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Minimal Residual Disease in Acute Myeloid Leukemia

RT-PCR—Based Studies of Fusion Transcripts

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Leukemia and Lymphoma

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Abstract

Acute myeloid leukemia (AML) is a biologically heterogeneous disease of the hematopoietic system characterized by a clonal accumulation of immature myeloid cells in the bone marrow. The management of this disease is clinically complex, with only approx 40% of the patients treated with conventional or highdose chemotherapy reaching a long-term complete remission (CR). Nonrandom chromosomal abnormalities are identified at the cytogenetic level in approx 55% of all adult primary or de novo AML patients and have long been recognized as important independent prognostic indicators for the achievement of CR, duration of first CR, and survival following intensive chemotherapy treatment (1,2). Among these recurrent aberrations, chromosome translocations and inversions often result in genomic structural rearrangements leading to the creation of chimeric fusion genes that, in turn, encode fusion transcripts readily detected in bone marrow (BM) and blood by highly sensitive molecular techniques such as the reverse transcription—polymerase chain reaction (RT-PCR). Because the fusion transcripts are thought to be specific to the leukemic cells, their detection in BM or blood from AML patients who achieve CR following intensive treatment has been used as a surrogate marker for minimal residual disease (MRD) (3–5). It was anticipated that those patients with a positive assay would inevitably relapse as a consequence of the treatment failure to completely eradicate the leukemogenic clone, whereas those patients with a negative RT-PCR status would remain in continuous CR (CCR).

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References

  1. Mrózek K and Bloomfield C. Chromosome aberrations in de novo acute myeloid leukemia in adults: clinical implications, Rev. Clin. Exp. Hematol., 5 (1998) 44.

    Google Scholar 

  2. Caligiuri M and Bloomfield C. The molecular biology of leukemia, in Principles and Practice of Oncology Cancer. DeVita VJ, Hellman S, and Rosenberg S. (eds). Philadelphia: JB Lippincott, 2000, p. 2389.

    Google Scholar 

  3. Yin JA and Tobal K. Detection of minimal residual disease in acute myeloid leukaemia: methodologies, clinical and biological significance, Br. J. Haematol., 106 (1999) 578.

    Article  PubMed  CAS  Google Scholar 

  4. Willman CL. Molecular evaluation of acute myeloid leukemias, Semin. Hematol., 36 (1999) 390.

    PubMed  CAS  Google Scholar 

  5. Radich JP. Clinical applicability of the evaluation of minimal residual disease in acute leukemia, Curr. Opin. Oncol., 12 (2000) 36.

    Article  PubMed  CAS  Google Scholar 

  6. Lion T. Monitoring of residual disease in chronic myelogenous leukemia by quantitative polymerase chain reaction and clinical decision making, [letter; comment], Blood, 94 (1999) 1486.

    Google Scholar 

  7. Diverio D, Rossi V, Avvisati G, De Santis S, Pistilli A, Pane F, et al. Early detection of relapse by prospective reverse transcriptase-polymerase chain reaction analysis of the PML/ RARalpha fusion gene in patients with acute promyelocytic leukemia enrolled in the GIMEMA-AIEOP multicenter “AIDA” trial. GIMEMA-AIEOP Multicenter “AIDA” Trial, Blood, 92 (1998) 784.

    PubMed  CAS  Google Scholar 

  8. Jurlander J, Caligiuri MA, Ruutu T, Baer MR, Strout MP, Oberkircher AR, et al. Persistence of the AML 1/ETO fusion transcript in patients treated with allogeneic bone marrow transplantation for t(8;21) leukemia, Blood, 88 (1996) 2183.

    Google Scholar 

  9. Marcucci G, Strout MP, Bloomfield CD, and Caligiuri MA. Detection of unique ALL1 (MLL) fusion transcripts in normal human bone marrow and blood: distinct origin of normal versus leukemic ALL1 fusion transcripts, Cancer Res., 58 (1998) 790.

    PubMed  CAS  Google Scholar 

  10. Marcucci G, Caligiuri MA, and Bloomfield CD. Molecular and clinical advances in core binding factor primary acute myeloid leukemia: a paradigm for translational research in malignant hematology, Cancer Invest., 18 (2000) 768.

    Article  PubMed  CAS  Google Scholar 

  11. Bloomfield CD, Lawrence D, Byrd JC, Carroll A, Pettenati MJ, Tantravahi R, et al. Frequency of prolonged remission duration after high-dose cytarabine intensification in acute myeloid leukemia varies by cytogenetic subtype, Cancer Res., 58 (1998) 4173.

