Therapy-related leukemias

Childhood Leukemias, Second Edition

Volumn , Issue , 2006, Pages 774-804

  Felix, Carolyn A ^a  

^a UNIVERSITY OF PENNSYLVANIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

EID: 33747879634     PISSN: None     EISSN: None     Source Type: Book    
DOI: 10.1017/CBO9780511471001.032     Document Type: Chapter

References (425)

1. Flannery, J.T., Boice, J.D., Jr., Devesa, S. S., et al. Cancerregistration in Connecticut and the study of multiple primary cancers, 1935-1982. Natl Cancer Inst Monogr, 1985; 68: 13-24.
2. Smith, M. A., McCaffrey, R. P., & Karp, J. E. The secondary leukemias: challenges and research directions. JNCI, 1996; 88: 407-18.
3. Felix, C. A. Secondary leukemias induced by topoisomerase targeted drugs. Biochimica et Biophysica Acta, 1998;1400: 233-55.
4. Felix, C. Chemotherapy-related second cancers. In A. I. Neugut, A. T. Meadows, & E. Robinson, eds., Multiple Primary Cancers: Incidence, Etiology, Diagnosis and Prevention (Baltimore, MD:Williams &Wilkins, 1999), pp. 137-64.
5. Meadows, A. T., Baum, E., Fossati-Bellani, F., et al. Second malignant neoplasms in children: an update from the late effects study group. J Clin Oncol, 1985; 3: 532-8.
6. Kaldor, J. Second cancer following chemotherapy and radiotherapy. An epidemiological perspective. Acta Oncol, 1990; 29: 647-55.
7. Donaldson, S. S. & Hancock, S. L. Second cancers after Hodgkin's disease in childhood. N Engl J Med, 1997; 334: 792-3.
8. Wolden, S. L., Lamborn, K. L., Cleary, S. F., Tate, D. J., &Donaldson, S. Second cancers following pediatric Hodgkin's disease. J Clin Oncol, 1998; 16: 536-44.
9. Ron, E., Lubin, J. H., Shore, R. E., et al. Thyroid cancer after exposure to external radiation: a pooled analysis of seven studies. Radiat Res, 1995; 141: 259-77.
10. Travis, L. B., Curtis, R. E., Boice, J. D., Jr., et al. Second malignant neoplasms among long-termsurvivors of ovarian cancer. Cancer Res, 1996; 56: 1564-70.
11. Tucker, M. A., Jones, P. H. M., Boice, J. D., Jr., et al. Therapeutic radiation at a young age is linked to secondary thyroid cancer. Cancer Res, 1991; 51: 2885-8.
12. Inskip, P. D. Second cancers following radiotherapy. In A. I. Neugut, A. T. Meadows, & E. Robinson, eds., Multiple Primary Cancers: Incidence, Etiology, Diagnosis and Prevention (Baltimore, MD:Williams &Wilkins, 1999), pp. 91-135.
13. UNSCEAR. United National Scientific Committee on the Effects of Atomic Radiation. UNSCEAR 2000 Report to General Assembly, with Scientific Annexes, Sources and Effects of Ionizing Radiation. UNSCEAR 2001. (New York: United Nations, 2001).
14. Rowley, J.D. & Olney, H. J. International workshop on the relationship of prior therapy to balanced chromosome aberrations in therapy-relatedmyelodysplastic syndromesandacute leukemia: overview report. Genes Chromosomes Cancer, 2002; 33: 331-45.
15. Smith, S. M., Le Beau, M.M., Huo, D., et al. Clinical-cytogenetic associations in 306 patients with therapy-related myelodysplasia and myeloid leukemia: the University of Chicago series. Blood, 2003; 102: 43-52.
16. Boice, J. D. Jr., Travis, L. B., & Curtis, L. B. Patterns of second cancers [abstract]. Proc AACR, 1997; 38: 645.
17. Kyle, R. A., Pierre, R. V., & Bayrd, E. D. Multiple myeloma and acute myelomonocytic leukemia: report of four cases possibly related to melphalan. N Engl J Med, 1970; 283: 1121-5.
18. Davies, S. M. Therapy-related leukemia associated with alkylating agents. Med Pediatr Oncol, 2001; 36: 536-40.
19. Pedersen-Bjergaard, J. Incidence, previous treatment and chromosome characteristics of secondary acute nonlymphocytic leukemia. Cancer Treat Rev, 1985; 12: 65-75.
20. Miser, J., Krailo, M., Smith, M., et al. Secondary leukemia (SL) or myelodysplastic syndrome (MDS) following therapy for Ewing's sarcoma (ES) [abstract]. Proc ASCO, 1997; 16: 518a.
21. Blayney, D.W., Longo, D. L., Young, R. C., et al. Decreasing risk of leukemia with prolonged follow-upafter chemotherapy and radiotherapy for Hodgkin's disease. N Engl J Med, 1987; 316: 710-4.
22. Meadows, A.T., Obringer, A. C., Marrero, O., et al.Secondmalignant neoplasms following childhood Hodgkin's disease: treatmentandsplenectomyas risk factors. Med Pediatr Oncol, 1989; 17: 477-84.
23. Bhatia, S., Robison, L. L., Oberlin, O., et al. Breast cancer and other second neoplasms after childhood Hodgkin's disease. N Engl J Med, 1997; 334: 745-51.
24. Schellong, G., Riepenhausen, M., Creutzig, U., et al. Low risk of secondary leukemias after chemotherapy without mechlorethamine in childhood Hodgkin's disease. J Clin Oncol, 1997; 15: 2247-53.
25. Greene, M.H., Harris, E. L., Gershenson, D. M., et al.Melphalan may be a more potent leukemogen than cyclophosphamide. Ann Intern Med, 1986; 105: 360-7.
26. Curtis, R. E., Boice, J, J. D., Stovall, M., et al. Risk of leukemia after chemotherapy and radiation treatment for breast cancer. NEngl J Med, 1992; 326: 1745-51.
27. Diamandidou, E., Buzdar, A. U., Smith, T. L., et al. Treatment-related leukemia in breast cancer patients treated with fluorouracil-doxorubicin-cyclophosphamide combination adjuvant chemotherapy: the University of Texas M. D. Anderson Cancer Center experience. J Clin Oncol, 1996; 14: 2722-30.
28. Tew, K. D., Colvin, M., & Chabner, B. A. Alkylating agents. In B. A. Chabner & D. L. Longo, eds., Cancer Chemotherapy and Biotherapy: Principles and Practice, vol. 1 (New York: Lippincott-Raven, 1996), pp. 297-332.
29. Friedman, H. S., Averbuch, S. D., & Kurtzberg, J. Nonclassic alkylating agents. In B. A. Chabner & D. L. Longo, eds., Cancer Chemotherapy and Biotherapy: Principles and Practice, vol. 1 (New York: Lippincott-Raven, 1996), pp. 333-56.
30. Reed, E., Dabholkar, M., & Chabner, B. A. Platinum analogues. In B. A. Chabner & D. L. Longo, eds., Cancer Chemotherapy and Biotherapy: Principles and Practice, vol. 1 (New York: Lippincott-Raven, 1996), pp. 357-78.
31. Chabner, B. A. &Myers, C. E. Clinical pharmacology of cancer chemotherapy. In V. T. De Vita, S. Hellman, & S. A. Rosenberg, eds., Principles and Practice of Oncology (Philadelphia, PA: J. B. Lippincott, 1989), pp. 349-95.
32. Greene, M. H. Is cisplatin a human carcinogen? J Natl Cancer Inst, 1992; 84: 306-12.
33. Pappo, A., Schneider, N. R., Sanders, J. M., & Buchanan, G. R. Secondary myelodysplastic syndrome complicating therapy for osteogenic sarcoma. Cancer, 1991; 68: 1373-5.
34. Panizo, C., Patino, A., Calasanz, J., et al. Emergence of secondary acute leukemia in a patient treated for osteosarcoma: implications of germline TP53 mutations. Med Pediatr Oncol, 1998; 30: 165-9.
35. Williams, T. M., Colas, C., Nowell, P. C., et al. Association of germlinep53replication error withmyelodysplastic syndrome following osteosarcomatreatment [abstract]. Proc AACR, 1999; 40: 683.
36. Jeha, S., Jaffe, N., & Robertson, R. Secondary acute nonlymphoblastic leukemia in two children following treatment with a cis-diamminechloroplatinum-II-based regimen for osteosarcoma. Med Pediatr Oncol, 1992; 20: 71-4.
37. De Vore, R., Whitlock, J., Hainsworth, J. D., & Johnson, D. H. Therapy-related acute nonlymphocytic leukemia with monocytic features and rearrangement of chromosome 11q. Ann Intern Med, 1989; 110: 740-2.
38. Nichols, C. R., Breeden, E. S., Loehrer, P. J., Williams, S. D., & Einhorn, L. H. Secondary leukemia associated with a conventional dose of etoposide: review of serial germ cell tumor protocols. J Natl Cancer Inst, 1993; 85: 36-40.
39. Pedersen-Bjergaard, J., Daugaard, G., Hansen, S. W., et al. Increased risk of myelodysplasia and leukaemia after etoposide, cisplatin, and bleomycin for germ-cell tumours. Lancet, 1991; 338: 359-63.
40. Travis, L. B., Holowaty, E. J., Bergfeldt, K., et al. Risk of leukemia after platinum-basedchemotherapy forovarian cancer. NEngl J Med, 1999; 340: 351-7.
41. Travis, L. B., Andersson, M., Gospodarowicz, M., et al. Treatment-related leukemia following testicular cancer. J Natl Cancer Institute, 2000; 92: 1165-71.
42. Tucker, M. A., Coleman, C. N., Cox, R. S., Varghese, A., & Rosenberg, S. A. Risk of second cancers after treatment for Hodgkin's disease. NEngl J Med, 1988; 318: 76-81.
43. Kaldor, J. M., Day, N. E., Clarke, E. A., et al. Leukemia following Hodgkin's disease. NEngl J Med, 1990; 22: 7-13.
44. Miller, J. S., Arthur, D. C., Litz, C. E., et al. Myelodysplastic syndrome after autologous bone marrow transplantation: an additional late complication of curative cancer therapy. Blood, 1994; 83: 3780-6.
45. Stone, R. M., Neuberg, D., Soiffer, R., et al. Myelodysplastic syndrome as a late complication following autologous bone marrow transplantation for non-Hodgkin's lymphoma. J Clin Oncol, 1994; 12: 2535-42.
46. Deeg, H. J. & Socie, G. Malignancies after hematopoietic stem cell transplantation: many questions, some answers. Blood, 1998; 91: 1833-44.
47. Pedersen-Bjergaard, J., Andersen, M. K., & Christiansen, D. H. Therapy-related acute myeloid leukemia and myelodysplasia after high-dose chemotherapy and autologous stem cell transplantation. Blood, 2000; 95: 3273-9.
48. Rege, K.P., Janes, S. L., Saso, R., et al.Secondaryleukaemiacharacterised bymonosomy7 occurring post-autologous stem cell transplantation for AML. Bone Marrow Transplant, 1998; 21: 853-5.
49. Micallef, I. N., Lillington, D. M., Apostolidis, J., et al. Therapyrelated myelodysplasia and secondary acute myelogenous leukemia after high-dose therapy with autologous hematopoietic progenitor-cell support for lymphoid malignancies. J Clin Oncol, 2000; 18: 947-55.
50. Armitage, J. O. Myelodysplasia and acute leukemia after autologous bone marrow transplantation [editorial]. J Clin Oncol, 2000; 18: 945-6.
51. Abruzzese, E., Radford, J. E., Miller, J. S., et al. Detection of abnormal pretransplant clones in progenitor cells of patients who developed myelodysplasia after autologous transplantation. Blood, 1999; 94: 1814-19.
52. Weber, M. H., Wenzel, U., Thiel, E., & Knauf, W. U. Chromosomal aberrations characteristic for sAML/sMDS are not detectable by random screening using FISH in peripheral blood-derived grafts used for autologous transplantation. J Hematother Stem Cell Res, 2000; 9: 861-5.
53. Kaneko, Y., Maseki, N., Sakurai, M., et al. Chromosome pattern in juvenile chronic myelogenous leukemia, myelodysplastic syndrome and acute leukemia associated with neurofibromatosis. Leukemia, 1989; 3: 36-41.
54. Perilongo, G., Felix, C. A., Meadows, A. T., et al. Sequential development of Wilms tumor, T-cell acute lymphoblastic leukemia, medulloblastoma and myeloid leukemia in a child with Type 1 neurofibromatosis: a clinical and cytogenetic case report. Leukemia, 1993; 7: 912-15.
