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31 - Therapy-related leukemias

from Part IV - Complications and supportive care

Published online by Cambridge University Press:  01 July 2010

Carolyn A. Felix
Affiliation:
Associate Professor of Pediatrics University of Pennsylvania School of Medicine, Attending Physician The Children's Hospital of Philadelphia, Abramson Research Center, Philadelphia, PA, USA
Ching-Hon Pui
Affiliation:
St. Jude Children's Research Hospital, Memphis
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Summary

Introduction

The estimated frequency of second cancers in long-term survivors of primary cancers is about 7%. Although leukemias comprise only a small fraction of all second cancers, they are the major second cancers resulting from chemotherapy. The two broad classes of cytotoxic drugs associated with leukemia are alkylating agents and DNA topoisomerase II inhibitors. This chapter will focus on the features that distinguish alkylating agent-related leukemias and DNA topoisomerase II inhibitor-related leukemias as the two major forms of leukemia attributed to chemotherapy. Chemotherapy has been implicated in acute myelogenous leukemia (AML) of virtually all morphologic subtypes, myelodysplastic syndrome (MDS), acute lymphoblastic leukemia (ALL) and chronic myelogenous leukemia (CML) (reviewed in Felix). By contrast, therapeutic radiation primarily induces solid tumors, but also has been linked to an increased risk of leukemia. There are many more reports of chemotherapy-related leukemias in adults than in children; however, leukemia has become an increasingly important complication of cytotoxic chemotherapy in children because they are more likely than adults to survive their primary cancers.

Epidemiology of treatment-related leukemias

Alkylating agent-related leukemias: incidence and risk

A minority of patients (40% in one large series) who develop therapy-related leukemia have received chemotherapy alone, and there is often overlap between alkylating agents and DNA topoisomerase II inhibitors in the chemotherapy regimen. The first observations of alkylating agent-related leukemia and MDS were reported in about 1970. Therapy-related MDS and AML can occur after administration of virtually all of the many different alkylating agents.

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Childhood Leukemias , pp. 774 - 804
Publisher: Cambridge University Press
Print publication year: 2006

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References

Flannery, J. T., Boice, J. D. Jr., Devesa, S. S., et al.Cancer registration in Connecticut and the study of multiple primary cancers, 1935–1982. Natl Cancer Inst Monogr, 1985; 68: 13–24.Google Scholar
Smith, M. A., McCaffrey, R. P., & Karp, J. E.The secondary leukemias: challenges and research directions. JNCI, 1996; 88: 407–18.CrossRefGoogle ScholarPubMed
Felix, C. A.Secondary leukemias induced by topoisomerase targeted drugs. Biochimica et Biophysica Acta, 1998; 1400: 233–55.CrossRefGoogle ScholarPubMed
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.Google Scholar
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.CrossRefGoogle ScholarPubMed
Kaldor, J.Second cancer following chemotherapy and radiotherapy. An epidemiological perspective. Acta Oncol, 1990; 29: 647–55.CrossRefGoogle ScholarPubMed
Donaldson, S. S. & Hancock, S. L.Second cancers after Hodgkin's disease in childhood. N Engl J Med, 1997; 334: 792–3.CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
Ron, E., Lubin, J. H., Shore, R. R., et al.Thyroid cancer after exposure to external radiation: a pooled analysis of seven studies. Radiat Res, 1995; 141: 259–77.CrossRefGoogle ScholarPubMed
Travis, L. B., Curtis, R. E., Boice, J. J. Jr., et al.Second malignant neoplasms among long-term survivors of ovarian cancer. Cancer Res, 1996; 56: 1564–70.Google ScholarPubMed
Tucker, M. A., Jones, P. P. 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.Google Scholar
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.Google Scholar
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).
Rowley, J. D. & Olney, H. J.International workshop on the relationship of prior therapy to balanced chromosome aberrations in therapy-related myelodysplastic syndromes and acute leukemia: overview report. Genes Chromosomes Cancer, 2002; 33: 331–45.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Boice, J. D. Jr., Travis, L. B., & Curtis, L. B.Patterns of second cancers [abstract]. Proc AACR, 1997; 38: 645.Google Scholar
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.CrossRefGoogle Scholar
Davies, S. M.Therapy-related leukemia associated with alkylating agents. Med Pediatr Oncol, 2001; 36: 536–40.CrossRefGoogle ScholarPubMed
Pedersen-Bjergaard, J.Incidence, previous treatment and chromosome characteristics of secondary acute non-lymphocytic leukemia. Cancer Treat Rev, 1985; 12: 65–75.CrossRefGoogle ScholarPubMed
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.Google Scholar
Blayney, D. W., Longo, D. L., Young, R. R., et al.Decreasing risk of leukemia with prolonged follow-up after chemotherapy and radiotherapy for Hodgkin's disease. N Engl J Med, 1987; 316: 710–4.CrossRefGoogle ScholarPubMed
Meadows, A. T., Obringer, A. C., Marrero, O., et al.Second malignant neoplasms following childhood Hodgkin's disease: treatment and splenectomy as risk factors. Med Pediatr Oncol, 1989; 17: 477–84.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
Greene, M. H., Harris, E. L., Gershenson, D. D., et al.Melphalan may be a more potent leukemogen than cyclophosphamide. Ann Intern Med, 1986; 105: 360–7.CrossRefGoogle ScholarPubMed
Curtis, R. E., Boice, J J. D., Stovall, M., et al.Risk of leukemia after chemotherapy and radiation treatment for breast cancer. N Engl J Med, 1992; 326: 1745–51.CrossRefGoogle ScholarPubMed
Diamandidou, E., Buzdar, A. U., Smith, T. T., 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.CrossRefGoogle ScholarPubMed
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.Google Scholar
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.Google Scholar
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.Google Scholar
Chabner, B. A. & Myers, C. E. Clinical pharmacology of cancer chemotherapy. In , V. T. DeVita, , S. Hellman, & , S. A. Rosenberg, eds., Principles and Practice of Oncology (Philadelphia, PA: J. B. Lippincott, 1989), pp. 349–95.Google Scholar
Greene, M. H.Is cisplatin a human carcinogen ?J Natl Cancer Inst, 1992; 84: 306–12.CrossRefGoogle ScholarPubMed
Pappo, A., Schneider, N. R., Sanders, J. J., & Buchanan, G. R.Secondary myelodysplastic syndrome complicating therapy for osteogenic sarcoma. Cancer, 1991; 68: 1373–5.3.0.CO;2-S>CrossRefGoogle ScholarPubMed
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: 165–9.3.0.CO;2-F>CrossRefGoogle Scholar