    PubMed  CAS  Google Scholar 

  12. Ferrant A, Labopin M, Frassoni F, et al. Karyotype in acute myeloblastic leukemia: prognostic significance for bone marrow transplantation in first remission: a European Group for Blood and Marrow Transplantation study. Acute Leukemia Working Party of the European Group for Blood and Marrow Transplantation (EBMT), Blood, 90 (8) (1997) 2931–2938.

    PubMed  CAS  Google Scholar 

  13. Downing JR. The AML1-ETO chimaeric transcription factor in acute myeloid leukaemia: biology and clinical significance, Br. J. Haematol., 106 (1999) 296.

    Article  PubMed  CAS  Google Scholar 

  14. Nucifora G, Birn DJ, Erickson P, Gao J, LeBeau MM, Drabkin HA, et al. Detection of DNA rearrangements in the AML1 and ETO loci and of an AML1/ETO fusion mRNA in patients with t(8;21) acute myeloid leukemia, Blood, 81 (1993) 883.

    PubMed  CAS  Google Scholar 

  15. Nucifora G, Larson RA, and Rowley JD. Persistence of the 8;21 translocation in patients with acute myeloid leukemia type M2 in long-term remission, Blood, 82 (1993) 712.

    PubMed  CAS  Google Scholar 

  16. Chang KS, Fan YH, Stass SA, Estey EH, Wang G, Trujillo JM, et al. Expression of AML1ETO fusion transcripts and detection of minimal residual disease in t(8;21)-positive acute myeloid leukemia, Oncogene, 8 (1993) 983.

    PubMed  CAS  Google Scholar 

  17. Kusec R, Laczika K, Knobl P, Friedl J, Greinix H, Kahls P, et al. AML1/ETO fusion mRNA can be detected in remission blood samples of all patients with t(8;21) acute myeloid leukemia after chemotherapy or autologous bone marrow transplantation, Leukemia, 8 (1994) 735.

    PubMed  CAS  Google Scholar 

  18. Saunders MJ, Tobal K, and Yin JA. Detection of t(8;21) by reverse transcriptase polymerase chain reaction in patients in remission of acute myeloid leukaemia type M2 after chemotherapy or bone marrow transplantation, Leukemia Res., 18 (1994) 891.

    Article  CAS  Google Scholar 

  19. Sakata N, Okamura T, Inoue M, Yumura-Yagi K, Hara J, Tawa A, et al. Rapid disappearance of AML1/ETO fusion transcripts in patients with t(8;21) acute myeloid leukemia following bone marrow transplantation and chemotherapy, Leuk. Lymphoma, 26 (1997) 141.

    PubMed  CAS  Google Scholar 

  20. Miyamoto T, Nagafuji K, Akashi K, Harada M, Kyo T, Akashi T, et al. Persistence of multipotent progenitors expressing AML1/ETO transcripts in long-term remission patients with t(8;21) acute myelogenous leukemia, Blood, 87 (1996) 4789.

    PubMed  CAS  Google Scholar 

  21. Elmaagacli AH, Beelen DW, Stockova J, Trzensky S, Kroll M, Schaefer UW, et al. Detection of AML1/ETO fusion transcripts in patients with t(8;21) acute myeloid leukemia after allogeneic bone marrow transplantation or peripheral blood progenitor cell transplantation, [letter]; comment, Blood, 90 (1997) 3230.

    PubMed  CAS  Google Scholar 

  22. Morschhauser F, Cayuela JM, Martini S, Baruchel A, Rousselot P, Socie G, et al. Evaluation of minimal residual disease using reverse-transcription polymerase chain reaction in t(8;21) acute myeloid leukemia: a multicenter study of 51 patients, J. Clin. Oncol., 18 (2000) 788.

    PubMed  CAS  Google Scholar 

  23. Lo Coco F, Diverio D, Falini B, Biondi A, Nervi C, and Pelicci PG. Genetic diagnosis and molecular monitoring in the management of acute promyelocytic leukemia, Blood, 94 (1999) 12.

    PubMed  Google Scholar 

  24. Tobal K, Saunders MJ, Grey MR, and Yin JA. Persistence of RAR alpha-PML fusion mRNA detected by reverse transcriptase polymerase chain reaction in patients in long-term remission of acute promyelocytic leukaemia, Br. J. Haematol., 90 (1995) 615.