55. Maris, J. M., Wiersma, S. R., Mahgoub, N., et al. Monosomy 7 myelodysplastic syndrome and other second malignant neoplasms in children with neurofibromatosis type 1. Cancer, 1997; 79: 1438-46.
56. Side, L., Taylor, B., Cayouette, M., et al. Homozygous inactivation of the NF1 gene in bone marrow cells from children with neurofibromatosis type 1 and malignant myeloid disorders. N Engl J Med, 1997; 336: 1713-20.
57. Mahgoub, N., Taylor, B. R., Le Beau, M.M., et al.Myeloid malignancies induced by alkylating agents in Nf1 mice. Blood, 1999; 93: 3617-23.
58. Felix, C. A., Hosler, M. R., Provisor, D., et al. The p53 gene in pediatric therapy-related leukemia and myelodysplasia. Blood, 1996; 87: 4376-81.
59. Diller, L., Sexsmith, E., Gottlieb, A., Li, F. P., & Malkin, D. Germline p53 mutations are frequently detected in young children with rhabdomyosarcoma. J Clin Invest, 1995; 95: 1606-11.
60. Felix, C. A., Megonigal, M. D., Chervinsky, D. S., et al. Association of germline p53 mutation with MLL segmental jumping translocation in treatment-related leukemia. Blood, 1998; 91: 4451-6.
61. McIntyre, J.F., Smith-Sorensen, B., Friend, S. H., et al.Germline mutations of the p53 tumor suppressor gene in children with osteosarcoma. J Clin Oncol, 1994; 12: 925-30.
62. Tanaka, K., Arif, M., Eguchi, M., et al. Frequent jumping translocations of chromosomalsegments involving the ABLoncogene alone or in combination with CD3-MLL genes in secondary leukemias. Blood, 1997; 89: 596-600.
63. Avet-Loiseau, H., Godon, C., Li, J. Y., et al. Amplification of the 11q23 region in acute myeloid leukemia. Genes Chromosomes Cancer, 1999; 26: 166-70.
64. Livingstone, L. R., White, A., Sprouse, J., et al. Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53. Cell, 1992; 70: 923-35.
65. Paulson, T. G., Almasan, A., Brody, L. L., & Wahl, G. M. Gene amplification in a p53-deficient cell line requires cell cycle progression under conditions that generate DNA breakage. Molec and Cell Biol, 1998; 18: 3089-100.
66. Seedhouse, C., Bainton, R., Lewis, M., et al. The genotype distribution of the XRCC1 gene indicates a role for base excision repair in the development of therapy-related acutemyeloblastic leukemia. Blood, 2002; 100: 3761-6.
67. Ben-Yehuda, D., Krichevsky, S., Caspi, O., et al. Microsatellite instabilityandp53mutations in therapy-related leukemia suggest mutator phenotype. Blood, 1996; 88: 4296-303.
68. Worrillow, L. J., Travis, L. B., Smith, A. G., et al. An intron splice acceptor polymorphism in hMSH2 and risk of leukemia after treatment with chemotherapeutic alkylating agents. Clin Cancer Res, 2003; 9: 3012-20.
69. Hayes, J.D.&Pulford, D. J. Theglutathione S-transferasesupergene family: regulation of GST and the contribution of the Cambridge Books Online (c) Cambridge University Press, 2009 Therapy-related leukemias 793 isoenzymes to cancer chemoprotection and drug resistance. Critical Rev Biochem Molec Biol, 1995; 30: 445-600.
70. Smith, G., Stanley, L. A., Sim, E., Strange, R. C., & Wolf, C. R. Metabolic polymorphisms and cancer susceptibility. Cancer Surveys, 1995; 25: 27-65.
71. Raunio, H., Husgafvel-Pursianen, K., Anttila, S., et al. Diagnosis of polymorphisms in carcinogen-activating and inactivating enzymes and cancer susceptibility. Gene, 1995; 159: 113-21.
72. Morgan, G. J.&Smith, M.T. Metabolicenzymepolymorphisms and susceptibility to acute leukemia in adults. Am J Pharmacogenomics, 2002; 2: 79-92.
73. Li, A. P., Kaminski, D. L., & Rasmussen, A. Substrates of human hepatic cytochrome P450 3A4. Toxicology, 1995; 104: 1-8.
74. Wrighton, S. & Stevens, J. The human hepatic cytochromes P450 involved in drug metabolism. Crit Rev Toxicol, 1992; 22: 1-21.
75. Felix, C. A., Walker, A. H., Lange, B. J., et al. Association of CYP3A4 genotype with treatment-related leukemia. Proc Natl Acad Sci U S A, 1998; 95: 13 176-81.
76. Kuehl, P., Zhang, J., Lin, Y., et al. Sequence diversity in CYP3A promoters and characterization of the genetic basis of polymorphic CYP3A5 expression. Nat Genet, 2001; 27: 383-91.
77. Roddam, P. L., Rollinson, S., Kane, E., et al. Poor metabolizers at the cytochromeP450 2D6 and 2C19 loci are at increased risk of developing adult acute leukaemia. Pharmacogenetics, 2000; 10: 605-15.
78. Chen, H., Sandler, D. P., Taylor, J. A., et al. Increased risk for myelodysplastic syndromes in individuals with glutathione transferase theta 1 (GSTT1) gene defect. Lancet, 1996; 347: 295-7.
79. Sasai, Y., Horiike, S., Misawa, S., et al. Genotype of glutathione S-transferase and other genetic configurations in myelodysplasia. Leuk Res, 1999; 23: 975-81.
80. Allan, J. M., Wild, C. P, Rollinson, S., et al. Polymorphism in glutathione S-transferase P1 is associated with susceptibility to chemotherapy-induced leukemia. Proc Natl Acad Sci U S A, 2001; 98: 11 592-7.
81. Ernster, L. DT-diaphorase: its structure, function, regulation, and role in antioxidant defence and cancer chemotherapy. In K. Yagi, ed., Pathophysiology of lipid peroxides and related free radicals. (Basel, Switzerland: Karger, 1998), pp. 149-68.
82. Ross, D. Quinone reductases. In F. P. Guengerich, ed., Comprehensive Toxicology, vol. 3 (New York: Pergamon Press, 1997), pp. 179-97.
83. Joseph, P., Long, D. J., Klein-Szanto, A. J., &Jaiswal, A. K. Role of NAD(P)H: quinone oxidoreductase 1 (DT diaphorase) in protection against quinone toxicity. Biochem Pharmacol, 2000;60: 207-14.
84. Benson, A. M., Hunkeler, M. J., & Talalay, P. Increase of NAD(P)H: quinone reductase by dietary antioxidants: possible role in protection against carcinogenesis and toxicity. Proc Natl Acad Sci U S A, 1980; 7: 5216-20.
85. Traver, R. D., Horikoshi, T., Danenberg, K. D., et al. NAD(P)H: quinone oxidoreductase gene expression in human colon carcinoma cells: characterization of a mutation which modulates DT-diaphorase activity and mitomycin sensitivity. Cancer Res, 1992; 52: 797-802.
86. Siegel, D., Winski, S. L., & Ross, D. Genotype-phenotype relationships in studies of a polymorphism in NAD(P)H: quinone oxidoreductase 1. Pharmacogenetics, 1999; 9: 113-21.
87. Rothman, N., Smith, M. T., Hayes, R. B., et al. Benzene poisoning, a risk factor for hematologic malignancy, is associated with NQO1 609 C->Tmutation and rapid fractional excretion of chlorzoxazone. Cancer Res, 1997; 57: 2839-42.
88. 609C->T polymorphism in the NAD(P)H: quinone oxidoreductase (NQO1) gene in patients with primary and therapy-related myeloid leukemia. Blood, 1999; 94: 803-7.
89. Naoe, T., Takeyama, K., Yokozawa, T., et al. Analysis of genetic polymorphism in NQO1, GST-M1, GST-T1, and CYP3A4 in 469 Japanese patients with therapy-related leukemia/myelodysplastic syndrome and de novo acute myeloid leukemia. Clin Cancer Res, 2000; 6: 4091-5.
90. Pui, C. H., Ribeiro, R. C., Hancock, M. L., et al. Acute myeloid leukemia in children treated with epipodophyllotoxins for acute lymphoblastic leukemia. NEngl J Med, 1991; 325: 1682-7.
91. Pui, C.-H., Hancock, M. L., Raimondi, S. C., et al. Myeloid neoplasia in children treated for solid tumours. Lancet, 1990; 336: 417-21.
92. Pui, C.-H., Behm, F. G., Raimondi, S. C., et al. Secondary acutemyeloid leukemia in children treated for acute lymphoid leukemia. NEngl J Med, 1989; 321: 136-42.
93. Winick, N., McKenna, R. W., Shuster, J. J., et al. Secondary acute myeloid leukemia in children with acute lymphoblastic leukemia treated with etoposide. J Clin Oncol, 1993; 11: 209-17.
94. Chak, L. Y., Sikic, B. I., Tucker, M. A., Horns, R. C., Jr., & Cox, R. S. Increased incidence of acute nonlymphocytic leukemia following therapy in patients with small cell carcinoma of the lung. J Clin Oncol, 1984; 2: 385-90.
95. Johnson, D. H., Porter, L. L., List, A. F., et al. Acute nonlymphocytic leukemia after treatment of small cell lung cancer. Am J Med, 1986; 81: 962-8.
96. Weh, H. J., Kabisch, H., Landbeck, G., & Hossfeld, D. K. Translocation (9;11)(p21q23) in a child with acute monoblastic leukemia following 2 1/2 years after successful chemotherapy for neuroblastoma. J Clin Oncol, 1986; 4: 1518-20.
97. Albain, K. S., Le Beau, M. M., Ullirsch, R., & Schumacher, H. Implications of prior treatment with drug combinations including inhibitors of topoisomerase II in therapy-related monocytic leukemia with a 9;11 translocation. Genes Chromosomes Cancer, 1990; 2: 53-8.
98. Verdeguer, A., Ruiz, J. G., Ferris, J., et al. Acute nonlymphoblastic leukemia in children treated for acute lymphoblastic leukemia with an intensive regimen including teniposide. Med Pediatr Oncol, 1992; 20: 48-52.
99. Heyn, R., Khan, F., Ensign, L. G., et al. Acute myeloid leukemia in patients treated for rhabdomyosarcoma with cyclophosphamide and low-dose etoposide on intergroup rhabdomyosarcoma study III: an interim report. Med Pediatr Oncol, 1994; 23: 99-106.
100. Whitlock, J. A., Greer, J. P., & Lukens, J. N. Epipodophyllotoxinrelated leukemia: identification of a new subset of secondary leukemia. Cancer, 1991; 68: 600-4.
101. Zeimet, A. G., Thaler, J., Abfalter, E., Marth, C., & Dapunt, O. Secondary leukaemias after etoposide. Lancet, 1992; 340: 379-80.
102. Hawkins, M. M. Secondary leukaemia after epipodophyllotoxins. Lancet, 1991; 338: 1408.
103. Hawkins, M. M., Kinnier-Wilson, L. M., Stovall, M. A., et al. Epipodophyllotoxins, alkylating agents, and radiation and risk of secondary leukaemia after childhood cancer. BMJ, 1992; 304: 951-8.
104. Pedersen-Bjergaard, J., Philip, P., Larsen, S. O., Jensen, G., & Byrsting, K. Chromosome aberrations and prognostic factors in therapy-related myelodysplasia and acute nonlymphocytic leukemia. Blood, 1990; 76: 1083-91.
105. Bajorin, D. F., Motzer, R. J., Rodriguez, E., Murphy, B., & Bosl, G. J. Acute nonlymphocytic leukemia in germ cell tumor patients treated with etoposide-containing chemotherapy. J Natl Cancer Inst, 1993; 85: 60-2.
106. Pedersen-Bjergaard, J., Daugaard, G., Hansen, S. W., et al. Increased risk of myelodysplasia and leukaemia after etoposide, cisplatin, and bleomycin for germ-cell tumours. Lancet, 1991; 338: 359-63.
107. Donatini, B. & Krupp, P. Secondary pre-leukaemia and etoposide. Lancet, 1991; 338: 1269.
108. Rose, V. L., Keppen, M. D., Eichner, E. R., Pitha, J. V., &Murray, J. L. Acute leukemia after successful chemotherapy for oat cell carcinoma. Am J Clin Pathol, 1983; 79: 122-4.
109. Bokemeyer, C. & Schmoll, H.-J. Secondary neoplasms following treatment of malignant germ cell tumors. J Clin Oncol, 1993; 11: 1703-9.