Williams, T. M., Colas, C., Nowell, P. C., et al.Association of germline p53 replication error with myelodysplastic syndrome following osteosarcoma treatment [abstract]. Proc AACR, 1999; 40: 683.Google Scholar
Jeha, S., Jaffe, N., & Robertson, R.Secondary acute non-lymphoblastic leukemia in two children following treatment with a cis-diamminechloroplatinum-II-based regimen for osteosarcoma. Med Pediatr Oncol, 1992; 20: 71–4.CrossRefGoogle ScholarPubMed
DeVore, 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.CrossRefGoogle ScholarPubMed
Nichols, C. R., Breeden, E. S., Loehrer, P. P., 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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Travis, L. B., Holowaty, E. J., Bergfeldt, K., et al.Risk of leukemia after platinum-based chemotherapy for ovarian cancer. N Engl J Med, 1999; 340: 351–7.CrossRefGoogle ScholarPubMed
Travis, L. B., Andersson, M., Gospodarowicz, M., et al.Treatment-related leukemia following testicular cancer. J Natl Cancer Institute, 2000; 92: 1165–71.CrossRefGoogle Scholar
Tucker, M. A., Coleman, C. N., Cox, R. R., Varghese, A., & Rosenberg, S. A.Risk of second cancers after treatment for Hodgkin's disease. N Engl J Med, 1988; 318: 76–81.CrossRefGoogle ScholarPubMed
Kaldor, J. M., Day, N. E., Clarke, E. E., et al.Leukemia following Hodgkin's disease. N Engl J Med, 1990; 22: 7–13.CrossRefGoogle Scholar
Miller, J. S., Arthur, D. C., Litz, C. C., et al.Myelodysplastic syndrome after autologous bone marrow transplantation: an additional late complication of curative cancer therapy. Blood, 1994; 83: 3780–6.Google ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Deeg, H. J. & Socie, G.Malignancies after hematopoietic stem cell transplantation: many questions, some answers. Blood, 1998; 91: 1833–44.Google ScholarPubMed
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.Google ScholarPubMed
Rege, K. P., Janes, S. L., Saso, R., et al.Secondary leukaemia characterised by monosomy 7 occurring post-autologous stem cell transplantation for AML. Bone Marrow Transplant, 1998; 21: 853–5.CrossRefGoogle ScholarPubMed
Micallef, I. N., Lillington, D. M., Apostolidis, J., et al.Therapy-related 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.CrossRefGoogle ScholarPubMed
Armitage, J. O.Myelodysplasia and acute leukemia after autologous bone marrow transplantation [editorial]. J Clin Oncol, 2000; 18: 945–6.CrossRefGoogle Scholar
Abruzzese, E., Radford, J. E., Miller, J. J., et al.Detection of abnormal pretransplant clones in progenitor cells of patients who developed myelodysplasia after autologous transplantation. Blood, 1999; 94: 1814–19.Google ScholarPubMed
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.CrossRefGoogle Scholar
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.Google ScholarPubMed
Perilongo, G., Felix, C. A., Meadows, A. A., 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.Google Scholar
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: 1438–46.3.0.CO;2-#>CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.Google ScholarPubMed
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.Google ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Felix, C. A., Megonigal, M. D., Chervinsky, D. D., et al.Association of germline p53 mutation with MLL segmental jumping translocation in treatment-related leukemia. Blood, 1998; 91: 4451–6.Google ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Tanaka, K., Arif, M., Eguchi, M., et al.Frequent jumping translocations of chromosomal segments involving the ABL oncogene alone or in combination with CD3-MLL genes in secondary leukemias. Blood, 1997; 89: 596–600.Google ScholarPubMed
Avet-Loiseau, H., Godon, C., Li, J. Y., et al.Amplification of the 11q23 region in acute myeloid leukemia. Genes Chromosomes Cancer, 1999; 26: 166–70.3.0.CO;2-P>CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
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 acute myeloblastic leukemia. Blood, 2002; 100: 3761–6.CrossRefGoogle ScholarPubMed
Ben-Yehuda, D., Krichevsky, S., Caspi, O., et al.Microsatellite instability and p53 mutations in therapy-related leukemia suggest mutator phenotype. Blood, 1996; 88: 4296–303.Google ScholarPubMed
Worrillow, L. J., Travis, L. B., Smith, A. A., 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.Google ScholarPubMed
Hayes, J. D. & Pulford, D. J.The glutathione S-transferase supergene family: regulation of GST and the contribution of the isoenzymes to cancer chemoprotection and drug resistance. Critical Rev Biochem Molec Biol, 1995; 30: 445–600.CrossRefGoogle ScholarPubMed
Smith, G., Stanley, L. A., Sim, E., Strange, R. C., & Wolf, C. R.Metabolic polymorphisms and cancer susceptibility. Cancer Surveys, 1995; 25: 27–65.Google ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Morgan, G. J. & Smith, M. T.Metabolic enzyme polymorphisms and susceptibility to acute leukemia in adults. Am J Pharmacogenomics, 2002; 2: 79–92.CrossRefGoogle ScholarPubMed
Li, A. P., Kaminski, D. L., & Rasmussen, A.Substrates of human hepatic cytochrome P450 3A4. Toxicology, 1995; 104: 1–8.CrossRefGoogle ScholarPubMed
Wrighton, S. & Stevens, J.The human hepatic cytochromes P450 involved in drug metabolism. Crit Rev Toxicol, 1992; 22: 1–21.CrossRefGoogle ScholarPubMed
Felix, C. A., Walker, A. H., Lange, B. B., et al.Association of CYP3A4 genotype with treatment-related leukemia. Proc Natl Acad Sci U S A, 1998; 95: 13176–81.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Roddam, P. L., Rollinson, S., Kane, E., et al.Poor metabolizers at the cytochrome P450 2D6 and 2C19 loci are at increased risk of developing adult acute leukaemia. Pharmacogenetics, 2000; 10: 605–15.CrossRefGoogle ScholarPubMed
Chen, H., Sandler, D. P., Taylor, J. J., et al.Increased risk for myelodysplastic syndromes in individuals with glutathione transferase theta 1 (GSTT1) gene defect. Lancet, 1996; 347: 295–7.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Allan, J. M., Wild, C. C.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: 11592–7.CrossRefGoogle ScholarPubMed
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.Google Scholar
Ross, D. Quinone reductases. In , F. P. Guengerich, ed., Comprehensive Toxicology, vol. 3 (New York: Pergamon Press, 1997), pp. 179–97.Google Scholar
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
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.Google ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Rothman, N., Smith, M. T., Hayes, R. R., et al.Benzene poisoning, a risk factor for hematologic malignancy, is associated with NQO1 609 C–>T mutation and rapid fractional excretion of chlorzoxazone. Cancer Res, 1997; 57: 2839–42.Google Scholar