    Article  PubMed  CAS  Google Scholar 

  25. Saunders MJ, Tobal K, Keeney S, and Liu Yin JA. Expression of diverse AML1/MTG8 transcripts is a consistent feature in acute myeloid leukemia with t(8;21) irrespective of disease phase, Leukemia, 10 (1996) 1139.

    Google Scholar 

  26. Miyamoto T, Weissman IL, and Akashi K. AML1/ETO-expressing nonleukemic stem cells in acute myelogenous leukemia with 8;21 chromosomal translocation, Proc. Natl. Acad. Sci. USA, 97 (2000) 7521.

    Article  PubMed  CAS  Google Scholar 

  27. Higuchi M, O’Brien D, Lenny N, Yang S, Cai Z, and Downing J. Expression of AML1-ETO immortalizes myeloid progenitors and cooperates with secondary mutations to induce granulocytic sarcoma/acute myeloid leukemia, Blood, 96 (2000) 222a.

    Google Scholar 

  28. Marcucci G, Livak KJ, Bi WL, Strout MP, Bloomfield CD, and Caligiuri MA. Detection of the AMLI/ETO fusion transcript in patients with t(8;21)-associated AML using a novel “real time” quantitative RT-PCR assay, Leukemia, 12 (1998) 1482.

    Google Scholar 

  29. Muto A, Mori S, Matsushita H, Awaya N, Ueno H, Takayama N, et al. Serial quantification of minimal residual disease of t(8;21) acute myelogenous leukaemia with RT-competitive PCR assay, Br. J. Haematol., 95 (1996) 85.

    Article  PubMed  CAS  Google Scholar 

  30. Tobal K and Yin JA. Monitoring of minimal residual disease by quantitative reverse transcriptase-polymerase chain reaction for AML1–MTG8 transcripts in AML-M2 with t(8; 21), Blood, 88 (1996) 3704.

    PubMed  CAS  Google Scholar 

  31. Tobal K, Newton J, Macheta M, Chang J, Morgenstern G, Evans PA, et al. Molecular quantitation of minimal residual disease in acute myeloid leukemia with t(8;21) can identify patients in durable remission and predict clinical relapse, Blood, 95 (2000) 815.

    PubMed  CAS  Google Scholar 

  32. Heid CA, Stevens J, Livak KJ, and Williams PM. Real time quantitative PCR, Genome Res., 6 (1996) 986.

    Article  PubMed  CAS  Google Scholar 

  33. Gibson UE, Heid CA, and Williams PM. A novel method for real time quantitative RT-PCR, Genome Res., 6 (1996) 995.

    Article  PubMed  CAS  Google Scholar 

  34. Marcucci G, Livak KJ, Bi W, Strout MP, Bloomfield CD, and Caligiuri MA. Detection of minimal residual disease in patients with AML1/ETO-associated acute myeloid leukemia using a novel quantitative reverse transcription polymerase chain reaction assay, Leukemia, 12 (1998) 1482.

    Google Scholar 

  35. Krauter J, Wattjes MP, Nagel S, Heidenreich O, Krug U, Kafert S, et al. Real-time RT-PCR for the detection and quantification of AML1/MTG8 fusion transcripts in t(8;21)-positive AML patients, Br. J. Haematol., 107 (1999) 80.

    Article  PubMed  CAS  Google Scholar 

  36. Sugimoto T, Das H, Imoto S, Murayama T, Gomyo H, Chakraborty S, et al. Quantitation of minimal residual disease in t(8;21)-positive acute myelogenous leukemia patients using real-time quantitative RT-PCR, Am. J. Hematol., 64 (2000) 101.

    Article  PubMed  CAS  Google Scholar 

  37. Wattjes MP, Krauter J, Nagel S, Heidenreich O, Ganser A, and Heil G. Comparison of nested competitive RT-PCR and real-time RT-PCR for the detection and quantification of AML1/MTG8 fusion transcripts in t(8;21) positive acute myelogenous leukemia, Leukemia, 14 (2000) 329.

    Article  PubMed  CAS  Google Scholar 

  38. Liu P, Tarle SA, Hajra A, Claxton DF, Marlton P, Freedman M, et al. Fusion between transcription factor CBFb/PEBP2b and a myosin heavy chain in acute myeloid leukemia, Science, 261 (1993) 1041.

    Article  PubMed  CAS  Google Scholar 

  39. Liu PP, Hajra A, Wijmenga C, and Collins FS. Molecular pathogenesis of the chromosome 16 inversion in the M4Eo subtype of acute myeloid leukemia, Blood, 85 (1995) 2289.