110. Secker-Walker, L. M., Stewart, E. L., & Todd, A. Acute lymphoblastic leukaemia with t(4;11) follows neuroblastoma: a late effect of treatment. Med Pediatr Oncol, 1985; 13: 48-50.
111. Ratain, M. J., Kaminer, L. S., Bitran, J. D., et al. Acute nonlymphocytic leukemia following etoposide and cisplatin combination chemotherapy for advanced non-small-cell carcinoma of the lung. Blood, 1987; 70: 1412-17.
112. Burden, D. A.&Osheroff, N. Mechanism of action of eukaryotic topoisomerase II and drugs targeted to the enzyme. Biochim Biophys Acta, 1998; 400: 139-54.
113. Fortune, J. M. & Osheroff, N. Topoisomerase II as a target for anticancer drugs: when enzymes stop being nice. Prog Nucleic Acid Res Mol Bio, 2000; 64: 221-53.
114. Robinson, M. J., Corbett, A. H., & Osheroff, N. Effects of topoisomerase II-targeted drugs on enzyme-mediated DNA cleavage and ATP hydrolysis: evidence for distinct drug interaction domains on topoisomerase II. Biochemistry, 1993; 32: 3638-43.
115. Andoh, T. & Ishida, R. Catalytic inhibitors of DNA topoisomerase II. Biochim Biophys Acta, 1998; 1400: 155-94.
116. Rivera, G. K., Pui, C. H., Santana, V. M., Pratt, C. B., & Crist, W. M. Epipodophyllotoxins in the treatment of childhood cancer. Cancer Chemother Pharmacol, 1994; 34: S89-95.
117. Giaccone, G. Teniposide alone and in combination chemotherapy in small cell lung cancer. Semin Oncol, 1992; 19: 75-80.
118. Giaccone, G., Splinter, T. A., Kirkpatrick, A., et al. The European Organizationfor Researchand Treatmentof Cancerexperience with teniposide: preliminary results of a randomized study in non-small cell lung cancer. Semin Oncol, 1992; 19: 98-102.
119. Muggia, F. M. Teniposide: overview of its therapeutic potential in adult cancers. Cancer Chemother Pharmacol, 1994; 34: S127-33.
120. Hirsch, F. R., Dombernowsky, P., &Hansen, H. H. Treatment of small cell lung cancer: the Copenhagenexperience. Anticancer Res, 1994; 14: 317-19.
121. Muggia, F. M. & Kelley, S. L. Teniposide in adult solid tumors: a historical perspective. Semin Oncol, 1992; 19: 43-50.
122. Weh, H. J., Kabisch, H., Landbeck, G., & Hossfeld, D. K. Translocation (9;11)(p21;q23) in a child with acute monoblastic leukemia following 2 1/2 years after successful chemotherapy for neuroblastoma. J Clin Oncol, 1986; 4: 1518-20.
123. Kreissman, S. G., Gelber, R. D., Cohen, H. J., et al. Incidence of secondary acute myelogenous leukemia after treatment of childhood acute lymphoblastic leukemia. Cancer, 1992; 70: 2208-13.
124. Pedersen-Bjergaard, J., Sigsgaard, T. C., Nielsen, D., et al. Acute monocytic or myelomonocytic leukemia with balanced chromosome translocations to band 11q23 after therapy with 4-epi-doxorubicin and cisplatin or cyclophosphamide for breast cancer. J Clin Oncol, 1992; 10: 1444-51.
125. Detourmignies, L., Castaigne, S., Stoppa, A. M., et al. Therapyrelated acute promyelocytic leukemia: a report on 16 cases. J Clin Oncol, 1992; 10: 1430-5.
126. Sandoval, C., Pui, C. H., Bowman, L. C., et al. Secondary acute myeloid leukemia in children previously treated with alkylating agents, intercalating topoisomerase II inhibitors, and irradiation. J Clin Oncol, 1993; 11: 1039-45.
127. Atlas, M., Head, D., Behm, F., et al. Cloning and sequence analysis of four t(9;11) therapy-related leukemia breakpoints. Leukemia, 1998; 12: 1895-902.
128. Kushner, B. H., Heller, G., Cheung, N. K., et al. High risk of leukemia after short-term dose-intensive chemotherapy in young patients with solid tumors. J Clin Oncol, 1998; 16: 3016-20.
129. Kushner, B. H., Cheung, N. K., Kramer, K., Heller, G., & Jhanwar, S. C. Neuroblastoma and treatment-related myelodysplasia/leukemia: the Memorial Sloan-Kettering experience and a literature review. J Clin Oncol, 1998; 16: 3880-9.
130. Megonigal, M. D., Cheung, N. K., Rappaport, E. F., et al. Detection of leukemia-associated MLL-GAS7 translocation early Cambridge Books Online (c) Cambridge University Press, 2009 Therapy-related leukemias 795 during chemotherapy with DNA topoisomerase II inhibitors. Proc Natl Acad Sci U S A, 2000; 97: 2814-19.
131. Vicari, A. M., Ciceri, F., Folli, F., et al. Acute promyelocytic leukemia following mitoxantrone as single agent for the treatment of multiple sclerosis [letter]. Leukemia, 1998; 12: 441-2.
132. Pedersen-Bjergaard, J. & Philip, P. Balanced translocations involving chromosome bands 11q23 and 21q22 are highly characteristic of myelodysplasia and leukemia following therapy with cytostatic agents targeting at DNA-topoisomerase II. Blood, 1991; 78: 1147-8.
133. Megonigal, M. D., Rappaport, E. F., Jones, D. H., et al. Panhandle PCR strategy to amplify MLL genomic breakpoints in treatment-related leukemias. Proc Natl Acad Sci U S A, 1997; 94: 11583-8.
134. Corbett, A.&Osheroff, N. Whengood enzymes go bad: conversion of topoisomerase II to a cellular toxin by antineoplastic drugs. Chem Res Toxicol, 1993; 6: 585-97.
135. Beaumont, M., Sanz, M., Carli, P. M., et al. Therapy-related acute promyelocytic leukemia. J Clin Oncol, 2003; 21: 2123-37.
136. Crump, M., Tu, D., Shepherd, L., et al. Risk of acute leukemia following epirubicin-based adjuvant chemotherapy: a report from the National Cancer Institute of Canada Clinical Trials Group. J Clin Oncol, 2003; 21: 3066-71.
137. Barker, D. E., Dragnani, T. A., Dunnick, J. K., et al. IARCMonographs on the Evaluation of Carcinogenic Risks to Humans. Some Antiviral and Antineoplastic drugs, and Other Pharmaceutical Agents, vol. 76. (Lyon, France: IARC Press, 2000).
138. Duffner, P. K., Krischer, J.P., Horowitz, M.E., et al.Secondmalignancies inyoungchildrenwith primarybraintumorsfollowing treatment with prolonged postoperative chemotherapy and delayed irradiation: a Pediatric Oncology Group study. Ann Neurol, 1998; 44: 313-16.
139. Sugita, K., Furukawa, T., Tsuchida, M., et al. High frequency of etoposide (VP-16)-related secondary leukemia in children with non-Hodgkin's lymphoma. Am J Pediatr Hematol Oncol, 1993; 15: 99-104.
140. Yagita, M., Ieki, Y., Onishi, R., et al. Therapy-related leukemia andmyelodysplasia followingoral administration of etoposide for recurrent breast cancer. Int J Oncol, 1998; 13: 91-6.
141. Bokemeyer, C., Schmoll, H. J., Kuczyk, M. A., Beyer, J., & Sieger, W. Risk of secondary leukemia following high cumulative doses of etoposide during chemotherapy for testicular cancer [letter]. J Natl Cancer Inst, 1995; 87: 58-60.
142. Boshoff, C., Begent, R. H., Oliver, R.T., et al.Secondarytumours following etoposide containing therapy for germ cell cancer. Ann Oncol, 1995; 8: 35-40.
143. Pedersen-Bjergaard, J.&Rowley, J.D. The balanced and unbalanced chromosome aberrations of acute myeloid leukemia may develop in different ways and may contribute to malignant transformation. Blood, 1994; 83: 2780-6.
144. Sano, K., Hayakawa, A., Piao, J.-H., Kosaka, Y., & Nakamura, H. Novel SH3 protein encoded by the AF3p21 gene is fused to the mixed lineage leukemia protein in a therapy-related leukemia with t(3;11)(p21;q23). Blood, 2000; 95: 1066-8.
145. _-monophosphate synthetase). Blood, 2000; 96: 4360-2.
146. Smith, M. A., Rubenstein, L., &Anderson, J. R., et al. Secondary leukemia or myelodysplastic syndrome after treatment with epipodophyllotoxins. J Clin Oncol, 1999; 17: 569-77.
147. Le Deley, M. C., Leblanc, T., Shamsaldin, A., et al. Risk of secondary leukemia after a solid tumor in childhood according to the dose of epipodophyllotoxins and anthracyclines: a case-control study by the Societe Francaise d'Oncologie Pediatrique. J Clin Oncol, 2003; 21: 1074-81.
148. Rivera, G. K., Pui, C.-H., & Crist, W. M. The epipodophyllotoxins: both sides of the coin. J Clin Oncol, 1993; 11: 1624-7.
149. Sandler, E. S., Friedman, D. J., Mustafa, M. M., et al. Treatment of childrenwith epipodophyllotoxin-induced secondary acute myeloid leukemia. Cancer, 1997; 79: 1049-54.
150. Pui, C.-H., Relling, M. V., Behm, F. G., et al. L-asparaginase may potentiate the leukemogenic effect of the epipodophyllotoxins. Leukemia, 1995; 9: 1680-4.
151. Winick, N., Buchanan, G. R., & Kamen, B. A. Secondary acute myeloid leukemia in Hispanic children. J Clin Oncol, 1993; 11: 1433.
152. Barnard, D. R., Lange, B., Alonzo, T. A., et al. Acute myeloid leukemia and myelodysplastic syndrome in children treated for cancer: comparison with primary presentation. Blood, 2002; 100: 427-34.
153. Haupt, R., Fears, T. R., Heise, A., et al. Risk of secondary leukemia after treatment with etoposide (VP-16) for Langerhans' cell histiocytosis in Italian and Austrian-German populations. Int J Cancer, 1997; 71: 9-13.
154. Ladisch, S., Gadner, H., Arico, M., et al. LCH-I: A randomized trial of etoposide versus vinblastine in disseminated Langerhans cell histiocytosis. Med Pediatr Oncol, 1994; 23: 107-10.
155. Horibe, K., Matsushita, T., Numata, S., et al. Acute promyelocytic leukemia with t(15;17) abnormality after chemotherapy containing etoposide for Langerhanscell histiocytosis. Cancer, 1993; 72: 3723-6.
156. Egeler, R. M., Neglia, J. P., Arico, M., et al. Acute leukemia in association with Langerhans cell histiocytosis. Med Pediatr Oncol, 1994; 23: 81-5.
157. Sandoval, C., Pui, C.-H., Bowman, L. C., et al. Secondary acute myeloid leukemia in children previously treated with alkylating agents, intercalating topoisomerase II inhibitors, and irradiation. J Clin Oncol, 1993; 11: 1039-45.
158. Krishnan, A., Bhatia, S., Slovak, M. L., et al. Predictors of therapy-related leukemia and myelodysplasia following autologous transplantation for lymphoma: an assessment of risk factors. Blood, 2000; 95: 1588-93.
159. Relling, M. V., Boyett, J. M., Blanco, J. G., et al. Granulocyte colony-stimulating factor and the risk of secondary myeloid malignancy after etoposide treatment. Blood, 2003; 101: 3862-7.
160. Felice, M. S., Rossi, J., Gallego, M., et al. Acute trilineage leukemiawithmonosomyofchromosome7followinganacute promyelocytic leukemia. Leuk Lymphoma, 1999; 34: 409-13.
161. Zompi, S., Legrand, O., Bouscary, D., et al. Therapy-related acute myeloid leukaemia after successful therapy for acute promyelocytic leukaemia with t(15;17): a report of two cases and a review of the literature. Br J Haematol, 2000; 110: 610-3.
162. Au, W. Y., Lam, C. C., Ma, E. S., et al. Therapy-relatedmyelodysplastic syndrome after eradication of acute promyelocytic leukemia: cytogenetic and molecular features. Hum Pathol, 2001; 32: 126-9.
163. Andersen, M.K.&Pedersen-Bjergaard, J. Therapy-related MDS and AML in acute promyelocytic leukemia. Blood, 2002; 100: 1928-9.
164. Latagliata, R., Petti, M. C., Fenu, S., et al. Therapy-related myelodysplastic syndrome-acute myelogenous leukemia in patients treated for acute promyelocytic leukemia: an emerging problem. Blood, 2002; 99: 822-4.