Larson, R. A., Wang, Y., Banerjee, M., et al.Prevalence of the inactivating 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.Google ScholarPubMed
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.Google ScholarPubMed
Pui, C. H., Ribeiro, R. C., Hancock, M. M., et al.Acute myeloid leukemia in children treated with epipodophyllotoxins for acute lymphoblastic leukemia. N Engl J Med, 1991; 325: 1682–7.CrossRefGoogle ScholarPubMed
Pui, C.-H., Hancock, M. L., Raimondi, S. S., et al.Myeloid neoplasia in children treated for solid tumours. Lancet, 1990; 336: 417–21.CrossRefGoogle ScholarPubMed
Pui, C.-H., Behm, F. G., Raimondi, S. S., et al.Secondary acute myeloid leukemia in children treated for acute lymphoid leukemia. N Engl J Med, 1989; 321: 136–42.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Chak, L. Y., Sikic, B. I., Tucker, M. M., 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.CrossRefGoogle ScholarPubMed
Johnson, D. H., Porter, L. L., List, A. A., et al.Acute nonlymphocytic leukemia after treatment of small cell lung cancer. Am J Med, 1986; 81: 962–8.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
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.CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Whitlock, J. A., Greer, J. P., & Lukens, J. N.Epipodophyllotoxin-related leukemia: identification of a new subset of secondary leukemia. Cancer, 1991; 68: 600–4.3.0.CO;2-F>CrossRefGoogle ScholarPubMed
Zeimet, A. G., Thaler, J., Abfalter, E., Marth, C., & Dapunt, O.Secondary leukaemias after etoposide. Lancet, 1992; 340: 379–80.CrossRefGoogle ScholarPubMed
Hawkins, M. M.Secondary leukaemia after epipodophyllotoxins. Lancet, 1991; 338: 1408.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.Google ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Donatini, B. & Krupp, P.Secondary pre-leukaemia and etoposide. Lancet, 1991; 338: 1269.CrossRefGoogle Scholar
Rose, V. L., Keppen, M. D., Eichner, E. E., Pitha, J. V., & Murray, J. L.Acute leukemia after successful chemotherapy for oat cell carcinoma. Am J Clin Pathol, 1983; 79: 122–4.CrossRefGoogle ScholarPubMed
Bokemeyer, C. & Schmoll, H.-J.Secondary neoplasms following treatment of malignant germ cell tumors. J Clin Oncol, 1993; 11: 1703–9.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
Ratain, M. J., Kaminer, L. S., Bitran, J. J., 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.Google ScholarPubMed
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.CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Andoh, T. & Ishida, R.Catalytic inhibitors of DNA topoisomerase II. Biochim Biophys Acta, 1998; 1400: 155–94.CrossRefGoogle ScholarPubMed
Rivera, G. K., Pui, C. H., Santana, V. V., Pratt, C. B., & Crist, W. M.Epipodophyllotoxins in the treatment of childhood cancer. Cancer Chemother Pharmacol, 1994; 34: S89–95.CrossRefGoogle ScholarPubMed
Giaccone, G.Teniposide alone and in combination chemotherapy in small cell lung cancer. Semin Oncol, 1992; 19: 75–80.Google ScholarPubMed
Giaccone, G., Splinter, T. A., Kirkpatrick, A., et al.The European Organization for Research and Treatment of Cancer experience with teniposide: preliminary results of a randomized study in non-small cell lung cancer. Semin Oncol, 1992; 19: 98–102.Google ScholarPubMed
Muggia, F. M.Teniposide: overview of its therapeutic potential in adult cancers. Cancer Chemother Pharmacol, 1994; 34: S127–33.CrossRefGoogle ScholarPubMed
Hirsch, F. R., Dombernowsky, P., & Hansen, H. H.Treatment of small cell lung cancer: the Copenhagen experience. Anticancer Res, 1994; 14: 317–19.Google ScholarPubMed
Muggia, F. M. & Kelley, S. L.Teniposide in adult solid tumors: a historical perspective. Semin Oncol, 1992; 19: 43–50.Google ScholarPubMed
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.CrossRefGoogle Scholar
Kreissman, S. G., Gelber, R. D., Cohen, H. H., et al.Incidence of secondary acute myelogenous leukemia after treatment of childhood acute lymphoblastic leukemia. Cancer, 1992; 70: 2208–13.3.0.CO;2-P>CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Detourmignies, L., Castaigne, S., Stoppa, A. M., et al.Therapy-related acute promyelocytic leukemia: a report on 16 cases. J Clin Oncol, 1992; 10: 1430–5.CrossRefGoogle ScholarPubMed
Sandoval, C., Pui, C. H., Bowman, L. L., 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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
Megonigal, M. D., Cheung, N. K., Rappaport, E. E., et al.Detection of leukemia-associated MLL-GAS7 translocation early during chemotherapy with DNA topoisomerase II inhibitors. Proc Natl Acad Sci U S A, 2000; 97: 2814–19.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
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.Google ScholarPubMed
Megonigal, M. D., Rappaport, E. F., Jones, D. D., 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.CrossRefGoogle ScholarPubMed
Corbett, A. & Osheroff, N.When good enzymes go bad: conversion of topoisomerase II to a cellular toxin by antineoplastic drugs. Chem Res Toxicol, 1993; 6: 585–97.CrossRefGoogle ScholarPubMed
Beaumont, M., Sanz, M., Carli, P. M., et al.Therapy-related acute promyelocytic leukemia. J Clin Oncol, 2003; 21: 2123–37.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Barker, D. E., Dragnani, T. A., Dunnick, J. K., et al.IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Some Antiviral and Antineoplastic drugs, and Other Pharmaceutical Agents, vol. 76. (Lyon, France: IARC Press, 2000).Google Scholar
Duffner, P. K., Krischer, J. P., Horowitz, M. M., et al.Second malignancies in young children with primary brain tumors following treatment with prolonged postoperative chemotherapy and delayed irradiation: a Pediatric Oncology Group study. Ann Neurol, 1998; 44: 313–16.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Yagita, M., Ieki, Y., Onishi, R., et al.Therapy-related leukemia and myelodysplasia following oral administration of etoposide for recurrent breast cancer. Int J Oncol, 1998; 13: 91–6.Google ScholarPubMed
Bokemeyer, C., Schmoll, H. J., Kuczyk, M. M., 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.CrossRefGoogle Scholar
Boshoff, C., Begent, R. H., Oliver, R. R., et al.Secondary tumours following etoposide containing therapy for germ cell cancer. Ann Oncol, 1995; 8: 35–40.CrossRefGoogle Scholar
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.Google ScholarPubMed
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.Google Scholar
Pegram, L. D., Megonigal, M. D., Lange, B. B., et al.t(3;11)(q25;q23) in treatment-related acute myeloid leukemia fuses MLL gene with GMPS (guanosine 5′-monophosphate synthetase). Blood, 2000; 96: 4360–2.Google Scholar
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Rivera, G. K., Pui, C.-H., & Crist, W. M.The epipodo phyllotoxins: both sides of the coin. J Clin Oncol, 1993; 11: 1624–7.CrossRefGoogle Scholar
