-induced apoptosis in lymphoma cells: involvement of hydrogen peroxide catabolism. Blood 2004. Epub ahead of print.
29. Huang C, Ma WY, Li J, Dong Z: Arsenic induces apoptosis through a c-Jun NH2-terminal kinase-dependent, p53-independent pathway. Cancer Res 1999, 59:3053-3058.
30. Davison K, Mann KK, Waxman S, Miller WH Jr: JNK activation is a mediator of arsenic trioxide-induced apoptosis in acute promyelocytic leukemia cells. Blood 2004, 103:3496-3502.
31. Khan MA, Oubrahim H, Stadtman ER: Inhibition of apoptosis in acute promyelocytic leukemia cells leads to increases in levels of oxidized protein and LMP2 immunoproteasome. Proc Natl Acad Sci USA 2004, 101:11560-11565. This paper demonstrated that arsenic trioxide treatment could lead to cellular pro-tein oxidation.
32. Liu L, Trimarchi JR, Navarro P, et al.: Oxidative stress contributes to arsenic-induced telomere attrition, chromosome instability, and apoptosis. J Biol Chem 2003, 278:31998-32004.
33. Sturlan S, Baumgartner M, Roth E, Bachleitner-Hofmann T: Docosahexaenoic acid enhances arsenic trioxide-mediated apoptosis in arsenic trioxide-resistant HL-60 cells. Blood 2003, 101:4990-4997.
34. Dyck JA, Maul GG, Miller WH Jr, et al.: A novel macromolecular structure is a target of the pramyelocyte-retinoic acid receptor oncoprotein. Cell 1994, 76:333-343.
35. Weis K, Rambaud S, Lavau C, et al.: Retinoic acid regulates aberrant nuclear localization of PML-RAR alpha in acute promyelocytic leukemia cells. Cell 1994, 76:345-356.
36. Wang ZG, Delva L, Gaboli M, et al.: Role of PML in cell growth and the retinoic acid pathway. Science 1998, 279:1547-1551.
37. Wang ZG, Ruggero D, Ronchetti S, et al.: PML is essential for multiple apoptotic pathways. Nat Genet 1998, 20:266-272.
38. Quignon F, De Bels F, Koken M, et al.: PML induces a novel caspase-independent death process. Nat Genet 1998, 20:259-265.
39. Zhu J, Koken MH, Quignon F, et al.: Arsenic-induced PML targeting onto nuclear bodies: implications for the treatment of acute promyelocytic leukemia. Proc Natl Acad Sci USA 1997, 94:3978-3983.
40. Muller S, Matunis MJ, Dejean A: Conjugation with the ubiquitin-related modifier SUMO-1 regulates the partitioning of PML within the nucleus. EMBO J 1998, 17:61-70.
41. 3-induced PML or PML/retinoic acid receptor alpha degradation. J Exp Med 2001, 193:1361-1371.
42. Hayakawa F, Privalsky ML: Phosphorylation of PML by mitogen-activated protein kinases plays a key role in arsenic trioxide-mediated apoptosis. Cancer Cell 2004, 5:389-401. This paper demonstrates that MAPK could enhance arsenic-mediated PML protein phosphorylation, and this process is associated with PML sumoylation and cell apoptosis.
43. Sternsdorf T, Puccetti E, Jensen K, et al.: PIC-1/SUMO-1-modified PML-retinoic acid receptor alpha mediates arsenic trioxide-induced apoptosis in acute promyelocytic leukemia. Mol Cell Biol 1999, 19:5170-5178.
44. Joshi S, Hughes JB: Inhibition of coupling factor B activity by cadmium ion, arsenite-2,3-dimercaptopropanol, and phenylarsine oxide, and preferential reactivation by dithiols. J Biol Chem 1981, 256:11112-11116.
45. Don AS, Kisker O, Dilda P, et al.: A peptide trivalent arsenical inhibits tumor angiogenesis by perturbing mitochondrial function in angiogenic endothelial cells. Cancer Cell 2003, 3:497-509. This paper devised a novel derivative of phenylarsenoxide to trigger MPTP opening by cross-linking the cysteine residues of adenine nucleotide translocator, leading to inhibition of angiogenesis.