165. Athanasiadou, A., Saloum, R., Zorbas, I., et al. Therapy-related myelodysplastic syndrome with monosomy 5 and 7 following successful therapy for acute promyelocytic leukemia with anthracyclines. Leuk Lymphoma, 2002; 43: 2409-11.
166. Andersen, M. K., Larson, R. A., Mauritzson, N., et al. Balanced chromosome abnormalities inv(16) and t(15;17) in therapyrelated myelodysplastic syndromes and acute leukemia: report from an international workshop. Genes Chromosomes Cancer, 2002; 33: 395-400.
167. Maanen, J. M. S. van, Retel, J., de Vries, J., & Pinedo, H. M. Mechanism of action of antitumor drug etoposide: A review. J Natl Cancer Inst, 1988; 80: 1526-33.
168. Mans, D. R. A., Retel, J., Maanen, J. M. S. van, et al. Role of the semi-quinone free radical of the anti-tumour agent etoposide (VP-16-213) in the inactivation of single-anddouble-stranded fX174 DNA. Br J Cancer, 1990; 62: 54-60.
169. Relling, M. V., Nemec, J., Schuetz, E. G., et al. O-demethylation of epipodophyllotoxins is catalyzed by human cytochrome P450 3A4. Mol Pharmacol, 1994; 45: 352-8.
170. Walker, A. H., Jaffe, J. M., Gunasegaram, S., et al. Characterization of an allelic variant in the nifedipine-specific element of CYP3A4: ethnic distribution and implications for prostate cancer risk. Hum Mutat, 1998; 12: 289.
171. Ben-Yehuda, D., Krichevsky, S., Shafran, S., et al. Therapyrelated leukemia: clinical characteristics and analysis of new molecular risk factors in 96 patients [abstract]. Blood, 2002; 100(Suppl. 1): 324a.
172. Blanco, J. G., Edick, M. J., Hancock, M. L., et al. Genetic polymorphisms in CYP3A5, CYP3A4 and NQO1 in children who developed therapy-related myeloid malignancies. Pharmacogenetics, 2002; 12: 605-11.
173. Kishi, S., Yang, W., Boureau, B., et al. Effects of prednisone and genetic polymorphisms on etoposide disposition in children with acute lymphoblastic leukemia. Blood, 2004; 103: 67-72.
174. Sinha, B. K., Politi, P. M., Eliot, H. M., Kerrigan, D., &Pommier, Y. Structure-activity relations, cytotoxicity and topoisomerase II dependent cleavage induced by pendulum ring analogues of etoposide. Eur J Cancer, 1990; 26: 590-3.
175. Gantchev, T. G.&Hunting, D. J. The ortho-quinone metabolite oftheanticancerdrugetoposide(VP-16)isapotentinhibitor of thetopoisomeraseII/DNAcleavablecomplex. Mol Pharmacol, 1998; 53: 422-8.
176. Lovett, B.D., Strumberg, D., Blair, I. A., et al.Etoposide metabolites enhance DNA topoisomerase II cleavage near leukemia associated MLL translocation breakpoints. Biochemistry, 2001; 40: 1159-70.
177. Stremetzne, S., Jaehde, U., Kasper, R., et al. Considerable plasma levels of a cytotoxic etoposide metabolite in patients undergoing high-dose chemotherapy [letter]. Eur J Cancer, 1997; 33: 978-9.
178. Relling, M. V., Yanishevski, Y., Nemec, J., et al. Etoposide and antimetabolite pharmacology in patients who develop secondary acute myeloid leukemia. Leukemia, 1998; 12: 346-52.
179. Pang, S., Zheng, N., Felix, C. A., Boston, R., & Blair, I. A. Simultaneous determination of etoposide and its catechol metabolite in the plasma of pediatric patients by liquid chromatography/tandem mass spectrometry. J Mass Spec, 2001; 36: 771-81.
180. Poll, M.E. vande, Relling, M.V., Schuetz, E. G., et al. Theeffect of atovaquone on etoposide pharmacokinetics in children with acute lymphoblastic leukemia. Cancer Chemother Pharmacol, 2001; 47: 467-72.
181. Zheng, N., Felix, C. A., Pang, S., et al. Plasma etoposide catechol increases in pediatric patients undergoing multiple-day chemotherapy with etoposide. Clin Cancer Res, 2004;10: 2977-85.
182. Chang, T. K., Yu, L., Maurel, P., & Waxman, D. J. Enhanced cyclophosphamide and ifosfamide activation in primary human hepatocyte cultures: response to cytochrome P-450 inducers and autoinduction by oxazaphosphorines. Cancer Res, 1997; 57: 1946-54.
183. Woo, M. H., Shuster, J., Chen, C.-L., et al. Glutathione Stransferase genotypes in children who develop treatmentrelated acute myeloid malignancies. Leukemia, 2000; 4: 232-7.
184. Relling, M. V., Hancock, M. L., Rivera, G. K., et al. Mercaptopurine therapy intoleranceandheterozygosity at the thiopurine S-methyltransferase gene locus. J Natl Cancer Inst, 1999; 91: 2001-8.
185. McLeod, H. L., Lin, J. S., Scott, E. P., Pui, C. H., & Evans, W. E. Thiopurine methyltransferase activity in American white subjects and black subjects. Clin Pharmacol Ther, 1994; 55: 15-20.
186. Echlin-Bell, D. R., Smith, L. L., Li, L., et al. Polymorphisms in the MLL breakpoint cluster region (BCR). Hum Genet, 2003; 113: 80-91.
187. Pedersen-Bjergaard, J., Andersen, M. K., Christiansen, D. H., & Nerlov, C. Geneticpathwaysin therapy-relatedmyelodysplasia and acute myeloid leukemia. Blood, 2002; 99: 1909-12.
188. Willman, C. L. Molecular genetic features of myelodysplastic syndromes (MDS). Leukemia, 1998; 12(Suppl. 1): S2-6.
189. Liang, H., Fairman, J., Claxton, D. F., et al. Molecular anatomy of chromosome 7q deletions in myeloid neoplasms: evidence for multiple critical loci. Proc Natl Acad Sci U S A, 1998; 95: 3781-5.
190. Bodner, S. M., Naeve, C.W., Rakestraw, K. M., et al. Cloning and chromosomal localization of the gene encoding human cyclin D-binding Myb-like protein (hDMP1). Gene, 1999; 229: 223-8.
191. Emerling, B. M., Bonifas, J., Kratz, C. P., et al. MLL5, a homolog of Drosophila trithorax located within a segment of chromosome band 7q22 implicated in myeloid leukemia. Oncogene, 2002; 21: 4849-54.
192. Kratz, C. P., Emerling, B. M., Donovan, S., et al. Candidate gene isolationandcomparative analysis of acommonlydeleted segment of 7q22 implicated in myeloid malignancies. Genomics, 2001; 77: 171-80.
193. Kratz, C.P., Emerling, B. M., Bonifas, J., et al.Genomicstructure of the PIK3CG gene on chromosome band 7q22 and evaluation as a candidatemyeloid tumor suppressor. Blood, 2002; 99: 372-4.
194. Boultwood, J., Lewis, S., & Wainscoat, J. S. The 5q-syndrome. Blood, 1994; 84: 3253-60.
195. Willman, C. L., Sever, C. E., Pallavicini, M. G., et al. Deletion of IRF-1, mapping to chromosome 5q31.1, in human leukemia and preleukemicmyelodysplasia. Science, 1993; 259: 968-71.
196. Zhao, N., Stoffel, A., Wang, P. W., et al. Molecular delineation of the smallest commonly deleted region of chromosome 5 in malignant myeloid diseases to 1-1.5 Mb and preparation of a PAC-based physical map. Proc Natl Acad Sci U S A, 1997; 94: 6948-53.
197. Lezon-Geyda, K., Najfeld, V., & Johnson, E. M. Deletions of PURA, at 5q31, and PURB, at 7p13, in myelodysplastic syndrome and progression to acute myelogenous leukemia. Leukemia, 2001; 15: 954-62.
198. Fairman, J., Wang, R. Y., Liang, H., et al. Translocations and deletions of 5q13.1 in myelodysplasia and acute myelogenous leukemia: evidence for a novel critical locus. Blood, 1996; 88: 2259-66.
199. Castro, P. D., Fairman, J., & Nagarajan, L. The unexplored 5q13 locus: a role in hematopoietic malignancies. Leuk Lymphoma, 1998; 30: 443-8.
200. Castro, P., Liang, H., Liang, J. C., & Nagarajan, L. A novel, evolutionarily conserved gene family with putative sequencespecific single-stranded DNA-binding activity. Genomics, 2002; 80: 78-85.
201. Castro, P. D., Liang, J. C., & Nagarajan, L. Deletions of chromosome 5q13.3 and 17p loci cooperate in myeloid neoplasms. Blood, 2000; 95: 2138-43.
202. Hall, A. The cellular functions of small GTP-binding proteins. Science, 1990; 249: 635-640.
203. Hall, A. Signal transduction through small GTPases-a tale of two GAPs. Cell, 1992; 69: 389-91.
204. Bourne, H. R., Sanders, D. A., & McCormick, F. The GTPase superfamily: a conserved switch for diverse cell functions. Nature, 1990; 348: 125-32.
205. Bourne, H. R., Sanders, D. A., & McCormick, F. The GTPase superfamily: conserved structure and molecular mechanism. Nature, 1991; 349: 117-27.
206. Boguski, M. S. &McCormick, F. Proteins regulating Ras and its relatives. Nature, 1993; 366: 643-54.
207. Aaronson, S. A. Growth factors and cancer. Science, 1991; 254: 1146-53.
208. Satoh, T., Nakafuku, M., Miyajima, A., &Kaziro, Y. Involvement of ras p21 protein in signal-transduction pathways frominterleukin 2, interleukin 3, and granulocyte/macrophage colonystimulating factor, but not from interleukin 4. Proc Natl Acad Sci U S A, 1991; 88: 3314-18.
209. Willman, C. L., Sever, C. E., Pallavicini, M. G., et al. Deletion of IRF-1, mapping to chromosome 5q31.1, in human leukemia and preleukemic myelodysplasia. Science, 1993; 259: 968-71.
210. Le Beau, M. M., Espinosa, R., Neuman, W. L., et al. Cytogenetic and molecular delineation of the smallest deleted region of chromososme 5 in malignant myeloid disorders. Proc Natl Acad Sci U S A, 1993; 90: 5484-8.
211. Side, L., Teel, K., Wang, P., et al. Activating RAS mutations in therapy-related myeloid disorders associated with deletions of chromosomes 5 and 7 [abstract]. Blood, 1996; 88: 566a.
212. Scheffzek, K., Ahmadian, M. R., Kabsch, W., et al. The Ras-RasGAP complex: structural basis for GTPase activation and its loss in oncogenic Ras mutations. Science, 1997; 277: 333-8.
213. Christiansen, D. H., Andersen, M. K., & Pedersen-Bjergaard, J. Mutations with loss of heterozygosity of p53 are common in therapy-related myelodysplasia and acute myeloid leukemia after exposure to alkylating agents and significantly associated with deletion or loss of 5q, a complex karyotype and a poor prognosis. J Clin Oncol, 2001; 19: 1405-13.
214. Leonard, D. G.B., Travis, L.B., Addya, K., et al. p53 mutations in leukemia andmyelodysplastic syndrome after ovarian cancer. Clin Cancer Res, 2002; 8: 973-85.
215. Andersen, M. K., Christiansen, D. H., Kirchhoff, M., & Pedersen-Bjergaard, J. Duplication or amplification of chromosomeband11q23, including the unrearranged MLLgene, is a recurrent abnormality in therapy-related MDS, and is closely related to mutation of the TP53 gene and to previous therapy with alkylating agents. Genes, Chromosomes Cancer, 2001; 31: 33-41.
216. Jonveaux, P., Fenaux, P., Quiquandon, I., et al.Mutations in the p53 gene in myelodysplastic syndromes. Oncogene, 1991; 6: 2243-7.
217. Sugimoto, K., Hirano, N., Toyoshima, H., et al. Mutations of the p53 gene in myelodysplastic syndrome (MDS) and MDSderived leukemia. Blood, 1993; 81: 3022-6.
218. Christiansen, D. H., Andersen, M. K., & Pedersen-Bjergaard, J. Methylation of p15INK4B is common, is associated with deletion of genesonchromosomearm7qandpredicts a poor prognosis in therapy-related myelodysplasia and acute myeloid leukemia. Leukemia, 2003; 17: 1813-19.