Sandler, E. S., Friedman, D. J., Mustafa, M. M., et al.Treatment of children with epipodophyllotoxin-induced secondary acute myeloid leukemia. Cancer, 1997; 79: 1049–54.3.0.CO;2-0>CrossRefGoogle ScholarPubMed
Pui, C.-H., Relling, M. V., Behm, F. F., et al.L-asparaginase may potentiate the leukemogenic effect of the epipodophyllotoxins. Leukemia, 1995; 9: 1680–4.Google ScholarPubMed
Winick, N., Buchanan, G. R., & Kamen, B. A.Secondary acute myeloid leukemia in Hispanic children. J Clin Oncol, 1993; 11: 1433.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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: 9–13.3.0.CO;2-Y>CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
Horibe, K., Matsushita, T., Numata, S., et al.Acute promyelocytic leukemia with t(15;17) abnormality after chemotherapy containing etoposide for Langerhans cell histiocytosis. Cancer, 1993; 72: 3723–6.3.0.CO;2-Y>CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.Google ScholarPubMed
Relling, M. V., Boyett, J. M., Blanco, J. J., et al.Granulocyte colony-stimulating factor and the risk of secondary myeloid malignancy after etoposide treatment. Blood, 2003; 101: 3862–7.CrossRefGoogle ScholarPubMed
Felice, M. S., Rossi, J., Gallego, M., et al.Acute trilineage leukemia with monosomy of chromosome 7 following an acute promyelocytic leukemia. Leuk Lymphoma, 1999; 34: 409–13.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
Au, W. Y., Lam, C. C., Ma, E. E., et al.Therapy-related myelodysplastic syndrome after eradication of acute promyelocytic leukemia: cytogenetic and molecular features. Hum Pathol, 2001; 32: 126–9.CrossRefGoogle ScholarPubMed
Andersen, M. K.& Pedersen-Bjergaard, J. Therapy-related MDS and AML in acute promyelocytic leukemia. Blood, 2002; 100: 1928–9.CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Andersen, M. K., Larson, R. A., Mauritzson, N., et al.Balanced chromosome abnormalities inv(16) and t(15;17) in therapy- related myelodysplastic syndromes and acute leukemia: report from an international workshop. Genes Chromosomes Cancer, 2002; 33: 395–400.CrossRefGoogle Scholar
Maanen, J. M. S., 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.CrossRefGoogle ScholarPubMed
Mans, D. R. A., Retel, J., Maanen, J. J. S., et al.Role of the semi-quinone free radical of the anti-tumour agent etoposide (VP-16–213) in the inactivation of single- and double-stranded fX174 DNA. Br J Cancer, 1990; 62: 54–60.CrossRefGoogle ScholarPubMed
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.Google ScholarPubMed
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.Google ScholarPubMed
Ben-Yehuda, D., Krichevsky, S., Shafran, S., et al.Therapy-related leukemia: clinical characteristics and analysis of new molecular risk factors in 96 patients [abstract]. Blood, 2002; 100(Suppl. 1): 324a.Google Scholar
Blanco, J. G., Edick, M. J., Hancock, M. M., et al.Genetic polymorphisms in CYP3A5, CYP3A4 and NQO1 in children who developed therapy-related myeloid malignancies. Pharmacogenetics, 2002; 12: 605–11.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Sinha, B. K., Politi, P. M., Eliot, H. H., 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.CrossRefGoogle ScholarPubMed
Gantchev, T. G. & Hunting, D. J.The ortho-quinone metabolite of the anticancer drug etoposide (VP-16) is a potent inhibitor of the topoisomerase II/DNA cleavable complex. Mol Pharmacol, 1998; 53: 422–8.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Poll, M. E. van de, Relling, M. V., Schuetz, E. E., et al.The effect of atovaquone on etoposide pharmacokinetics in children with acute lymphoblastic leukemia. Cancer Chemother Pharmacol, 2001; 47: 467–72.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.Google ScholarPubMed
Woo, M. H., Shuster, J., Chen, C.-L., et al.Glutathione S-transferase genotypes in children who develop treatment-related acute myeloid malignancies. Leukemia, 2000; 4: 232–7.CrossRefGoogle Scholar
Relling, M. V., Hancock, M. L., Rivera, G. G., et al.Mercaptopurine therapy intolerance and heterozygosity at the thiopurine S-methyltransferase gene locus. J Natl Cancer Inst, 1999; 91: 2001–8.CrossRefGoogle ScholarPubMed
McLeod, H. L., Lin, J. S., Scott, E. E., Pui, C. H., & Evans, W. E.Thiopurine methyltransferase activity in American white subjects and black subjects. Clin Pharmacol Ther, 1994; 55: 15–20.CrossRefGoogle ScholarPubMed
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.Google Scholar
Pedersen-Bjergaard, J., Andersen, M. K., Christiansen, D. D., & Nerlov, C.Genetic pathways in therapy-related myelodysplasia and acute myeloid leukemia. Blood, 2002; 99: 1909–12.CrossRefGoogle ScholarPubMed
Willman, C. L.Molecular genetic features of myelodysplastic syndromes (MDS). Leukemia, 1998; 12(Suppl. 1): S2–6.Google Scholar
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.CrossRefGoogle ScholarPubMed
Bodner, S. M., Naeve, C. W., Rakestraw, K. K., et al.Cloning and chromosomal localization of the gene encoding human cyclin D-binding Myb-like protein (hDMP1). Gene, 1999; 229: 223–8.CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
Kratz, C. P., Emerling, B. M., Donovan, S., et al.Candidate gene isolation and comparative analysis of a commonly deleted segment of 7q22 implicated in myeloid malignancies. Genomics, 2001; 77: 171–80.CrossRefGoogle ScholarPubMed
Kratz, C. P., Emerling, B. M., Bonifas, J., et al.Genomic structure of the PIK3CG gene on chromosome band 7q22 and evaluation as a candidate myeloid tumor suppressor. Blood, 2002; 99: 372–4.CrossRefGoogle ScholarPubMed
Boultwood, J., Lewis, S., & Wainscoat, J. S.The 5q-syndrome. Blood, 1994; 84: 3253–60.Google ScholarPubMed
Willman, C. L., Sever, C. E., Pallavicini, M. M., et al.Deletion of IRF-1, mapping to chromosome 5q31.1, in human leukemia and preleukemic myelodysplasia. Science, 1993; 259: 968–71.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.Google ScholarPubMed
Castro, P. D., Fairman, J., & Nagarajan, L.The unexplored 5q13 locus: a role in hematopoietic malignancies. Leuk Lymphoma, 1998; 30: 443–8.CrossRefGoogle ScholarPubMed
Castro, P., Liang, H., Liang, J. C., & Nagarajan, L.A novel, evolutionarily conserved gene family with putative sequence-specific single-stranded DNA-binding activity. Genomics, 2002; 80: 78–85.CrossRefGoogle ScholarPubMed
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.Google ScholarPubMed
Hall, A.The cellular functions of small GTP-binding proteins. Science, 1990; 249: 635–640.CrossRefGoogle ScholarPubMed
Hall, A.Signal transduction through small GTPases – a tale of two GAPs. Cell, 1992; 69: 389–91.CrossRefGoogle ScholarPubMed
Bourne, H. R., Sanders, D. A., & McCormick, F.The GTPase superfamily: a conserved switch for diverse cell functions. Nature, 1990; 348: 125–32.CrossRefGoogle ScholarPubMed