    PubMed  CAS  Google Scholar 

  40. Dissing M, Le Beau MM, and Pedersen-Bjergaard J. Inversion of chromosome 16 and uncommon rearrangements of the CBFB and MYH l 1 genes in therapy-related acute myeloid leukemia: rare events related to DNA-topoisomerase II inhibitors?, J. Clin. Oncol., 16 (1998) 1890.

    PubMed  CAS  Google Scholar 

  41. Marcucci G, Caligiuri M, and Bloomfield C. Defining the “absence” of the CBFb/MYH11 fusion transcript in patients with acute myeloid leukemia and inversion of chromosome 16 to predict long-term complete remission: a call for definitions, Blood, 90 (1997) 5022.

    PubMed  CAS  Google Scholar 

  42. Claxton DF, Liu P, Hsu HB, Marlton P, Hester J, Collins F, et al. Detection of fusion transcripts generated by the inversion 16 chromosome in acute myelogenous leukemia, Blood, 83 (1994) 1750.

    PubMed  CAS  Google Scholar 

  43. Martinelli G, Ottaviani E, Testoni N, Visani G, Terragna C, Amabile M, et al. Molecular remission in PCR-positive acute myeloid leukemia patients with inv(16): role of bone marrow transplantation procedures, Bone Marrow Transplant., 24 (1999) 694.

    Article  PubMed  CAS  Google Scholar 

  44. Poirel H, Radford-Weiss I, Rack K, Troussard X, Veil A, Valensi F, et al. Detection of the chromosome 16 CBF beta-MYH 11 fusion transcript in myelomonocytic leukemias, Blood, 85 (1995) 1313.

    Google Scholar 

  45. Hebert J, Cayuela JM, Daniel MT, Berger R, and Sigaux F. Detection of minimal residual disease in acute myelomonocytic leukemia with abnormal marrow eosinophils by nested polymerase chain reaction with allele specific amplification, Blood, 84 (1994) 2291.

    PubMed  CAS  Google Scholar 

  46. Costello R, Sainty D, Blaise D, Gastaut JA, Gabert J, Poirel H, et al. Prognosis value of residual disease monitoring by polymerase chain reaction in patients with CBF beta/MYH 11-positive acute myeloblastic leukemia, Blood, 89 (1997) 2222.

    PubMed  CAS  Google Scholar 

  47. Martin G, Barragan E, Bolufer P, Chillon C, Garcia-Sanz R, Gomez T, et al. Relevance of presenting white blood cell count and kinetics of molecular remission in the prognosis of acute myeloid leukemia with CBFbeta/MYH11 rearrangement, Haematologica, 85 (2000) 699.

    PubMed  CAS  Google Scholar 

  48. Tobal K, Johnson PR, Saunders MJ, Harrison CJ, and Liu Yin JA. Detection of CBFB/MYH 11 transcripts in patients with inversion and other abnormalities of chromosome 16 at presentation and remission, Br. J. Haematol., 91 (1995) 104.

    Article  PubMed  CAS  Google Scholar 

  49. Elmaagacli AH, Beelen DW, Kroll M, Trzensky S, Stein C, and Schaefer UW. Detection of CBFbeta/MYH11 fusion transcripts in patients with inv(16) acute myeloid leukemia after allogeneic bone marrow or peripheral blood progenitor cell transplantation, Bone Marrow Transplant., 21 (1998) 159.

    Article  PubMed  CAS  Google Scholar 

  50. Evans PA, Short MA, Jack AS, Norfolk DR, Child JA, Shiach CR, et al. Detection and quantitation of the CBFbeta/MYH11 transcripts associated with the inv(16) in presentation and follow-up samples from patients with AML, Leukemia, 11 (1997) 364.

    Article  PubMed  CAS  Google Scholar 

  51. Laczika K, Novak M, Hilgarth B, Mitterbauer M, Mitterbauer G, Scheidel-Petrovic A, et al. Competitive CBFbeta/MYH11 reverse-transcriptase polymerase chain reaction for quantitative assessment of minimal residual disease during postremission therapy in acute myeloid leukemia with inversion(16): a pilot study, J. Clin. Oncol., 16 (1998) 1519.

    Google Scholar 

  52. Marcucci G, Caligiuri M, Maghraby E, Archer K, Dohner K, Schlenk R, et al. Quantification of the CBFb/MYH11 fusion transcript in inv(16) acute myeloid leukemia by real time RT-PCR, Blood, 94 (1999) 625a.