219. Qian, Z., Fernald, A. A., Godley, L. A., Larson, R. A., & Le Beau, M. M. Expression profiling of CD34+ hematopoietic stem/progenitor cells reveals distinct subtypes of therapyrelated acutemyeloid leukemia. Proc Natl Acad SciUS A, 2002; 99: 14 925-30.
220. Harada, H., Harada, Y., Tanaka, H., Kimura, A., & Inaba, T. Implications of somatic mutations in the AML1 gene in radiation-associated and therapy-related myelodysplastic syndrome/acute myeloid leukemia. Blood, 2003; 101: 673-80.
221. Voso, M. T., Scardocci, A., Guidi, F., et al. Aberrant methylation of DAP-kinase in therapy-related acute myeloid leukemia and myelodysplastic syndromes. Blood, 2004; 103: 698-700.
222. Gattermann, N., Wulfert, M., Junge, B., et al. Ineffective hematopoiesis linked with a mitochondrial tRNA mutation (G3242A) in a patient with myelodysplastic syndrome. Blood, 2004; 103: 1499-502.
223. Carew, J. S., Zhou, Y., Albitar, M., et al. Mitochondrial DNA mutations in primary leukemia cells after chemotherapy: clinical significance and therapeutic implications. Leukemia, 2003; 17: 1437-47.
224. Olney, H. J., Mitelman, F., Johansson, B., et al. Unique balanced chromosome abnormalities in treatment-related myelodysplastic syndromes and acute myeloid leukemia: report from an international workshop. Genes Chromosomes Cancer, 2002; 33: 413-23.
225. Thirman, M. J., Gill, H. J., Burnett, R. C., et al. Rearrangement of the MLL gene in acute lymphoblastic and acute myeloid leukemias with 11q23 chromosomal translocations. N Engl J Med, 1993; 329: 909-14.
226. Rubin, C. M., Arthur, D. C., Woods, W. G., et al. Therapy-related myelodysplastic syndrome and acute myeloid leukemia in children: correlation between chromosomal abnormalities and prior therapy. Blood, 1991; 78: 2982-8.
227. Rowley, J. D., Vignon, C., Gollin, S. M., et al. Rearrangements involving chromosome band 11q23 in acute leukemia. NEngl J Med, 1996; 334: 601-3.
228. Rubnitz, J. E., Behm, F. G., & Downing, J. R. 11q23 rearrangements in acute leukemia. Leukemia, 1996; 10: 74-82.
229. Pui, C.-H., Relling, M. V., Rivera, G. K., et al. Epipodophyllotoxin-related acute myeloid leukemia: a study of 35 cases. Leukemia, 1995; 9: 1990-6.
230. Kantarjian, H. M., Keating, M. J., Walters, R. S., et al. The association of specific "favorable" cytogenetic abnormalities with secondary leukemia. Cancer, 1986; 58: 924-7.
231. Quensel, B., Kantarjian, H., Pedersen-Bjergaard, J., et al. Therapy-related acute myeloid leukemia with t(8;21), inv(16), and t(8;16): a report on 25 cases and review of the literature. J Clin Oncol, 1993; 11: 2370-9.
232. Larson, R. A., Le Beau, M., Ratain, M.J., &Rowley, J.D. Balanced translocations involving chromosome bands11q23 and 21q22 in therapy-related leukemia. Blood, 1992; 79: 1892-3.
233. Rubin, C. M., Larson, R. A., Anastasi, J., et al. t(3;21)(q26;q22): a recurring chromosomal abnormality in therapy-related myelodysplastic syndrome and acute myeloid leukemia. Blood, 1990; 76: 2594-8.
234. Nucifora, G., Birn, D. J., Espinosa, R., III, et al. Involvement of the AML1 gene in the t(3;21) in therapy-related leukemia and in chronic myeloid leukemia in blast crisis. Blood, 1993; 81: 2728-34.
235. Nucifora, G.&Rowley, J.D.AML1and the 8;21 and 3;21 translocations in acute and chronic myeloid leukemia. Blood, 1995; 86: 1-14.
236. Roulston, D., Espinosa, R., III, Nucifora, G., et al. CBFA2(AML1) translocations with novel partner chromosomes in myeloid leukemias: association with prior therapy. Blood, 1998; 92: 2879-85.
237. Slovak, M. L., Bedell, V., Popplewell, L., et al. 21q22 balanced chromosome aberrations in therapy-related hematopoietic disorders: report froman international workshop. Genes Chromosomes Cancer, 2002; 33: 379-94.
238. Raiker, A., Green, W., Shabaik, A., & Perlin, E. Acute promyelocytic leukemia following treatment of non-Hodgkin's lymphoma. Cancer, 1989; 63: 1402, a6.
239. Lopez-Andreu, J. A., Ferris, J., Verdeguer, A., et al. Secondary acute promyelocytic leukemia in a child treated with epipodophyllotoxins. Am J Pediatr Hematol Oncol, 1994; 16: 384-6.
240. Pedersen-Bjergaard, J., Andersen, M. K., & Johansson, B. Balanced chromosome aberrations in leukemias following chemotherapy with DNA-topoisomerase II inhibitors. J Clin Oncol, 1998; 16: 1897-8.
241. Wiernick, P. H. & Muse, I. M. Acute promyelocytic leukemia after treatmentof malignant glioma in a patient with Von Recklinghausen's disease: a case report and review of the literature. Leukemia, 1996; 10: 178-91.
242. Fenaux, P., Lucidarme, D., Lai, J. L., &Bauters, F. Favorable cytogenetic abnormalities in secondary leukemia. Cancer, 1989; 3: 2505-8.
243. Pedersen-Bjergaard, J., Brondum-Nielsen, K., Karle, H., & Johansson, B. Chemotherapy-related-and late occurring-Philadelphia chromosome in AML, ALL and CML. Similar events related to treatment with DNA topoisomerase II inhibitors? Leukemia, 1997; 11: 1571-4.
244. Stark, B., Jeison, M., Shohat, M., et al. Involvement of 11p15 and 2q21q26 9n therapy-related myeloid leukemia (t-ML) in children. Cancer Genet Cytogenet, 1994; 75: 11-22.
245. Kobayashi, H., Arai, Y., Hosoda, F., et al. Inversion of chromosome 11 inv(11)(p15q22), as a recurring chromosomal aberration associated with de novo and secondary myeloid malignancies: identification of a P1 clone spanning the 11q22 breakpoint. Genes Chromosomes Cancer, 1997; 19: 150-5.
246. Felix, C. A., Hosler, M. R., Winick, N. J., et al. ALL-1 gene rearrangements in DNA topoisomerase II inhibitor-related leukemia in children. Blood, 1995; 85: 3250-6.
247. Raza-Egilmez, S. Z., Jani-Sait, S. N., Grossi, M., et al. NUP98-HOXD13 gene fusion in therapy-related acute myelogenous leukemia. Cancer Res, 1998; 58: 4269-73.
248. Aria, Y., Hosoda, F., Kobayashi, H., et al. The inv(11)(p15q22) chromosome translocation of de novo and therapy-related myeloid malignancies results in fusion of the nucleoporin gene, NUP98, with a putative RNA helicase gene, DDX10. Blood, 1997; 89: 3936-44.
249. Nakamura, T., Largaespada, D. A., Lee, M. P., et al. Fusion of the nucleoporin gene NUP98 to HOXA9 by chromosomal translocation t(7;11)(p15;p15) in human myeloid leukemia. Nat Genet, 1996; 12: 154-8.
250. Borrow, J., Shearman, A. M., Stanton, V. P. Jr., et al. The t(7;11)(p15;p15) translocation in acutemyeloid leukemia fuses Cambridge Books Online (c) Cambridge University Press, 2009 Therapy-related leukemias 799 the genes for nucleoporin NUP98 to class I homeoprotein HOXA9. Nat Genet, 1996; 12: 159-67.
251. Nakamura, T., Yamazaki, Y., Hatano, Y., & Miura, I. NUP98 is fused to PMX1 homeobox gene in human acute myelogenous leukemia with chromosome translocation t(1;11)(q23;p15). Blood, 1999; 94: 741-7.
252. Yasuhito, A., Hosoda, F., Kobayashi, H., et al. The inv(11)(p15q22) chromosome translocation of de novo and therapy-related myeloid malignancies results in fusion of the nucleoporin gene NUP98 with the putative RNA helicase gene DDX10. Blood, 1997; 89: 3936-44.
253. Ahuja, H. G., Felix, C. A., & Aplan, P. D. The t(11;20)(p15;q11) chromosomal translocation associated with therapy-related myelodysplastic syndrome results in NUP98-TOP1 fusion. Blood, 1999; 94: 3258-61.
254. Djabali, M., Selleri, L., Parry, P., et al. A Trithorax-like gene is interrupted by chromosome 11q23 translocations in acute leukemias. Nat Genet, 1992; 2: 113-18.
255. Gu, Y., Nakamura, T., Alder, H., et al. The t(4;11) chromosome translocation of human acute leukemias fuses the ALL-1 gene, related to Drosophila Trithorax, to the AF-4 gene. Cell, 1992; 71: 701-8.
256. Tkachuk, D. C., Kohler, S., Cleary, M. L. Involvement of a homolog of Drosophila Trithorax by 11q23 chromosomal translocations in acute leukemias. Cell, 1992; 71: 691-700.
257. Ma, Q., Alder, H., Nelson, K. K., et al. Analysis of the murine All-1 gene reveals conserved domains with human ALL-1 and identifies a motif shared with DNA methyltransferases. Proc Natl Acad Sci U S A, 1993; 90: 6350-4.
258. Domer, P. H., Fakharzadeh, S. S., Chen, C.-S., et al. Acute mixed-lineage leukemia t(4;11)(q21;q23) generates an MLLAF4 fusion product. Proc Natl Acad Sci U S A, 1993; 90: 7884-8.
259. Rasio, D., Schichman, S. A., Negrini, M., Canaani, E., & Croce, C. M. Complete exon structure of the ALL1 gene. Cancer Res, 1996; 56: 1766-9.
260. Yu, B.D., Hanson, R.D., Hess, J. L., Horning, S. E., &Korsmeyer, S. J. MLL, a mammalian trithorax-group gene, functions as a transcriptional maintenance factor in morphogenesis. Proc Natl Acad Sci U S A, 1998; 95: 10 632-6.
261. Mahmoudi, T. & Verrijzer, C. P. Chromatin silencing and activation by Polycomb and trithorax group proteins. Oncogene, 2001; 20: 3055-66.
262. Hanson, R.D., Hess, J. L., Yu, B.D., et al. Mammalian Trithorax and Polycomb-group homologues are antagonistic regulators of homeotic development. Proc Natl Acad Sci U S A, 1999; 96: 14 372-7.
263. Yu, B.D., Hess, J. L., Horning, S. E., Brown, G. A. J., &Korsmeyer, S. J. Altered Hox expression and segmental identity in Mllmutant mice. Nature, 1995; 378: 505-8.
264. Hess, J. L., Yu, B.D., Li, B., Hanson, R., &Korsmeyer, S. J. Defects in yolk-sac hematopoiesis in Mll-null embryos. Blood, 1997; 90: 1799-806.
265. Caslini, C., Alarcon, A. S., Hess, J. L., et al. The amino terminus targets the mixed lineage leukemia (MLL) protein to the nucleolus, nuclear matrix and mitotic chromosomal scaffolds. Leukemia, 2000; 14: 1898-908.
266. Caslini, C., Shilatifard, A., Yang, L., & Hess, J. L. The amino terminus of the mixed lineage leukemia protein (MLL) promotes cell cycle arrest and monocytic differentiation. Proc Natl Acad Sci U S A, 2000; 97: 2797-802.
267. Fair, K., Anderson, M., Bulanova, E., et al. Protein interactions of the MLL PHD fingers modulate MLL target gene regulation in human cells. Mol Cell Biol, 2001; 21: 3589-97.
268. Rozenblatt-Rosen, O., Rozovskaia, T., Burakov, D., et al. The C-terminal SET domains of ALL-1 and TRITHORAX interact with the INI1 and SNR1 proteins, components of the SWI/SNF complex. Proc Natl Acad Sci U S A, 1998; 95: 4152-7.
269. Milne, T. A., Briggs, S. D., Brock, H. W., et al. MLL targets SET domainmethyltransferase activity to Hoxgenepromoters. Mol Cell, 2002; 10: 1107-17.
270. Nakamura, T., Mori, T., Tada, S., et al. ALL-1 is a histone methyltransferase that assembles a supercomplex of proteins involved in transcriptional regulation. Mol Cell, 2002;10:1119-28.