Bourne, H. R., Sanders, D. A., & McCormick, F.The GTPase superfamily: conserved structure and molecular mechanism. Nature, 1991; 349: 117–27.CrossRefGoogle ScholarPubMed
Boguski, M. S. & McCormick, F.Proteins regulating Ras and its relatives. Nature, 1993; 366: 643–54.CrossRefGoogle ScholarPubMed
Aaronson, S. A.Growth factors and cancer. Science, 1991; 254: 1146–53.CrossRefGoogle ScholarPubMed
Satoh, T., Nakafuku, M., Miyajima, A., & Kaziro, Y.Involvement of ras p21 protein in signal-transduction pathways from interleukin 2, interleukin 3, and granulocyte/macrophage colony-stimulating factor, but not from interleukin 4. Proc Natl Acad Sci U S A, 1991; 88: 3314–18.CrossRefGoogle Scholar
Willman, C. L., Sever, C. E., Pallavicini, M. M., et al.Deletion of IRF-1, mapping to chromosome 5q31.1, in human leukemia and preleukemic myelodysplasia. Science, 1993; 259: 968–71.CrossRefGoogle ScholarPubMed
LeBeau, 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.CrossRefGoogle Scholar
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.Google Scholar
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.CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
Leonard, D. G. B., Travis, L. B., Addya, K., et al.p53 mutations in leukemia and myelodysplastic syndrome after ovarian cancer. Clin Cancer Res, 2002; 8: 973–85.Google ScholarPubMed
Andersen, M. K., Christiansen, D. H., Kirchhoff, M., & Pedersen-Bjergaard, J.Duplication or amplification of chromosome band 11q23, including the unrearranged MLL gene, 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.CrossRefGoogle ScholarPubMed
Jonveaux, P., Fenaux, P., Quiquandon, I., et al.Mutations in the p53 gene in myelodysplastic syndromes. Oncogene, 1991; 6: 2243–7.Google ScholarPubMed
Sugimoto, K., Hirano, N., Toyoshima, H., et al.Mutations of the p53 gene in myelodysplastic syndrome (MDS) and MDS-derived leukemia. Blood, 1993; 81: 3022–6.Google ScholarPubMed
Christiansen, D. H., Andersen, M. K., & Pedersen-Bjergaard, J.Methylation of p15INK4B is common, is associated with deletion of genes on chromosome arm 7q and predicts a poor prognosis in therapy-related myelodysplasia and acute myeloid leukemia. Leukemia, 2003; 17: 1813–19.CrossRefGoogle ScholarPubMed
Qian, Z., Fernald, A. A., Godley, L. L., Larson, R. A., & Le Beau, M. M.Expression profiling of CD34+ hematopoietic stem/progenitor cells reveals distinct subtypes of therapy-related acute myeloid leukemia. Proc Natl Acad Sci U S A, 2002; 99: 14925–30.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Thirman, M. J., Gill, H. J., Burnett, R. R., 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.CrossRefGoogle ScholarPubMed
Rubin, C. M., Arthur, D. C., Woods, W. W., et al.Therapy-related myelodysplastic syndrome and acute myeloid leukemia in children: correlation between chromosomal abnormalities and prior therapy. Blood, 1991; 78: 2982–8.Google ScholarPubMed
Rowley, J. D., Vignon, C., Gollin, S. M., et al.Rearrangements involving chromosome band 11q23 in acute leukemia. N Engl J Med, 1996; 334: 601–3.CrossRefGoogle Scholar
Rubnitz, J. E., Behm, F. G., & Downing, J. R.11q23 rearrangements in acute leukemia. Leukemia, 1996; 10: 74–82.Google ScholarPubMed
Pui, C.-H., Relling, M. V., Rivera, G. G., et al.Epipodo phyllotoxin-related acute myeloid leukemia: a study of 35 cases. Leukemia, 1995; 9: 1990–6.Google Scholar
Kantarjian, H. M., Keating, M. J., Walters, R. R., et al.The association of specific “favorable” cytogenetic abnormalities with secondary leukemia. Cancer, 1986; 58: 924–7.3.0.CO;2-Y>CrossRefGoogle ScholarPubMed
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.Google Scholar
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.Google ScholarPubMed
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.Google Scholar
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.Google Scholar
Nucifora, G. & Rowley, J. D.AML1 and the 8;21 and 3;21 translocations in acute and chronic myeloid leukemia. Blood, 1995; 86: 1–14.Google ScholarPubMed
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.Google ScholarPubMed
Slovak, M. L., Bedell, V., Popplewell, L., et al.21q22 balanced chromosome aberrations in therapy-related hematopoietic disorders: report from an international workshop. Genes Chromosomes Cancer, 2002; 33: 379–94.CrossRefGoogle ScholarPubMed
Raiker, A., Green, W., Shabaik, A., & Perlin, E.Acute promyelocytic leukemia following treatment of non-Hodgkin's lymphoma. Cancer, 1989; 63: 1402, a6.3.0.CO;2-#>CrossRefGoogle ScholarPubMed
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.Google Scholar
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.CrossRefGoogle ScholarPubMed
Wiernick, P. H. & Muse, I. M.Acute promyelocytic leukemia after treatment of malignant glioma in a patient with Von Recklinghausen's disease: a case report and review of the literature. Leukemia, 1996; 10: 178–91.Google Scholar
Fenaux, P., Lucidarme, D., Lai, J. L., & Bauters, F.Favorable cytogenetic abnormalities in secondary leukemia. Cancer, 1989; 3: 2505–8.3.0.CO;2-Z>CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
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: 150–5.3.0.CO;2-X>CrossRefGoogle ScholarPubMed
Felix, C. A., Hosler, M. R., Winick, N. N., et al.ALL-1 gene rearrangements in DNA topoisomerase II inhibitor-related leukemia in children. Blood, 1995; 85: 3250–6.Google ScholarPubMed
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.Google ScholarPubMed
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.Google Scholar
Nakamura, T., Largaespada, D. A., Lee, M. M., 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.CrossRefGoogle Scholar
Borrow, J., Shearman, A. M., Stanton, V. P. Jr., et al.The t(7;11)(p15;p15) translocation in acute myeloid leukemia fuses the genes for nucleoporin NUP98 to class I homeoprotein HOXA9. Nat Genet, 1996; 12: 159–67.CrossRefGoogle Scholar
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.Google Scholar
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.Google Scholar
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.Google Scholar
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.CrossRefGoogle Scholar
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.CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Domer, P. H., Fakharzadeh, S. S., Chen, C.-S., et al.Acute mixed-lineage leukemia t(4;11)(q21;q23) generates an MLL-AF4 fusion product. Proc Natl Acad Sci U S A, 1993; 90: 7884–8.CrossRefGoogle Scholar
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.Google ScholarPubMed
Yu, B. D., Hanson, R. D., Hess, J. J., 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: 10632–6.CrossRefGoogle ScholarPubMed
Mahmoudi, T. & Verrijzer, C. P.Chromatin silencing and activation by Polycomb and trithorax group proteins. Oncogene, 2001; 20: 3055–66.CrossRefGoogle ScholarPubMed
