Acute Leukemias - Republican Scientific Medical Library

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176 Chapter 13 · Treatment of Adult ALL According to Protocols of the German Multicenter Study Group for Adult ALL (GMALL) 9. Arnold R, Beelen D, Bunjes D, et al. (2003) Phenotype predicts outcome after allogeneic stem cell transplantation in adult high risk ALL patients. Blood 102:(abstr #1719) 10. Ottmann OG, Druker BJ, Sawyers CL, et al. (2002) A phase II study of imatinib mesylate (Glivec) in patients with relapsed or refractory Philadelphia chromosome-positive acute lymphoid leukemias. Blood 100:1965–1971 11. Wassmann B, Pfeifer H, Scheuring U, et al. (2002) Therapy with imatinib mesylate (Glivec) preceding allogeneic stem cell transplantation (SCT) in relapsed or refractory Philadelphia-positive acute lymphoblastic leukemia (Ph+ALL). Leukemia 16:2358–2365 12. Scheuring UJ, Pfeifer H, Wassmann B, et al. (2003) 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 101:85– 90 13. Wassmann B, Pfeifer H, Gökbuget N, et al. (2006) Alternating versus concurrent schedules of Imatinib and chemotherapy as frontline therapy for Philadelphia-positive acute lymphoblastic leukemia (Ph+ALL). Blood 108:1469–1477 14. Wassmann B, Pfeifer H, Stadler M, et al. (2005) Early molecular response to posttransplantation imatinib determines outcome in MRD+ Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL). Blood 106:458–463 15. Gökbuget N, de Wit M, Gerhardt A, et al. (2000) Results of a shortened, dose reduced treatment protocol in elderly patients with acute lymphoblastic leukemia (ALL). Blood 96:3104a(abstr) 16. Ottmann OG, Wassmann B, Pfeifer H, et al. (2007) Imatinib compared with chemotherapy as front-line treatment of elderly patients with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ALL). Cancer 109:2068–2076 17. Hofmann WK, de Vos S, Elashoff D, et al. (2002) Relation between resistance of Philadelphia-chromosome-positive acute lymphoblastic leukaemia to the tyrosine kinase inhibitor STI571 and gene-expression profiles: A gene-expression study. Lancet 359: 481–486 18. Pfeifer H, Wassmann B, Pavlova A, et al. (2007) Kinase domain mutations of BCR-ABL frequently precede imatinib-based therapy and give rise to relapse in patients with de novo Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL). Blood 110:727–734 19. Hoelzer D, Ludwig W-D, Thiel E, et al. (1996) Improved outcome in adult B-cell acute lymphoblastic leukemia. Blood 87:495–508 20. Hoelzer D, Arnold R, Diedrich H, et al. (2002) Successful treatment of Burkitt’s NHL and other high-grade NHL according to a protocol for mature B-ALL. Blood 100:159a(abstr 595) 21. Hoelzer D, Baur K-H, Giagounidis A, et al. (2003) Short intensive chemotherapy with rituximab seems successful in Burkitt NHL, mature B-ALL and other high-grade B-NHL. Blood 102:(abstr 236) 22. Hoffmann C, Wolf E, Wyen C, et al. (2006) AIDS-associated Burkitt or Burkitt-like lymphoma: Short intensive polychemotherapy is feasible and effective. Leuk Lymphoma 47:1872–1880 23. Thiel E, Hoelzer D, Dörken B, et al. (1987) Clinical relevance of blast cell phenotype as determined with monoclonal antibodies in acute lymphoblastic leukemia of adults. Haematol Blood Transf 30:95–103 24. Bene MC, Castoldi G, Knapp W, et al. (1995) Proposal for the immunological classification of acute leukemias. Leukemia 9:1783– 1786 25. Ludwig WD, Raghavachar A, Thiel E (1994) Immunophenotypic classification of acute lymphoblastic leukemia. Bailliere’s Clin Haematol 7(2):235 26. Thiel E, Kranz BR, Raghavachar A, et al. (1989) Prethymic phenotype and genotype of pre-T(CD+/ER–)-cell leukemia and its clinical significance within adult acute lymphoblastic leukemia. Blood 73:1247–1258 27. Hoelzer D, Arnold R, Freund M, et al. (1999) Characteristics, outcome and risk factors in adult T-lineage acute lymphoblastic leukemia (ALL). Blood 94:2926a 28. Ludwig WD (1996) Immunophenotypic features of childhood and adult acute lymphoblastic leukemia (ALL): experience of the German Multicentre Trials ALL-BFM and GMALL. Leuk Lymphoma 13:71 29. Gleissner B, Gökbuget N, Rieder H, et al. (2005) CD10-negative pre-B acute lymphoblastic leukemia (ALL): A distinct high-risk subgroup of adult ALL associated with a high frequency of MLL aberrations. Results of the German Multicenter Trials for Adult ALL (GMALL). Blood 106:4054–4056 30. Gleissner B, Gökbuget N, Bartram CR, et al. (2002) Leading prognostic relevance of the BCR-ABL translocation in adult acute Blineage lymphoblastic leukemia: A prospective study of the German Multicenter Trial Group and confirmed polymerase chain reaction analysis. Blood 99:1536–1543 31. Burmeister T, Gökbuget N, Reinhardt R, et al. (2006) NUP214-ABL1 in adult T-ALL: The GMALL study group experience. Blood 108:3556–3559 32. Burmeister T, Marschalek R, Schneider B, et al. (2006) Monitoring