271. Yokoyama, A., Kitabayashi, I., Ayton, P. M., Cleary, M. L., & Ohki, M. Leukemia proto-oncoprotein MLL is proteolytically processedinto2fragmentswithoppositetranscriptionalproperties. Blood, 2002; 100: 3710-8.
272. Hsieh, J. J., Cheng, E. H., & Korsmeyer, S. J. Taspase1: a threonine aspartase required for cleavage of MLL and proper HOX gene expression. Cell, 2003; 115: 293-303.
273. Hsieh, J. J., Ernst, P., Erdjument-Bromage, H., Tempst, P., & Korsmeyer, S. J. Proteolytic cleavage of MLL generates a complex of N-and C-terminal fragments that confers protein stability and subnuclear localization. Mol Cell Biol, 2003; 23: 186-94.
274. Gurney, J. G., Ross, J. A., Wall, D. A., et al. Infant cancer in the U.S.: histology-specific incidence and trends, 1973-1992. J Pediatr Hematol/Oncol, 1997; 19: 428-32.
275. Domer, P. H., Head, D. R., Renganathan, N., et al. Molecular analysis of 13 cases of MLL/11q23 secondary acute leukemia and identification of topoisomerase II consensus binding sequences near the chromosomal breakpoint of a secondary leukemia with the t(4;11). Leukemia, 1995; 9: 1305-12.
276. Lovett, B. D., Lo Nigro, L., Rappaport, E. F., et al. Near-precise interchromosomal recombination and functional DNA topoisomerase II cleavage sites at MLL and AF-4 genomic breakpoints in treatment-related acute lymphoblastic leukemia with t(4;11) translocation. Proc Natl Acad Sci U S A, 2001; 98: 9802-7.
277. Raffini, L. J., Slater, D. J., Rappaport, E. F., et al. Panhandle and reverse panhandle PCR enable cloning of der(11) and der(other) genomic breakpoint junctions of MLL translocations and identify complex translocation of MLL, AF-4 and CDK6. Proc Natl Acad Sci U S A, 2002; 99: 4568-73.
278. Ayton, P. M & Cleary, M. L. MLL in normal and malignant hematopoiesis. In K. Ravid & J. D. Licht eds., Transcription Factors: Normal and Malignant Development of Blood Cells (New York:Wiley-Liss, 2001).
279. Rowley, J. D. The critical role of chromosome translocations in human leukemias. Annu Rev Genet, 1998; 32: 495-519.
280. Felix, C. A. Acute lymphoblastic leukemia in infants. In Pediatric Acute Lymphoblastic Leukemia: Challenges and Controversies in 2000. Hematology 2000. Education program of the American Society of Hematology (Washington, DC: American Society of Hematology, 2000), pp. 294-8.
281. Morrissey, J., Tkachuk, D. C., Milatovich, A., et al. A serine/proline-rich protein is fused to HRX in t(4;11) acute leukemias. Blood, 1993; 81: 1124-31.
282. Taki, T., Hayashi, Y., Taniwaki, M., et al. Fusion of the MLLgene with two different genes, AF-6 and AF-5alpha, by a complex translocation involving chromosomes 5, 6, 8 and 11 in infant leukemia. Oncogene, 1996; 13: 2121-30.
283. Taki, T., Kano, H., Taniwaki, M., et al. AF5q31, a newly identified AF4-relatedgene, is fused to MLLin infantacutelymphoblastic leukemia with ins(5;11)(q31;q13q23). Proc Natl Acad SciUS A, 1999; 96: 14 535-40.
284. Hillion, J., Le Coniat, M., Jonveaux, P., Berger, R., & Bernard, O. A. AF6q21, a novel partner of the MLL gene in t(6;11)(q21;q23), defines a Forkhead transcriptional factor subfamily. Blood, 1997; 9: 3714-19.
285. Chaplin, T., Bernard, O., Beverloo, H. B., et al. The t(10;11) translocation in acute myeloid leukemia (M5) consistently fuses the leucine zipper motif of AF10 onto the HRX gene. Blood, 1995; 86: 2073-6.
286. Schichman, S. A., Caligiuri, M. A., Gu, Y., et al. ALL-1 partial duplication in acute leukemia. Proc Natl Acad Sci, 1994; 91: 6236-9.
287. Prasad, R., Leshkowitz, D., Gu, Y., et al. Leucine-zipper dimerization motif encoded by the AF17 gene fused to ALL-1 (MLL) in acute leukemia. Proc Natl Acad SciUS A, 1994; 91: 8107-11.
288. Nakamura, T., Alder, H., Gu, Y., et al. Genes on chromosomes 4, 9, and 19 involved in 11q23 abnormalities in acute leukemia share sequence homology and/or common motifs. Proc Natl Acad Sci U S A, 1993; 90: 4631-5.
289. Borkhardt, A., Repp, R., Haas, O., et al. Cloning and characterization of AFX, the gene that fuses to MLL in acute leukemias with a t(X;11)(q13;q23). Oncogene, 1997; 14: 195-202.
290. Sobulo, O. M., Borrow, J., Tomek, R., et al. MLL is fused to CBP, a histone acetyltransferase, in therapy related acute myeloid leukemia with a t(11;16)(q23;p13.3). Proc Natl Acad Sci U S A, 1997; 94: 8732-7.
291. Taki, T., Sako, M., Tsuchida, M., & Hayashi, Y. The t(11;16)(q23;p13) translocation in myelodysplastic syndrome fuses the MLL gene to the CBP gene. Blood, 1997; 89: 3945-50.
292. Thirman, M. J., Levitan, D. A., Kobayashi, H., Simon, M. C., & Rowley, J. D. Cloning of ELL, a gene that fuses to MLL in a t(11;19)(q23;p13.1) in acute myeloid leukemia. Proc Natl Acad Sci U S A, 1994; 91: 12 110-4.
293. Ida, K., Kitabayashi, I., Taki, T., et al.Adenoviral E1A-associated protein p300 is involved in acute myeloid leukemia with t(11;22)(q23;q13). Blood, 1997; 90: 4699-704.
294. Ono, R., Taki, T., Taketani, T., et al. LCX, leukemia-associated protein with a CXXC domain, is fused to MLL in acute myeloid leukemia with trilineage dysplasia having t(10;11)(q22;q23). Cancer Res, 2002; 62: 4075-80.
295. Lorsbach, R.B., Moore, J., Mathew, S., et al. TET1, amemberofa novel protein family, is fused to MLL in acutemyeloidleukemia containing the t(10;11)(q22;q23). Leukemia, 2003; 17: 637-41.
296. Hayette, S., Tigaud, I., Vanier, A., et al. AF15q14, a novel partner genefusedto the MLL geneinan acutemyeloidleukaemia with a t(11;15)(q23;q14). Oncogene, 2000; 19: 4446-50.
297. Bernard, O., Mauchauffe, M., Mecucci, C., Berghe, H. Van Den, & Berger, R. A novel gene, AF-1p, fused to HRX in t(1;11)(p32;q23), is not related to AF-4, AF-9 nor ENL. Oncogene, 1994; 9: 1039-45.
298. Tse, W., Zhu, W., Chen, H. S., & Cohen, A. A novel gene, AF1q, fused to MLL in t(1;11) (q21;q23), is specifically expressed in leukemic and immature hematopoietic cells. Blood, 1995; 85: 650-6.
299. Daheron, L., Veinstein, A., Brizard, F., et al. Human LLP gene is fused to MLL in a secondary acute leukemia with a t(3;11)(q28;q23). Genes Chromosomes Cancer, 2001; 31: 382-9.
300. Borkhardt, A., Bojesen, S., Haas, O. A., et al. The human GRAF gene is fused to MLL in a unique t(5;11)(q31;q23) and both alleles are disrupted in three cases of myelodysplastic syndrome/acute myeloid leukemia with a deletion 5q. Proc Natl Acad Sci U S A, 2000; 97: 9168-73.
301. Fuchs, U., Rehkamp, G., Haas, O. A., et al. The human forminbinding protein 17 (FBP17) interacts with sorting nexin, SNX2, and is an MLL-fusion partner in acute myelogeneous leukemia. Proc Natl Acad Sci U S A, 2001; 98: 8756-61.
302. Taki, T., Shibuya, N., Taniwaki, M., et al. ABI-1, a human homolog to mouse Abl-1 interactor 1, fuses the MLL gene in acute myeloid leukemia with t(10;11)(p11.2;q23). Blood, 1998; 92: 1125-30.
303. Fu, J., Hsu, J., Tang, T., & Shih, L. Identification of CBL, a protooncogene at 11q23.3, as anovelMLLfusion partner in a patient with de novo acute myeloid leukemia. Genes Chromosomes Cancer, 2003; 37: 214-19.
304. Chinwalla, V., Chien, A., Odero, M., et al. A t(11;15) fuses MLL to two different genes, AF15q14 and a novel gene MPFYVE on chromosome 15. Oncogene, 2003; 22: 1400-10.
305. Strehl, S., Borkhardt, A., Slany, R., et al. The human LASP1 gene is fused to MLL in an acute myeloid leukemia with t(11;17)(q23;q21). Oncogene, 2003; 22: 157-60.
306. So, C., Caldas, C., Liu, M.-M., et al. EEN encodes for a member ofanewfamilyofproteinscontaininga Srchomology3domain and is the third gene located on chromosome 19p13 that fuses to MLL in human leukemia. Proc Natl Acad SciUS A, 1997; 99: 2563-8.
307. Megonigal, M. D., Rappaport, E. F., Jones, D. H., et al. t(11;22)(q23;q11.2) in acute myeloid leukemia of infant twins fuses MLL with hCDCrel, a cell division cycle gene in the genomic region of deletion in Di George and velocardiofacial syndromes. Proc Natl Acad Sci U S A, 1998; 95: 6413-18.
308. Osaka, M., Rowley, J. D., & Zeleznik-Le, N. J. MSF (MLL septinlike fusion), a fusion partner gene of MLL, in a therapy-related Cambridge Books Online (c) Cambridge University Press, 2009 Therapy-related leukemias 801 acute myeloid leukemia with a t(11;17)(q23;q25). Proc Natl Acad Sci U S A, 1999; 96: 6428-33.
309. Taki, T., Ohnishi, H., Shinohara, K., et al. AF17q25, a putative septin family gene, fuses the MLL gene in acute myeloid leukemia with t(11;17)(q23;q25). Cancer Res, 1999; 59: 4261-5.
310. Borkhardt, A., Teigler-Schlegel, A., Fuchs, U., et al. An ins(X;11)(q24;q23) fuses the MLL and the Septin 6/KIAA0128 gene an infant with AML-M2. Genes Chromosomes Cancer, 2001; 32: 82-8.
311. Ono, R., Taki, T., Taketani, T., et al. SEPTIN6, a human homologue tomouse Septin6, is fused to MLL in infant acutemyeloid leukemia with complex chromosomal abnormalities involving 11q23 and Xq24. Cancer Res, 2002; 62: 333-7.
312. Slater, D. J., Hilgenfeld, E., Rappaport, E. F., et al. MLL-SEPTIN6 fusion recurs in novel translocation of chromosomes 3, X and 11 in infant acute myelomonocytic leukemia and in t(X;11) in infant acute myeloid leukemia, and MLL genomic breakpoint in complex MLL-SEPTIN6 rearrangement is a DNA topoisomerase II cleavage site. Oncogene, 2002; 21: 4706-14.
313. Eguchi, M., Eguchi-Ishimae, M., Seto, M., et al. GPHN, a novel partner gene fused to MLL in a leukemia with t(11;14) (q23;q24). Genes Chromosomes Cancer, 2001; 32: 212-21.
314. Wechsler, D. S., Engstrom, L.D., Alexander, B. M., Motto, D. G., & Roulston, D. A novel chromosomal inversion at 11q23 in infant acute myeloid leukemia fuses MLL to CALM, a gene thatencodesaclathrinassemblyprotein. Genes, Chromosomes Cancer, 2003; 36: 26-36.
315. Kourlas, P. J., Strout, M. P., Becknell, B., et al. Identification of a gene at 11q23 encoding a guanine nucleotide exchange factor: evidence for its fusion with MLL in acute myeloid leukemia. Proc Natl Acad Sci U S A, 2000; 97: 2145-50.
316. Prasad, R., Gu, Y., Alder, H., et al. Cloning of the ALL-1 fusion partner, the AF-6 gene, involved in acute myeloid leukemias with the t(6;11) chromosome translocation. Cancer Res, 1993; 53: 5624-8.
317. Lo Nigro, L., Slater, D. J., Rappaport, E. F., et al. Two new partner genes of MLL and additional heterogeneity in t(11;19)(q23;p13) translocations [abstract]. Blood, 2002; 100(Suppl. 1): 531a.