Hanson, R. D., Hess, J. L., Yu, B. B., et al.Mammalian Trithorax and Polycomb-group homologues are antagonistic regulators of homeotic development. Proc Natl Acad Sci U S A, 1999; 96: 14372–7.CrossRefGoogle ScholarPubMed
Yu, B. D., Hess, J. L., Horning, S. S., Brown, G. G. J., & Korsmeyer, S. J.Altered Hox expression and segmental identity in Mll-mutant mice. Nature, 1995; 378: 505–8.CrossRefGoogle ScholarPubMed
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.Google ScholarPubMed
Caslini, C., Alarcon, A. S., Hess, J. J., 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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Milne, T. A., Briggs, S. D., Brock, H. H., et al.MLL targets SET domain methyltransferase activity to Hox gene promoters. Mol Cell, 2002; 10: 1107–17.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Yokoyama, A., Kitabayashi, I., Ayton, P. M., Cleary, M. M., & Ohki, M.Leukemia proto-oncoprotein MLL is proteolytically processed into 2 fragments with opposite transcriptional properties. Blood, 2002; 100: 3710–8.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Gurney, J. G., Ross, J. A., Wall, D. D., et al.Infant cancer in the U.S.: histology-specific incidence and trends, 1973–1992. J Pediatr Hematol/Oncol, 1997; 19: 428–32.CrossRefGoogle Scholar
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.Google Scholar
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.CrossRefGoogle Scholar
Raffini, L. J., Slater, D. J., Rappaport, E. E., 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.CrossRefGoogle ScholarPubMed
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).Google Scholar
Rowley, J. D.The critical role of chromosome translocations in human leukemias. Annu Rev Genet, 1998; 32: 495–519.CrossRefGoogle ScholarPubMed
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.Google ScholarPubMed
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.Google Scholar
Taki, T., Hayashi, Y., Taniwaki, M., et al.Fusion of the MLL gene 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.Google ScholarPubMed
Taki, T., Kano, H., Taniwaki, M., et al.AF5q31, a newly identified AF4-related gene, is fused to MLL in infant acute lymphoblastic leukemia with ins(5;11)(q31;q13q23). Proc Natl Acad Sci U S A, 1999; 96: 14535–40.CrossRefGoogle Scholar
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.Google Scholar
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.Google Scholar
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.CrossRefGoogle ScholarPubMed
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 Sci U S A, 1994; 91: 8107–11.CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
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.CrossRefGoogle Scholar
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.Google Scholar
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: 12110–4.CrossRefGoogle Scholar
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.Google Scholar
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.Google Scholar
Lorsbach, R. B., Moore, J., Mathew, S., et al.TET1, a member of a novel protein family, is fused to MLL in acute myeloid leukemia containing the t(10;11)(q22;q23). Leukemia, 2003; 17: 637–41.CrossRefGoogle Scholar
Hayette, S., Tigaud, I., Vanier, A., et al.AF15q14, a novel partner gene fused to the MLL gene in an acute myeloid leukaemia with a t(11;15)(q23;q14). Oncogene, 2000; 19: 4446–50.CrossRefGoogle Scholar
Bernard, O., Mauchauffe, M., Mecucci, C., Berghe, H., & 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.Google Scholar
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.Google Scholar
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.CrossRefGoogle Scholar
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.CrossRefGoogle Scholar
Fuchs, U., Rehkamp, G., Haas, O. A., et al.The human formin-binding 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.CrossRefGoogle ScholarPubMed
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.Google Scholar
Fu, J., Hsu, J., Tang, T., & Shih, L.Identification of CBL, a proto-oncogene at 11q23.3, as a novel MLL fusion partner in a patient with de novo acute myeloid leukemia. Genes Chromosomes Cancer, 2003; 37: 214–19.CrossRefGoogle Scholar
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.CrossRefGoogle Scholar
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.CrossRefGoogle Scholar
So, C., Caldas, C., Liu, M.-M., et al.EEN encodes for a member of a new family of proteins containing a Src homology 3 domain and is the third gene located on chromosome 19p13 that fuses to MLL in human leukemia. Proc Natl Acad Sci U S A, 1997; 99: 2563–8.CrossRefGoogle Scholar
Megonigal, M. D., Rappaport, E. F., Jones, D. D., 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 DiGeorge and velocardiofacial syndromes. Proc Natl Acad Sci U S A, 1998; 95: 6413–18.CrossRefGoogle Scholar
Osaka, M., Rowley, J. D., & Zeleznik-Le, N. J.MSF (MLL septin-like fusion), a fusion partner gene of MLL, in a therapy-related acute myeloid leukemia with a t(11;17)(q23;q25). Proc Natl Acad Sci U S A, 1999; 96: 6428–33.CrossRefGoogle Scholar
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.Google Scholar
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.CrossRefGoogle ScholarPubMed
Ono, R., Taki, T., Taketani, T., et al.SEPTIN6, a human homologue to mouse Septin6, is fused to MLL in infant acute myeloid leukemia with complex chromosomal abnormalities involving 11q23 and Xq24. Cancer Res, 2002; 62: 333–7.Google ScholarPubMed
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.CrossRefGoogle Scholar
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.CrossRefGoogle Scholar
Wechsler, D. S., Engstrom, L. D., Alexander, B. B., Motto, D. G., & Roulston, D.A novel chromosomal inversion at 11q23 in infant acute myeloid leukemia fuses MLL to CALM, a gene that encodes a clathrin assembly protein. Genes, Chromosomes Cancer, 2003; 36: 26–36.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.Google Scholar
LoNigro, L., Slater, D. J., Rappaport, E. E., 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.Google Scholar
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.CrossRefGoogle Scholar
LoNigro, 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.Google Scholar
Megonigal, M. D., Rappaport, E. F., Wilson, R. R., 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.CrossRefGoogle ScholarPubMed
Rowley, J. D., Reshmi, S., Sobulo, O., et al.All patients with t(11;16)(q23;p13.3) that involve MLL and CBP have treatment-related hematologic disorders. Blood, 1997; 90: 535–41.Google Scholar
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].Google Scholar
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
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.