    Google Scholar 

  53. Strout MP, Marcucci G, Caligiuri MA, and Bloomfield CD. Core-binding factor (CBF) and MLL-associated primary acute myeloid leukemia: biology and clinical implications, Ann. Hematol., 78 (1999) 251.

    Article  PubMed  CAS  Google Scholar 

  54. Caligiuri MA, Schichman SA, Strout MP, Mrozek K, Baer MR, Frankel SR, et al. Molecular rearrangement of the ALL-1 gene in acute myeloid leukemia without cytogenetic evidence of 11g23 chromosomal translocations, Cancer Res., 54 (1994) 370.

    PubMed  CAS  Google Scholar 

  55. Schichman SA, Canaani E, and Croce CM. Self-fusion of the ALLI gene. A new genetic mechanism for acute leukemia, [review], JAMA, 273 (1995) 571.

    Google Scholar 

  56. Mrozek K, Heinonen K, Lawrence D, Carroll AJ, Koduru PRK, Rao KW, et al. Adult patients with de novo acute myeloid leukemia and t(9;11)(p22;g23) have a superior outcome to patients with other translocations involving 11g23: a Cancer and Leukemia Group B study, Blood, 90 (1997) 4532.

    PubMed  CAS  Google Scholar 

  57. Mitterbauer G, Zimmer C, Pirc-Danoewinata H, Haas OA, Hojas S, Schwarzinger I, et al. Monitoring of minimal residual disease in patients with MLL-AF6-positive acute myeloid leukaemia by reverse transcriptase polymerase chain reaction, Br. J. Haematol., 109 (2000) 622.

    Article  PubMed  CAS  Google Scholar 

  58. Mitterbauer G, Zimmer C, Fonatsch C, Haas O, Thalhammer-Scherrer R, Schwarzinger I, et al. Monitoring of minimal residual leukemia in patients with MLL-AF9 positive acute myeloid leukemia by RT-PCR, Leukemia, 13 (1999) 1519.

    Google Scholar 

  59. Caligiuri MA, Strout MP, Schichman SA, Mrozek K, Arthur DC, Herzig GP, et al. Partial tandem duplication of ALL1 as a recurrent molecular defect in acute myeloid leukemia with trisomy 11, Cancer Res., 56 (1996) 1416.

    Google Scholar 

  60. Caligiuri MA, Strout MP, Lawrence D, Arthur DC, Baer MR, Yu F, et al. Rearrangement of ALL] in acute myeloid leukemia with normal cytogenetics, Cancer Res., 58 (1998) 55.

    PubMed  CAS  Google Scholar 

  61. Caldas C, So CW, MacGregor A, Ford A, McDonald B, and Wiedermann LM. Exon scrambling of MLL transcripts occur commonly and mimic partial genomic duplication of the gene, Gene, 208 (1998) 167.

    Article  PubMed  CAS  Google Scholar 

  62. Schnittger S, Wormann B, Hiddemann W, and Griesinger F. Partial tandem duplications of the MLL gene are detectable in peripheral blood and bone marrow of nearly all healthy donors, Blood, 92 (1998) 1728.

    Google Scholar 

  63. Inoue K, Sugiyama H, Ogawa H, Nakagawa M, Yamagami T, Miwa H, et al. WT1 as a new prognostic factor and a new marker for the detection of minimal residual disease in acute leukemia, Blood, 84 (1994) 3071.

    PubMed  CAS  Google Scholar 

  64. Sugiyama H. Wilms tumor gene (WT1) as a new marker for the detection of minimal residual disease in leukemia, Leuk. Lymphoma, 30 (1998) 55.

    Article  PubMed  CAS  Google Scholar 

  65. Inoue K, Ogawa H, Yamagami T, Soma T, Tani Y, Tatekawa T, et al. Long-term follow-up of minimal residual disease in leukemia patients by monitoring WT1 (Wilms tumor gene) expression levels, Blood, 88 (1996) 2267.

    Google Scholar 

  66. Gaiger A, Schmid D, Heinze G, Linnerth B, Greinix H, Kalhs P, et al. Detection of the WT1 transcript by RT-PCR in complete remission has no prognostic relevance in de novo acute myeloid leukemia, Leukemia, 12 (1998) 1886.