318. Fu, J. E., Hsu, H. C., Shih, L. Y. MLL is fused to EB1 (MAPRE1), which encodes a microtubule-associated protein, in a patient with acute lymphoblastic leukemia. Genes Chromosomes Cancer, 2005; 43: 206-10.
319. Lo Nigro, L., Slater, D. J., Mirabile, E., et al. Reverse panhandle PCR identifies RIBOSOMAL PROTEIN S3 (RPS3) as a new partner gene of MLL in a three-way MLL rearrangement in infant acute monoblastic leukemia. Blood, 2003; 102: 184-5b.
320. Megonigal, M.D., Rappaport, E. F., Wilson, R. B., et al. Panhandle PCR for cDNA: a rapid method for isolation of MLL fusion transcripts involving unknown partner genes. Proc Natl Acad Sci U S A, 2000; 97: 9597-602.
321. Rowley, J. D., Reshmi, S., Sobulo, O., et al. All patients with t(11;16)(q23;p13.3) that involve MLL and CBP have treatmentrelated hematologic disorders. Blood, 1997; 90: 535-41.
322. Robinson, B. W., Lee, A., Cheung, N.-K. V., & Felix, C. A. Bone marrow replacement with a clone harboring novel t(4;11)(p12;q23) involving MLL during neuroblastoma treatment is not associated with leukemia. Blood, 2004; 104: 793a [abstract].
323. Teuffel, O., Betts, D. R., Thali, M. et al. Clonal expansion of a new MLL rearrangement in the absence of leukemia. Blood, 2005; 105: 4151-2.
324. Nilson, I., Reichel, M., Ennas, M. G., et al. Exon/intron structure of the AF-4 gene, a member of the AF-4/LAF-4/FMR-2 gene family coding for a nuclear protein with structural alterations in acute leukaemia. Br J Haematol, 1997; 98: 157-69.
325. Huret, J. L. 11q23 rearrangements in leukaemia. In Atlas of Genetics and Cytogenetics in Oncology and Haematology, 2001. http://www.infobiogen.fr/services/chromcancer/Anomalies/11q23ID1030.html.
326. Tatsumi, K., Taki, T., Taniwaki, M., et al. The CDCREL1 gene is fused to MLL in de novo acute myeloid leukemia with t(11;22)(q23;q11.2) and its frequent expression in myeloid leukemia cell lines. Genes Chromosomes Cancer, 2001; 30: 230-5.
327. So, C. W. & Cleary, M. L. MLL-AFX requires the transcriptional effector domains of AFX to transformmyeloid progenitors and transdominantly interfere with forkheadprotein function. Mol Cell Biol, 2002; 22: 6542-52.
328. So, C. W. & Cleary, M. L. Common mechanism for oncogenic activation of MLL by forkhead family proteins. Blood, 2003; 101: 633-9.
329. Corral, J., Lavenir, I., Impey, H., et al. An Mll-AF9 fusion gene made by homologous recombination causes acute leukemia in chimeric mice: a method to create fusion oncogenes. Cell, 1996; 85: 853-61.
330. Lavau, C., Szilvassy, S. J., Slany, R., &Cleary, M. L. Immortalization and leukemic transformation of a myelomonocytic precursor by retrovirally transduced HRX-ENL. EMBO J, 1997; 16: 4226-37.
331. Lavau, C., Luo, R. T., Du, C., & Thirman, M. J. Retrovirusmediated gene transfer of MLL-ELL transforms primary myeloid progenitors and causes acute myeloid leukemias in mice. Proc Natl Acad Sci U S A, 2000; 97: 10 984-9.
332. Lavau, C., Du, C., Thirman, M., & Zeleznik-Le, N. Chromatinrelated properties of CBP fused to MLL generate a myelodysplastic-like syndrome that evolves into myeloid leukemia. EMBO J, 2000; 19: 4655-64.
333. So, C. W., Karsunky, H., Passegue, E., et al. MLL-GAS7 transforms multipotent hematopoietic progenitors and induces mixed lineage leukemias in mice. Cancer Cell, 2003; 3: 161-71.
334. Liedman, D. & Zeleznik-Le, N. Retroviral transduction model ofmixedlineage leukemia fused to CREB binding protein. Curr Opin Hematol, 2001; 8: 218-23.
335. Ayton, P. M. & Cleary, M. L. Molecular mechanisms of leukemogenesis mediated by MLL fusion proteins. Oncogene, 2001; 20: 5695-707.
336. Zeisig, B. B., Schreiner, S., Garcia-Cuellar, M. P., & Slany, R. K. Transcriptional activation is a key function encoded by MLL fusion partners. Leukemia, 2003; 17: 359-65.
337. Rubnitz, J. E., Morrissey, J., Savage, P. A., &Cleary, M.L.ENL, the gene fused with HRX in t(11;19) leukemias, encodes a nuclear protein with transcriptional activation potential in lymphoid and myeloid cells. Blood, 1994; 84: 1747-52.
338. Di Martino, J. F., Miller, T., Ayton, P. M., et al.Acarboxy-terminal domain of ELL is required and sufficient for immortalization of myeloid progenitors by MLL-ELL. Blood, 2000; 96: 3887-93.
339. Adler, H. T., Chinery, R., Wu, D. Y., et al. Leukemic HRX fusion proteins inhibit GADD34-induced apoptosis and associate with the GADD34 and hSNF5/INI1 proteins. Mol Cell Biol, 1999; 19: 7050-60.
340. Armstrong, S. A., Staunton, J. E., Silverman, L. B., et al. MLL translocations specify a distinct gene expression profile that distinguishes a unique leukemia. Nat Genet, 2002; 30: 41-7.
341. Zeisig, B. B., Milne, T., Garcia-Cuellar, M. P., et al. Hoxa9 and Meis1 are key targets for MLL-ENL-mediated cellular immortalization. Mol Cell Biol, 2004; 24: 617-28.
342. Ayton, P. M.&Cleary, M. L. Transformation ofmyeloid progenitors by MLL oncoproteins is dependent on Hoxa7 and Hoxa9. Genes Dev, 2003; 17: 2298-307.
343. So, C. W., Karsunky, H., Wong, P., Weissman, I. L., & Cleary, M. L. Leukemic transformation of hematopoietic progenitors by MLL-GAS7 in the absence of Hoxa7 or Hoxa9. Blood, 2004; 103: 3192-9.
344. So, C. W., Lin, M., Ayton, P. M., Chen, E. H., & Cleary, M. L. Dimerization contributes to oncogenic activation of MLL chimeras in acute leukemias. Cancer Cell, 2003; 4: 99-110.
345. Megonigal, M. D., Rappaport, E. F., Nowell, P. C., Lange, B. J., & Felix, C. A. Potential role for wild-type p53 in leukemias with MLL gene translocations. Oncogene, 1998; 16: 1351-6.
346. Armstrong, S. A., Kung, A. L., Mabon, M. E., et al. Inhibition of FLT3 in MLL. Validation of a therapeutic target identified by gene expression based classification. Cancer Cell, 2003; 3: 173-83.
347. Taketani, T., Taki, T., Sugita, K., et al. FLT3 mutations in the activation loop of tyrosine kinase domain are frequently found in infant ALL with MLL rearrangements and pediatric ALL with hyperdiploidy. Blood, 2004; 103: 1085-8.
348. Libura, M., Asnafi, V., Tu, A., et al. FLT3 and MLL intragenic abnormalities in AML reflect a common category of genotoxic stress. Blood, 2003; 102: 2198-204.
349. Thiede, C., Steudel, C., Mohr, B., et al. Analysis of FLT3-activating mutations in 979 patients with acute myelogenous leukemia: association with FAB subtypes and identification of subgroups with poor prognosis. Blood, 2002; 99: 4326-35.
350. Blanco, J. G., Dervieux, T., Edick, M. J., et al. Molecular emergence of acute myeloid leukemia during treatment for acute lymphoblastic leukemia. Proc Natl Acad Sci U S A, 2001; 98: 10 338-43.
351. Ford, A.M., Ridge, S. A., Cabrera, M.E., et al. In uterorearrangements in the trithorax-related oncogene in infant leukaemias. Nature, 1993; 363: 358-60.
352. Gale, K., Ford, A., Repp, R., et al. Backtrackingleukemiato birth: Identification of clonotypic gene fusion sequences in neonatal bloodspots. Proc Natl Acad Sci U S A, 1997; 94: 13950-4.
353. Maia, A. T., Koechling, J., Corbett, R., et al. Protracted postnatal natural histories in childhood leukemia. Genes Chromosomes Cancer, 2004; 39: 335-40.
354. Felix, C. A. & Megonigal, M. D. Molecular biology of chemotherapy-related leukemias. InAmerican Society of Clinical Oncology Educational Book 2001 (Alexandria, VA: ASCO), pp. 578-90.
355. Felix, C. A. Leukemias related to treatment with DNA topoisomerase II inhibitors. Med Pediatr Oncol, 2001; 36: 525-35.
356. Rowley, J. D. The role of chromosome translocations in leukemogenesis. Semin Hematol, 1999; 36: 59-72.
357. Broeker, P. L., Super, H. G., Thirman, M. J., et al. Distribution of 11q23 breakpoints within the MLL breakpoint cluster region in de novo acute leukemia and in treatment-related acute myeloid leukemia: correlation with scaffold attachment regions and topoisomerase II consensus binding sites. Blood, 1996; 87: 1912-22.
358. Langer, T., Metzler, M., Reinhardt, D., et al. Analysis of t(9;11) chromosomal breakpoint sequences in childhood acute leukemia: almost identical MLL breakpoints in therapyrelated AML after treatment without etoposides. Genes Chromosomes Cancer, 2003; 36: 393-401.
359. _ sequence in MLL and AF-9 create homologous single-stranded overhangs that anneal to form der(11) and der(9) genomic breakpoint junctions in treatment-related AML without further processing. Oncogene, 2003; 22: 8448-59.
360. Relling, M. V., Evans, R., Dass, C., Desiderio, D. M., & Nemec, J. Human cytochrome P450 metabolism of teniposide and etoposide. J Pharmacol Exp Ther, 1992; 261: 491-6.
361. Maanen, J. M. van, Lafleur, M. V., Mans, D. R., et al. Effects of the ortho-quinone and catechol of the antitumor drug VP-16-213 on the biological activity of single-stranded and doublestranded fX174 DNA. Biochem Pharmacol, 1988; 37: 3579-89.
362. Bolton, J. L., Trush, M.A., Penning, T.M., Dryhurst, G., &Monks, T. J. Role of quinones in toxicology. Chem Res Toxicol, 2000; 13: 135-60.
363. Haim, N., Nemec, J., Roman, J., & Sinha, B. K. In vitro metabolismof etoposide (VP-16-213)by livermicrosomesand irreversible binding of reactive intermediates to microsomal proteins. Biochem Pharmacol, 1987; 36: 527-36.
364. Maanen, J. M. van, de Ruiter, C., Kootstra, P. R., et al. Inactivation of fX174 DNA by the ortho-quinone derivative or its reduction product of the antitumor agent VP16-213. Eur J Cancer Clin Oncol, 1985; 21: 1215-18.
365. Maanen, J. M. van, de Vries, J., Pappie, D., et al. Cytochrome P-450-mediated O-demethylation: a route in the metabolic activation of etoposide (VP-16-213). Cancer Res, 1987; 47: 4658-62.
366. Kingma, P. S., Corbett, A. H., Burcham, P. C., Marnett, L. J., & Osheroff, N. Abasic sites stimulate double-stranded DNA cleavage mediatedby topoisomerase II. J Biol Chem, 1995; 270: 21 441-4.
367. Kingma, P. S.&Osheroff, N. Apurinic sites are position-specific topoisomerase II poisons. J Biol Chem, 1997; 272: 1148-55.
368. Betti, C. J., Villalobos, M. J., Diaz, M. O., & Vaughan, A. T. M. Apoptotic triggers initiate translocations within the MLL gene involving the nonhomologous end joining repair system. Cancer Res, 2001; 61: 4550-5.
369. Sim, S.-P. & Liu, L. F. Nucleolytic cleavage of the mixed lineage leukemia breakpoint cluster region during apoptosis. J Biol Chem, 2001; 276: 31590-5.
370. Betti, C. J., Villalobos, M. J., Diaz, M. O., & Vaughan, A. T. Apoptotic stimuli initiate MLL-AF9 translocations that are transcribed in cells capable of division. Cancer Res, 2003; 63: 1377-81.