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: 230–5.3.0.CO;2-J>CrossRefGoogle Scholar
So, C. W. & Cleary, M. L.MLL-AFX requires the transcriptional effector domains of AFX to transform myeloid progenitors and transdominantly interfere with forkhead protein function. Mol Cell Biol, 2002; 22: 6542–52.CrossRefGoogle ScholarPubMed
So, C. W. & Cleary, M. L.Common mechanism for oncogenic activation of MLL by forkhead family proteins. Blood, 2003; 101: 633–9.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Lavau, C., Luo, R. T., Du, C., & Thirman, M. J.Retrovirus-mediated 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: 10984–9.CrossRefGoogle ScholarPubMed
Lavau, C., Du, C., Thirman, M., & Zeleznik-Le, N.Chromatin-related properties of CBP fused to MLL generate a myelodysplastic-like syndrome that evolves into myeloid leukemia. EMBO J, 2000; 19: 4655–64.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Liedman, D.& Zeleznik-Le, N. Retroviral transduction model of mixed lineage leukemia fused to CREB binding protein. Curr Opin Hematol, 2001; 8: 218–23.CrossRefGoogle ScholarPubMed
Ayton, P. M. & Cleary, M. L.Molecular mechanisms of leukemogenesis mediated by MLL fusion proteins. Oncogene, 2001; 20: 5695–707.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.Google Scholar
DiMartino, J. F., Miller, T., Ayton, P. M., et al.A carboxy-terminal domain of ELL is required and sufficient for immortalization of myeloid progenitors by MLL-ELL. Blood, 2000; 96: 3887–93.Google ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Armstrong, S. A., Staunton, J. E., Silverman, L. L., et al.MLL translocations specify a distinct gene expression profile that distinguishes a unique leukemia. Nat Genet, 2002; 30: 41–7.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Ayton, P. M. & Cleary, M. L.Transformation of myeloid progenitors by MLL oncoproteins is dependent on Hoxa7 and Hoxa9. Genes Dev, 2003; 17: 2298–307.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
So, C. W., Lin, M., Ayton, P. M., Chen, E. E., & Cleary, M. L.Dimerization contributes to oncogenic activation of MLL chimeras in acute leukemias. Cancer Cell, 2003; 4: 99–110.CrossRefGoogle ScholarPubMed
Megonigal, M. D., Rappaport, E. F., Nowell, P. P., Lange, B. J., & Felix, C. A.Potential role for wild-type p53 in leukemias with MLL gene translocations. Oncogene, 1998; 16: 1351–6.CrossRefGoogle ScholarPubMed
Armstrong, S. A., Kung, A. L., Mabon, M. M., et al.Inhibition of FLT3 in MLL. Validation of a therapeutic target identified by gene expression based classification. Cancer Cell, 2003; 3: 173–83.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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: 10338–43.CrossRefGoogle ScholarPubMed
Ford, A. M., Ridge, S. A., Cabrera, M. M., et al.In utero rearrangements in the trithorax-related oncogene in infant leukaemias. Nature, 1993; 363: 358–60.CrossRefGoogle ScholarPubMed
Gale, K., Ford, A., Repp, R., et al.Backtracking leukemia to birth: Identification of clonotypic gene fusion sequences in neonatal bloodspots. Proc Natl Acad Sci U S A, 1997; 94: 13950–4.CrossRefGoogle Scholar
Maia, A. T., Koechling, J., Corbett, R., et al.Protracted postnatal natural histories in childhood leukemia. Genes Chromosomes Cancer, 2004; 39: 335–40.CrossRefGoogle ScholarPubMed
Felix, C. A. & Megonigal, M. D. Molecular biology of chemotherapy-related leukemias. In American Society of Clinical Oncology Educational Book 2001 (Alexandria, VA: ASCO), pp. 578–90.
Felix, C. A.Leukemias related to treatment with DNA topoisomerase II inhibitors. Med Pediatr Oncol, 2001; 36: 525–35.CrossRefGoogle ScholarPubMed
Rowley, J. D.The role of chromosome translocations in leukemogenesis. Semin Hematol, 1999; 36: 59–72.Google ScholarPubMed
Broeker, P. L., Super, H. G., Thirman, M. M., 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.Google ScholarPubMed
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 therapy-related AML after treatment without etoposides. Genes Chromosomes Cancer, 2003; 36: 393–401.CrossRefGoogle Scholar
Whitmarsh, R., Saginario, C., Zhuo, Y., et al.Reciprocal DNA topoisomerase II cleavage events at 5′-TATTA-3′ 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.CrossRefGoogle ScholarPubMed
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.Google ScholarPubMed
Maanen, J. M., Lafleur, M. V., Mans, D. D., et al.Effects of the ortho-quinone and catechol of the antitumor drug VP-16–213 on the biological activity of single-stranded and double-stranded fX174 DNA. Biochem Pharmacol, 1988; 37: 3579–89.CrossRefGoogle ScholarPubMed
Bolton, J. L., Trush, M. A., Penning, T. T., Dryhurst, G., & Monks, T. J.Role of quinones in toxicology. Chem Res Toxicol, 2000; 13: 135–60.CrossRefGoogle Scholar
Haim, N., Nemec, J., Roman, J., & Sinha, B. K.In vitro metabolism of etoposide (VP-16–213) by liver microsomes and irreversible binding of reactive intermediates to microsomal proteins. Biochem Pharmacol, 1987; 36: 527–36.CrossRefGoogle ScholarPubMed
Maanen, J. M., 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.CrossRefGoogle ScholarPubMed
Maanen, J. M., 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.Google Scholar
Kingma, P. S., Corbett, A. H., Burcham, P. P., Marnett, L. J., & Osheroff, N.Abasic sites stimulate double-stranded DNA cleavage mediated by topoisomerase II. J Biol Chem, 1995; 270: 21441–4.CrossRefGoogle ScholarPubMed
Kingma, P. S. & Osheroff, N.Apurinic sites are position-specific topoisomerase II poisons. J Biol Chem, 1997; 272: 1148–55.CrossRefGoogle ScholarPubMed
Betti, C. J., Villalobos, M. J., Diaz, M. M., & Vaughan, A. A. M.Apoptotic triggers initiate translocations within the MLL gene involving the nonhomologous end joining repair system. Cancer Res, 2001; 61: 4550–5.Google ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Betti, C. J., Villalobos, M. J., Diaz, M. M., & Vaughan, A. T.Apoptotic stimuli initiate MLL-AF9 translocations that are transcribed in cells capable of division. Cancer Res, 2003; 63: 1377–81.Google ScholarPubMed
Super, H. G., Strissel, P. L., Sobulo, O. O., 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: 185–95.3.0.CO;2-#>CrossRefGoogle Scholar
Felix, C. A., Kim, C. S., Megonigal, M. M., et al.Panhandle PCR amplifies genomic translocation breakpoint involving unknown partner gene. Blood, 1997; 90: 4679–86.Google ScholarPubMed
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.CrossRefGoogle Scholar
Felix, C. A., Hosler, M. R., Slater, D. D., et al.Duplicated regions of AF-4 intron 4 at t(4;11) translocation breakpoints. Molecular Diagnosis, 1999; 4: 269–83.CrossRefGoogle Scholar
Whitmarsh, R., Saginario, C., Zhuo, Y., et al.Reciprocal DNA topoisomerase II cleavage events at 5′;-TATTA-3′ 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.Google Scholar
Jackson, S. P.Sensing and repairing DNA double-strand breaks. Carcinogenesis, 2002; 23: 687–96.CrossRefGoogle ScholarPubMed
Wiedemann, L. M., MacGregor, A., & Caldas, C.Analysis of the region of the 5′ end of the MLL gene involved in genomic duplication events. Br J Haematol, 1999; 105: 256–64.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Smith, M. A., Rubenstein, L., & Ungerleider, R. S.Therapy-related acute myeloid leukemia following treatment with epipodophyllotoxins: estimating the risks. Med Pediatr Oncol, 1994; 23: 86–98.CrossRefGoogle ScholarPubMed