minimal residual disease by quantification of genomic chromosomal breakpoint sequences in acute leukemias with MLL aberrations. Leukemia 20:451–457 33. Baak U, Burmeister T, Gökbuget N, et al. (2004) Prognostic impact of the expression of the TLX1 (HOX11) and TLX3 (HOX11L2) oncogenes in adult ALL: Experience of the German Multicenter <strong>Acute</strong> Lymphoblastic Leukemia (GMALL) Therapy Study Group. Session Type: Poster Session 229-I. Blood 104:#1075 34. Baldus CD, Burmeister T, Martus P, et al. (2006) High expression of the ETS transcription factor ERG predicts adverse outcome in acute T-lymphoblastic leukemia in adults. J Clin Oncol 24:4714– 4720 35. Baldus CD, Martus P, Burmeister T, et al. (2007) Low ERG and BAALC expression identifies a new subgroup of adult acute T-lymphoblastic leukemia with a highly favorable outcome. J Clin Oncol (accepted) 36. Bruggemann M, Raff T, Flohr T, et al. (2006) Clinical significance of minimal residual disease quantification in adult patients with standard-risk acute lymphoblastic leukemia. Blood 107:1116– 1123 37. Raff T, Gökbuget N, Luschen S, et al. (2007) Molecular relapse in adult standard-risk ALL patients detected by prospective MRD monitoring during and after maintenance treatment: Data from the GMALL 06/99 and 07/03 trials. Blood 109:910–915 38. Gökbuget N, Raff R, Brugge-Mann M, et al. (2004) Risk/MRD adapted GMALL trials in adult ALL. Ann Hematol 83(Suppl 1): S129–S131 39. 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Philadelphia Chromosome-Positive <strong>Acute</strong> Lymphoblastic Leukemia Olga Sala-Torra, Jerald P. Radich Contents 14.1 Introduction ................... 177 14.2 Molecular Biology of the Ph Chromosome ........................ 177 14.2.1 Lineage Restriction of the Ph Chromosome .............. 179 14.2.2 The Molecular and Cell Biology of the Ph Chromosome ....... 179 14.2.3 The Biology of p190 Versus p210 BCR-ABL ................. 180 14.3 Treatment of Ph+ ALL ............ 180 14.3.1 Pediatric Ph+ ALL ........... 180 14.3.2 Adult Ph+ ALL ............. 181 14.3.3 Imatinib-based Therapy of Ph+ ALL 182 14.4 Hematopoietic Stem Cell Transplantation ................. 183 14.5 The Detection of Minimal Residual Disease ....................... 184 14.6 Conclusion .................... 184 References ......................... 184 14.1 Introduction The Philadelphia chromosome (Ph) is the shortened chromosome 22 resulting from the reciprocal translocation between 5' part of the BCR gene from chromosome 22 combines with the 3' part of the ABL gene, resulting in an chimeric BCR-ABL tyrosine kinase that is constitutively activated and oncogenic. The Ph is the genetic hallmark of chronic myeloid leukemia (CML), and it is also the most frequent cytogenetic abnormality in adult acute lymphoblastic leukemia (Ph+ ALL), where it is present in roughly 25% of cases. The Ph occurs less often in pediatric ALL, with a prevalence of < 5%. In both age groups the Ph chromosome describes a subgroup of ALL with a poor prognosis. Thus, patients with Ph+ ALL are usually offered a hematopoietic stem cell transplant if a suitable donor is available. The tyrosine kinase inhibitor, imatinib mesylate, has been found to block the activity of the BCR-ABL tyrosine kinase and has made an impact in the short-term management of Ph+ ALL. Unfortunately the effect of Imatinib monotherapy tends to be short-lived in Ph+ ALL, and it is by no means curative. Therefore, recent approaches are investigating combinations of Imatinib with either other small molecular inhibitors, chemotherapy, and transplant regimens. Although the numbers of patients reported are still small, the results suggest that these combinations using Imatinib with other therapies may improve clinical outcomes for this highly recalcitrant malignancy. 14.2 Molecular Biology of the Ph Chromosome The most common breakpoints of the BCR and ABL sequences yield two fusion BCR-ABL genes in Ph+ ALL (Fig. 14.1) [1–4]. These two different BCR-ABL variants result from the different breakpoint locations in the BCR gene, while the breakpoint in ABL occurs reliably 5' to ABL exon 2, except in rare circumstances. The typical 210 kD BCR-ABL fusion protein, found in CML and Ph+ ALL, involves a break in the major breakpoint clus-
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E.H. Estey · S.H. Faderl · H. M.
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E. H. Estey Department of Leukemia
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VI Table of Contents 14 Philadelphi
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VIII Contributors S. H. Faderl Depa
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X Contributors D. Wartenberg Depart
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Therapy of AML Elihu Estey Contents
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a 1.2 · Standard Therapy 3 Table 1