371. Super, H. G., Strissel, P. L., Sobulo, O. M., et al. Identification of complex genomic breakpoint junctions in the t(9;11) MLL-AF-9 fusion gene in acute leukemia. Genes Chromosomes Cancer, 1997; 20: 185-95.
372. Felix, C. A., Kim, C. S., Megonigal, M. D., et al. Panhandle PCR amplifies genomic translocation breakpoint involving unknown partner gene. Blood, 1997; 90: 4679-86.
373. Gillert, E., Leis, T., Repp, R., et al. A DNA damage repair mechanism is involved in the origin of chromosomal translocations t(4;11) in primary leukemic cells. Oncogene, 1999; 18: 4663-71.
374. Felix, C. A., Hosler, M. R., Slater, D. J., et al. Duplicated regions of AF-4 intron 4 at t(4;11) translocation breakpoints. Molecular Diagnosis, 1999; 4: 269-83.
375. _ sequence in MLL and AF-9 create homologous single-stranded overhangs that anneal to form der(11) and der(9) genomic breakpoint junctions in treatment-related AML without further processing [abstract]. Blood, 2002; 100(Suppl. 1): 530-1a.
376. Jackson, S.P. Sensingandrepairing DNA double-strandbreaks. Carcinogenesis, 2002; 23: 687-96.
377. _ end of the MLL gene involved in genomic duplication events. Br J Haematol, 1999; 105: 256-64.
378. Mistry, A. R., Felix, C. A., Whitmarsh, R. J., et al. DNA topoisomerase II in therapy-related acute promyelocytic leukemia. N Eng J Med, 2005; 352: 529-38.
379. Smith, M. A., Rubenstein, L., & Ungerleider, R. S. Therapyrelated acute myeloid leukemia following treatment with epipodophyllotoxins: estimating the risks. Med Pediatr Oncol, 1994; 23: 86-98.
380. Satake, N., Ishida, Y., Otoh, Y., et al.Novel MLL-CBPfusion transcript in therapy-related chronic myelomonocytic leukemia with a t(11;16)(q23;p13) chromosome translocation. Genes Chromosomes Cancer, 1997; 20: 60-3.
381. Hunger, S. P., Sklar, J., & Link, M. P. Acute lymphoblastic leukemia occurring as a second malignant neoplasm in childhood: report of three cases and review of the literature. J Clin Oncol, 1992; 10: 156-63.
382. Pedersen-Bjergaard, J. Acute promyelocytic leukemia with t(15;17) following inhibition of DNA topoisomerase II. Ann Oncol, 1995; 6: 751-3.
383. Preisler, H. D., Early, A. P., Raza, A., et al. Therapy of secondary acute nonlymphocytic leukemia with cytarabine. NEngl J Med, 1983; 308: 21-3.
384. Longmore, G., Guinan, E. C., Weinstein, H. J., et al. Bone marrow transplantation for myelodysplasia and secondary acute nonlymphoblastic leukemia. J Clin Oncol, 1990; 8: 1707-14.
385. Cortes, J., O'Brien, S., Kantarjian, H., et al.Abnormalities in the long armof chromosome11 (11q) in patients with de novo and secondary acutemyelogenous leukemiasandmyelodysplastic syndromes. Leukemia, 1994; 8: 2174-8.
386. de Witte, T., Suciu, S., Peetermans, M., et al. Intensive chemotherapy for poor prognosis myelodysplasia (MDS) and secondary acute myeloid leukemia (sAML) following MDS of more than 6 months duration. A pilot study by the Leukemia Cooperative Group of the European Organisation for Research and Treatment in Cancer (EORTC-LCG). Leukemia, 1995; 9: 1805-11.
387. O'Donnell, M. R., Long, G. D., Parker, P. M., et al. Busulfan/cyclophosphamide as conditioning regimen for allogeneicbonemarrowtransplantation formyelodysplasia. J Clin Oncol, 1995; 13: 2973-9.
388. Gardin, C., Chaibi, P., de Revel, T., et al. Intensive chemotherapy with idarubicin, cytosine arabinoside, and granulocyte colony-stimulating factor (G-CSF) in patients with secondary and therapy-related acute myelogenous leukemia. Leukemia, 1997; 11: 16-21.
389. Anderson, J. E., Gooley, T. A., Schoch, G., et al. Stem cell transplantation for secondary acute myeoid leukemia: Evaluation of transplantation as initial therapy or following induction chemotherapy. Blood, 1997; 89: 2578-85.
390. Laver, J. H., Yusuf, U., Cantu, E. S., et al. Transient therapy-related myelodysplastic syndrome associated with monosomy 7 and 11q23 translocation. Leukemia, 1997; 11: 448-55.
391. Applebaum, F. R., Le Beau, M. M., & Willman, C. L. Secondary leukemia. In Hematology 1996. Education program of the American Society of Hematology (Washington, DC: American Society of Hematology, 1996), pp. 33-47.
392. Tohyama, K., Tsutani, H., Wano, Y., et al. Anti-leukemia chemotherapy of high-risk myelodysplastic syndromes. Oncologist, 1997; 2: 160-3.
393. List, A., Beran, M., Di Persio, J., et al.Opportunities for Trisenox (arsenic trioxide) in the treatment of myelodysplastic syndromes. Leukemia, 2003; 17: 1499-507.
394. Stasi, R., Brunetti, M., Terzoli, E., & Amadori, S. Sustained response to recombinanthumanerythropoietin and intermittent all-trans retinoic acid in patients with myelodysplastic syndromes. Blood, 2002; 99: 1578-84.
395. Negrin, R. S., Stein, R., Doherty, K., et al. Maintenance treatmentoftheanemiaofmyelodysplasticsyndromeswithrecombinant human granulocyte colony-stimulating factor and erythropoiet In evidence for in vivo synergy. Blood, 1996; 87: 4076-81.
396. Rowe, J. M. Therapy of secondary leukemia. Leukemia, 2002; 16: 748-50.
397. Geller, R. B., Vogelsang, G. B., Wingard, J. R., et al. Successful marrowtransplantation for acutemyelocytic leukemia following therapy for Hodgkin's disease. J Clin Oncol, 1988; 6: 1558-61.
398. Kantarjian, H. M., Estey, E. H., & Keating, M. J. Treatment of therapy-related leukemia and myelodysplastic syndrome. Hematol Oncol Clin North Am, 1993; 7: 81-107.
399. Witherspoon, R. P.&Deeg, H. J. Allogeneic bone marrowtransplantation for secondary leukemia ormyelodysplasia. Haematologica, 1999; 84: 1085-7.
400. Yakoub-Agha, I., de La Salmoniere, P., Ribaud, P., et al. Allogeneic bone marrow transplantation for therapy-related myelodysplastic syndrome and acute myeloid leukemia: a long-term study of 70 patients-report of the French society of Bone Marrow Transplantation. J Clin Oncol, 2000; 18: 963-71.
401. Arnold, R., de Witte, T., Biezen, A. van, et al. Unrelated bone marrowtransplantation in patients with myelodysplastic syndromes and secondary acutemyeloid leukemia: anEBMTsurvey. European Bloodand Marrow Transplantation Group. Bone Marrow Transplant, 1998; 21: 1213-16.
402. Mantadakis, E., Shannon, K. M., Singer, D. A., et al. Transient monosomy 7: a case series in children and review of the literature. Cancer, 1999; 85: 2655-61.
403. Leung, E. W., Woodman, R. C., Roland, B., et al. Transient myelodysplastic syndrome associated with isochromosome 7q abnormality. Pediatr Hematol Oncol, 2003; 20: 539-45.
404. Bullinger, L., Dohner, K., Bair, E., et al. Use of gene-expression profiling to identify prognostic subclasses in adult acute myeloid leukemia. NEngl J Med, 2004; 350: 1605-16.
405. Valk, P. J., Verhaak, R. G., Beijen, M. A., et al. Prognostically useful gene-expression profiles in acute myeloid leukemia. N Engl J Med, 2004; 350: 1617-28.
406. Grimwade, D., Walker, H., Oliver, F., et al. The importance of diagnostic cytogenetics on outcome in AML: analysis of 1, 612 patients entered into the MRC AML 10 trial. The Medical Research Council Adult and Children's Leukaemia Working Parties. Blood, 1998; 92: 2322-33.
407. Hale, G. A., Heslop, H. E., Bowman, L. C., et al. Bone marrow transplantation for therapy-induced acute myeloid leukemia in children with previous lymphoid malignancies. Bone Marrow Transplant, 1999; 24: 735-9.
408. Leahey, A. M., Friedman, D. L., & Bunin, N. J. Bone marrow transplantation in pediatric patients with therapy-related myelodysplasia and leukemia. Bone Marrow Transplant, 1999; 23: 21-5.
409. Anargyrou, K., Vaiopoulos, G., Terpos, E., et al. Low dose melphalan is a treatment option in elderly patients with high risk myelodysplastic syndrome or secondary acute myeloblastic leukaemia. Haematologia (Budap), 2002; 32: 169-73.
410. Ballen, K. K. & Antin, J. H. Treatment of therapy-related acute myelogenous leukemia and myelodysplastic syndromes. Hematol Oncol Clin North Am, 1993; 7: 477-93.
411. Fung, H. C., Cohen, S., Rodriguez, R., et al. Reducedintensity allogeneic stem cell transplantation for patients whose prior autologous stem cell transplantation for hematologicmalignancyfailed. Biol Blood Marrow Transplant, 2003;9: 649-56.
412. Taussig, D. C., Davies, A. J., Cavenagh, J. D., et al. Durable remissions of myelodysplastic syndrome and acute myeloid leukemia after reduced-intensity allografting. J Clin Oncol, 2003; 21: 3060-5.
413. Hasle, H., Kerndrup, G., Yssing, M., et al. Intensive chemotherapy in childhood myelodysplastic syndrome. A comparison with results in acute myeloid leukemia. Leukemia, 1996; 10: 1269-73.
414. Goldman, J. M. & Melo, J. V. Chronic myeloid leukemia-advances in biology and new approaches to treatment. NEng J Med, 2003; 349: 1451-64.
415. Scheuring, U. J., Pfeifer, H., Wassmann, B., et al. Early minimal residual disease (MRD) analysis during treatment of Philadelphia chromosome/Bcr-Abl-positive acute lymphoblastic leukemia with the Abl-tyrosine kinase inhibitor imatinib (STI571). Blood, 2003; 101: 85-90.
416. Ottmann, O. G., Druker, B. J., Sawyers, C. L., et al. A phase 2 study of imatinib in patients with relapsed or refractory Philadelphia chromosome-positive acute lymphoid leukemias. Blood, 2002; 100: 1965-71.
417. Kindler, T., Breitenbuecher, F., Marx, A., et al. Sustained complete hematologic remission after administration of the tyrosine kinase inhibitor imatinib mesylate in a patient with refractory, secondary AML. Blood, 2003; 101: 2960-2.
418. Spiekermann, K., Dirschinger, R. J., Schwab, R., et al. The protein tyrosine kinase inhibitor SU5614 inhibits FLT3 and induces growth arrest and apoptosis in AML-derived cell lines expressing a constitutively activated FLT3. Blood, 2003; 101: 1494-504.
419. Karamouzis, M.V., Gorgoulis, V. G., &Papavassiliou, A. G. Transcription factors and neoplasia: vistas in novel drug design. Clin Cancer Res, 2002; 8: 949-61.
420. Rabbitts, T. H. & Stocks, M. R. Chromosomal translocation products engender new intracellular therapeutic technologies. Nat Med, 2003; 9: 383-6.
421. Kawagoe, H., Kawagoe, R., & Sano, K. Targeted downregulation of MLL-AF9 with antisense oligodeoxyribonucleotide reduces the expression of the HOXA7 and-A10 genes and induces apoptosis in a human leukemia cell line, THP-1. Leukemia, 2001; 15: 1743-9.
422. Niitsu, N., Hayashi, Y., & Honma, Y. Downregulation of MLLCBP fusion gene expression is associated with differentiation of SN-1 cells with t(11;16)(q23;p13). Oncogene, 2001; 20: 375-84.
423. Johnstone, R. W., Gerber, M., Landewe, T., et al. Functional analysis of the leukemia protein ELL: evidence for a role in the regulation of cell growth and survival. Mol Cell Biol, 2001; 21: 1672-81.
424. Akao, Y., Mizoguchi, H., Misiura, K., et al. Antisense oligodeoxyribonucleotide against the MLL-LTG19 chimeric transcript inhibits cell growth and induces apoptosis in cells of an infantile leukemia cell line carrying the t(11;19) chromosomal translocation. Cancer Res, 1998; 58: 3773-6.
425. _-deoxycytidine (decitabine) treatment. Blood, 2002; 100: 2957-64.