    Google Scholar 

  67. Elmaagacli AH, Beelen DW, Trenschel R, and Schaefer UW. The detection of wt-1 transcripts is not associated with an increased leukemic relapse rate in patients with acute leukemia after allogeneic bone marrow or peripheral blood stem cell transplantation, Bone Marrow Transplant, 25 (2000) 91–96.

    Article  PubMed  CAS  Google Scholar 

  68. Nakao M, Janssen JW, Erz D, Seriu T, and Bartram CR. Tandem duplication of the FLT3 gene in acute lymphoblastic leukemia: a marker for the monitoring of minimal residual disease, [letter], Leukemia, 14 (2000) 522.

    Article  PubMed  CAS  Google Scholar 

  69. Nakao M, Yokota S, Iwai T, Kaneko H, Horiike S, Kashima K, et al. Internal tandem duplication of the flt3 gene found in acute myeloid leukemia, Leukemia, 10 (1996) 1911.

    Google Scholar 

  70. Yokota S, Kiyoi H, Nakao M, Iwai T, Misawa S, Okuda T, et al. Internal tandem duplication of the FLT3 gene is preferentially seen in acute myeloid leukemia and myelodysplastic syndrome among various hematological malignancies. A study on a large series of patients and cell lines, Leukemia, 11 (1997) 1605.

    Google Scholar 

  71. Xu F, Taki T, Yang HW, Hanada R, Hongo T, Ohnishi H, et al. Tandem duplication of the FLT3 gene is found in acute lymphoblastic leukaemia as well as acute myeloid leukaemia but not in myelodysplastic syndrome or juvenile chronic myelogenous leukaemia in children, Br. J. Haematol., 105 (1999) 155.

    Article  PubMed  CAS  Google Scholar 

  72. Baylin SB, Herman JG, Graff JR, Vertino PM, and Issa JP. Alterations in DNA methylation: a fundamental aspect of neoplasia, Adv. Cancer Res., 72 (1998) 141.

    Article  PubMed  CAS  Google Scholar 

  73. Issa JP, Baylin SB, and Herman JG. DNA methylation changes in hematologic malignancies: biologic and clinical implications, Leukemia, 11 (1997) S7.

    PubMed  Google Scholar 

  74. Plass C, Yu F, Yu L, Strout MP, El-Rifai W, Elonen E, et al. Restriction landmark genome scanning for aberrant methylation in primary refractory and relapsed acute myeloid leukemia; involvement of the WIT-1 gene, Oncogene, 18 (1999) 3159.

    Article  PubMed  CAS  Google Scholar 

  75. Xiong Z and Laird PW. COBRA: a sensitive and quantitative DNA methylation assay, Nucleic Acids Res., 25 (1997) 2532.

    Google Scholar 

  76. Eads CA, Danenberg KD, Kawakami K, Saltz LB, Blake C, Shibata D, et al. MethyLight: a high-throughput assay to measure DNA methylation, Nucleic Acids Res., 28 (2000) E32.

    Article  PubMed  CAS  Google Scholar 

  77. Lo YM, Wong IH, Zhang J, Tein MS, Ng MH, and Hjelm NM. Quantitative analysis of aberrant p16 methylation using real-time quantitative methylation-specific polymerase chain reaction, Cancer Res., 59 (1999) 3899.

    PubMed  CAS  Google Scholar 

  78. Castilla LH, Garrett L, Adya N, Orlic D, Dutra A, Anderson S, et al. The fusion gene CbfbMYH11 blocks myeloid differentiation and predisposes mice to acute myelomonocytic leukaemia, [letter], Nat. Genet., 23 (1999) 144.

    Article  PubMed  CAS  Google Scholar 

  79. Golub TR, Slonim DK, Tamayo P, Huard C, Gaasenbeek M, Mesirov JP, et al. Molecular classification of cancer: class discovery and class prediction by gene expression monitoring, Science, 286 (1999) 531.

    Article  PubMed  CAS  Google Scholar 

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Authors
  1. Guido Marcucci
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  2. Michael A. Caligiuri
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Editors and Affiliations

  1. Houston, TX, USA

    Theodore F. Zipf PhD, MD

  2. Department of Biomathematics, MD Anderson Cancer Center, Houston, TX, USA

    Dennis A. Johnston PhD

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Marcucci, G., Caligiuri, M.A. (2003). Minimal Residual Disease in Acute Myeloid Leukemia. In: Zipf, T.F., Johnston, D.A. (eds) Leukemia and Lymphoma. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-318-7_9

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  • DOI: https://doi.org/10.1007/978-1-59259-318-7_9

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