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a 1.2 · Standard Therapy 5 Table 1
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a 1.2 · Standard Therapy 7 tween G
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a 1.2 · Standard Therapy 9 Fig. 1.
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a 1.2 · Standard Therapy 11 of tre
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a 1.2 · Standard Therapy 13 Table
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a 1.2 · Standard Therapy 15 permit
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a References 17 19. Care RS, Valk P
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a References 19 6-thioguanine in th
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Acute Myeloid Leukemia: Epidemiolog
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a 3.1 · Epidemiology 49 3.1.4 Gend
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a 3.2 · Etiology 51 part of the in
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a 3.2 · Etiology 53 for the develo
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a References 55 38. Crane MM, Stom
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Relapsed and Refractory Acute Myelo
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a 4.2 · Prognostic Factors in Pati
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a 4.3 · Treatment of Relapsed and
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a 4.4 · Hematopoietic Stem Cell Tr
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a 4.6 · Gemtuzumab Ozogamicin 65 T
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a 4.7 · Relapsed and Refractory Ac
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a 4.7 · Relapsed and Refractory Ac
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a References 71 The ability of immu
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a References 73 39. Vogler WR, McCa
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a References 75 95. Sievers EL, Lar
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Part II - Acute Lymphoblastic Leuke
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78 Chapter 5 · Acute Lymphoblastic
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Molecular Biology and Genetics Meir
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a 6.3 · Structural Aberrations 97
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a 6.3 · Structural Aberrations 99
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a 6.5 · Molecular Aberrations 101
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a References 103 clear that homozyg
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a References 105 53. Chim CS, Tam C
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a References 107 122. Lennard L, Li
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Diagnosis of Acute Lymphoblastic Le
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a 8.3 · Cytochemistry and Immunoph
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a 8.5 · Cytogenetic and Molecular
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a 8.5 · Cytogenetic and Molecular
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a References 127 including the reti
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a References 129 47. Kita K, Shirak
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Acute Lymphoblastic Leukemia: Clini
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Page 143 and 144: ALL Therapy: Review of the MD Ander
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228 Chapter 17 · The Role of Allog
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230 Chapter 18 · The Role of Autol
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238 Chapter 19 · Novel Therapies i
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248 Chapter 20 · Minimal Residual
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264 Chapter 21 · Central Nervous S
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276 Chapter 22 · Relapsed Acute Ly
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278 Chapter 22 · Relapsed Acute Ly
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Emergencies in Acute Lymphoblastic
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a 23.5 · Hyperleukocytosis 283 LA
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a 23.9 · Neurological Complication
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a References 287 29. Hingorani AD,
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Subject Index A aberrant methylatio
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a Subject Index 291 CREB, see enhan
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a Subject Index 293 MUD, see matche
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