Satake, N., Ishida, Y., Otoh, Y., et al.Novel MLL-CBP fusion transcript in therapy-related chronic myelomonocytic leukemia with a t(11;16)(q23;p13) chromosome translocation. Genes Chromosomes Cancer, 1997; 20: 60–3.3.0.CO;2-7>CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
Pedersen-Bjergaard, J.Acute promyelocytic leukemia with t(15;17) following inhibition of DNA topoisomerase II. Ann Oncol, 1995; 6: 751–3.CrossRefGoogle Scholar
Preisler, H. D., Early, A. P., Raza, A., et al.Therapy of secondary acute nonlymphocytic leukemia with cytarabine. N Engl J Med, 1983; 308: 21–3.CrossRefGoogle ScholarPubMed
Longmore, G., Guinan, E. C., Weinstein, H. H., et al.Bone marrow transplantation for myelodysplasia and secondary acute nonlymphoblastic leukemia. J Clin Oncol, 1990; 8: 1707–14.CrossRefGoogle ScholarPubMed
Cortes, J., O'Brien, S., Kantarjian, H., et al.Abnormalities in the long arm of chromosome 11 (11q) in patients with de novo and secondary acute myelogenous leukemias and myelodysplastic syndromes. Leukemia, 1994; 8: 2174–8.Google Scholar
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.Google Scholar
O'Donnell, M. R., Long, G. D., Parker, P. P., et al.Busulfan/cyclophosphamide as conditioning regimen for allogeneic bone marrow transplantation for myelodysplasia. J Clin Oncol, 1995; 13: 2973–9.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.Google ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.Google Scholar
Tohyama, K., Tsutani, H., Wano, Y., et al.Anti-leukemia chemotherapy of high-risk myelodysplastic syndromes. Oncologist, 1997; 2: 160–3.Google ScholarPubMed
List, A., Beran, M., DiPersio, J., et al.Opportunities for Trisenox (arsenic trioxide) in the treatment of myelodysplastic syndromes. Leukemia, 2003; 17: 1499–507.CrossRefGoogle ScholarPubMed
Stasi, R., Brunetti, M., Terzoli, E., & Amadori, S.Sustained response to recombinant human erythropoietin and intermittent all-trans retinoic acid in patients with myelodysplastic syndromes. Blood, 2002; 99: 1578–84.CrossRefGoogle ScholarPubMed
Negrin, R. S., Stein, R., Doherty, K., et al.Maintenance treatment of the anemia of myelodysplastic syndromes with recombinant human granulocyte colony-stimulating factor and erythropoietIn evidence for in vivo synergy. Blood, 1996; 87: 4076–81.Google ScholarPubMed
Rowe, J. M.Therapy of secondary leukemia. Leukemia, 2002; 16: 748–50.CrossRefGoogle ScholarPubMed
Geller, R. B., Vogelsang, G. B., Wingard, J. J., et al.Successful marrow transplantation for acute myelocytic leukemia following therapy for Hodgkin's disease. J Clin Oncol, 1988; 6: 1558–61.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Witherspoon, R. P. & Deeg, H. J.Allogeneic bone marrow transplantation for secondary leukemia or myelodysplasia. Haematologica, 1999; 84: 1085–7.Google ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Arnold, R., de Witte, T., Biezen, A., et al.Unrelated bone marrow transplantation in patients with myelodysplastic syndromes and secondary acute myeloid leukemia: an EBMT survey. European Blood and Marrow Transplantation Group. Bone Marrow Transplant, 1998; 21: 1213–16.CrossRefGoogle ScholarPubMed
Mantadakis, E., Shannon, K. M., Singer, D. D., et al.Transient monosomy 7: a case series in children and review of the literature. Cancer, 1999; 85: 2655–61.3.0.CO;2-W>CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Bullinger, L., Dohner, K., Bair, E., et al.Use of gene-expression profiling to identify prognostic subclasses in adult acute myeloid leukemia. N Engl J Med, 2004; 350: 1605–16.CrossRefGoogle ScholarPubMed
Valk, P. J., Verhaak, R. G., Beijen, M. M., et al.Prognostically useful gene-expression profiles in acute myeloid leukemia. N Engl J Med, 2004; 350: 1617–28.CrossRefGoogle ScholarPubMed
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.Google ScholarPubMed
Hale, G. A., Heslop, H. E., Bowman, L. L., et al.Bone marrow transplantation for therapy-induced acute myeloid leukemia in children with previous lymphoid malignancies. Bone Marrow Transplant, 1999; 24: 735–9.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle ScholarPubMed
Fung, H. C., Cohen, S., Rodriguez, R., et al.Reduced-intensity allogeneic stem cell transplantation for patients whose prior autologous stem cell transplantation for hematologic malignancy failed. Biol Blood Marrow Transplant, 2003; 9: 649–56.CrossRefGoogle ScholarPubMed
Taussig, D. C., Davies, A. J., Cavenagh, J. J., et al.Durable remissions of myelodysplastic syndrome and acute myeloid leukemia after reduced-intensity allografting. J Clin Oncol, 2003; 21: 3060–5.CrossRefGoogle ScholarPubMed
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.Google ScholarPubMed
Goldman, J. M. & Melo, J. V.Chronic myeloid leukemia – advances in biology and new approaches to treatment. N Eng J Med, 2003; 349: 1451–64.CrossRefGoogle Scholar
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.CrossRefGoogle Scholar
Ottmann, O. G., Druker, B. J., Sawyers, C. C., 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.CrossRefGoogle ScholarPubMed
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.CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
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.Google ScholarPubMed
Rabbitts, T. H. & Stocks, M. R.Chromosomal translocation products engender new intracellular therapeutic technologies. Nat Med, 2003; 9: 383–6.CrossRefGoogle ScholarPubMed
Kawagoe, H., Kawagoe, R., & Sano, K.Targeted down-regulation 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.CrossRefGoogle Scholar
Niitsu, N., Hayashi, Y., & Honma, Y.Downregulation of MLL-CBP fusion gene expression is associated with differentiation of SN-1 cells with t(11;16)(q23;p13). Oncogene, 2001; 20: 375–84.CrossRefGoogle Scholar
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.CrossRefGoogle ScholarPubMed
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.Google Scholar
Daskalakis, M., Nguyen, T. T., Nguyen, C., et al.Demethy lation of a hypermethylated P15/INK4B gene in patients with myelodysplastic syndrome by 5-Aza-2′-deoxycytidine (decitabine) treatment. Blood, 2002; 100: 2957–64.CrossRefGoogle Scholar

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  • Therapy-related leukemias
    • By Carolyn A. Felix, Associate Professor of Pediatrics University of Pennsylvania School of Medicine, Attending Physician The Children's Hospital of Philadelphia, Abramson Research Center, Philadelphia, PA, USA
  • Edited by Ching-Hon Pui
  • Book: Childhood Leukemias
  • Online publication: 01 July 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511471001.032
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  • Therapy-related leukemias
    • By Carolyn A. Felix, Associate Professor of Pediatrics University of Pennsylvania School of Medicine, Attending Physician The Children's Hospital of Philadelphia, Abramson Research Center, Philadelphia, PA, USA
  • Edited by Ching-Hon Pui
  • Book: Childhood Leukemias
  • Online publication: 01 July 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511471001.032
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  • Therapy-related leukemias
    • By Carolyn A. Felix, Associate Professor of Pediatrics University of Pennsylvania School of Medicine, Attending Physician The Children's Hospital of Philadelphia, Abramson Research Center, Philadelphia, PA, USA
  • Edited by Ching-Hon Pui
  • Book: Childhood Leukemias
  • Online publication: 01 July 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511471001.032
Available formats
×