46. Gurr JR, Bau DT, Liu F, et al.: Dithiothreitol enhances arsenic trioxide-induced apoptosis in NB4 cells. Mol Pharmacol 1999, 56:102-109.
47. Grignani F, De Matteis S, Nervi C, et al.: Fusion proteins of the retinoic acid receptor-alpha recruit histone deacetylase in promyelocytic leukaemia. Nature 1998, 391:815-818.
48. Lin RJ, Nagy L, Inoue S, et al.: Role of the histone deacetylase complex in acute promyelocytic leukaemia. Nature 1998, 391:811-814.
49. 3 exerts dose-dependent dual effects on APL cells. Blood 1997, 89:3345-3353.
50. Hong SH, Yang Z, Privalsky ML: Arsenic trioxide is a potent inhibitor of the interaction of SMRT corepressor with its transcription factor partners, including the PML-retinoic acid receptor alpha oncoprotein found in human acute promyelocytic leukemia. Mol Cell Biol 2001, 21:7172-7182.
51. Chou WC, Hawkins AL, Barrett JF, et al.: Arsenic inhibition of telomerase transcription leads to genetic instability. J Clin Invest 2001, 108:1541-1547.
52. Mathas S, Lietz A, Janz M, et al.: Inhibition of NF-kappaB essentially contributes to arsenic-induced apoptosis. Blood 2003, 102:1028-1034.
53. Park JW, Choi YJ, Jang MA, et al.: Arsenic trioxide induces G2/M growth arrest and apoptosis after caspase-3 activation and bcl-2 phosphorylation in promonocytic U937 cells. Biochem Biophys Res Commun 2001, 286:726-734.
54. Liu Q, Hilsenbeck S, Gazitt Y: Arsenic trioxide-induced apoptosis in myeloma cells: p53-dependent G1 or G2/M cell cycle arrest, activation of caspase-8 or caspase-9, and synergy with APO2/TRAIL. Blood 2003, 101:4078-4087.
55. Ruchaud S, Duprez E, Gendron MC, et al.: Two distinctly regulated events, priming and triggering, during retinoid-induced maturation and resistance of NB4 promyelocytic leukemia cell line. Proc Natl Acad Sci USA 1994, 91:8428-8432.
56. Zhu Q, Zhang JW, Zhu HQ, et al.: Synergic effects of arsenic trioxide and cAMP during acute promyelocytic leukemia cell maturation subtends a novel signaling cross-talk. Blood 2002, 99:1014-1022.
57. Guillemin MC, Raffoux E, Vitoux D, et al.: In vivo activation of cAMP signaling induces growth arrest and differentiation in acute promyelocytic leukemia. J Exp Med 2002, 196:1373-1380.
58. Bazarbachi A, El-Sabban ME, Nasr R, et al.: Arsenic trioxide and interferon-alpha synergize to induce cell cycle arrest and apoptosis in human T-cell lymphotropic virus type I-transformed cells. Blood 1999, 93:278-283.
59. El-Sabban ME, Nasr R, Dbaibo G, et al.: Arsenic-interferon-alpha- triggered apoptosis in HTLV-I transformed cells is associated with tax down-regulation and reversal of NF-kappa B activation. Blood 2000, 96:2849-2855.
60. Chelbi-alix MK, Bobe P, Benoit G, et al.: Arsenic enhances the activation of Stat1 by interferon gamma leading to synergistic expression of IRF-1. Oncogene 2003, 22:9121-9130.
61. Dai J, Weinberg RS, Waxman S, Jing Y: Malignant cells can be sensitized to undergo growth inhibition and apoptosis by arsenic trioxide through modulation of the glutathione redox system. Blood 1999, 93:268-277.
62. Maeda H, Hori S, Ohizumi H, et al.: Effective treatment of advanced solid tumors by the combination of arsenic trioxide and L-buthionine-sulfoximine. Cell Death Differ 2004, 11:737-746.
63. Grad JM, Bahlis NJ, Reis I, et al.: Ascorbic acid enhances arsenic trioxide-induced cytotoxicity in multiple myeloma cells. Blood 2001, 98:805-813.