Acute Leukemias - Republican Scientific Medical Library

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118 Chapter 7 · <strong>Acute</strong> Lymphoblastic Leukemia: Clinical Presentation, Diagnosis, and Classification cule expression, and architectural features. Am J Clin Pathol 114(1):66–75 39. van Wering ER, van der Linden-Schrever BE, Szczepanski T, Willemse MJ, Baars EA, van Wijngaarde-Schmitz HM, et al. (2000) Regenerating normal B-cell precursors during and after treatment of acute lymphoblastic leukaemia: Implications for monitoring of minimal residual disease. Br J Haematol 110(1):139–146 40. Anastasi J, Feng J, Dickstein JI, Le Beau MM, Rubin CM, Larson RA, et al. (1996) Lineage involvement by BCR/ABL in Ph+ lymphoblastic leukemias: Chronic myelogenous leukemia presenting in lymphoid blast vs. Ph+ acute lymphoblastic leukemia. Leukemia 10(5):795–802 41. Le Beau MM, Larson RA (2000) Cytogenetics and Neoplasia. In: Hoffman R BJE, Shattil SJ, et al. (eds) Hematology: Basic principles and practice, 3rd edn. Churchill Livingstone, Philadelphia, pp 848– 869 42. van Dongen JJ, Seriu T, Panzer-Grumayer ER, Biondi A, Pongers- Willemse MJ, Corral L, et al. (1998) Prognostic value of minimal residual disease in acute lymphoblastic leukaemia in childhood. Lancet 352(9142):1731–1738 43. Cave H, van der Werff ten Bosch J, Suciu S, Guidal C, Waterkeyn C, Otten J, et al. (1998) Clinical significance of minimal residual disease in childhood acute lymphoblastic leukemia. European Organization for Research and Treatment of Cancer7Childhood Leukemia Cooperative Group. N Engl J Med 339(9):591–598
General Approach to the Therapy of Adult <strong>Acute</strong> Lymphoblastic Leukemia S.H. Faderl, H. M. Kantarjian Contents 9.1 Introduction .................... 131 9.2 The General Treatment Outline of ALL 131 9.3 New Agents .................... 133 9.4 Conclusion ..................... 134 References ......................... 134 9.1 Introduction Remarkable progress has been made in the treatment and outcome of adult acute lymphoblastic leukemia (ALL) over the past 3 decades. This progress is the result of an accumulation of a mosaic of knowledge and experience, which have led to a more profound understanding of the biology of the disease, and at the same time the development of new drugs and treatment strategies. Advances in the understanding of the biology has highlighted significant differences between childhood and adult ALL (e.g., high frequency of Philadelphia-positive ALL and low incidence of TEL-AML1-positive disease in adults) and thus explains at least partly the divergence of outcomes that is still observed between children and adults. Moreover, ALL is increasingly recognized as a group of heterogeneous disease entities with unique responses to therapy and prognosis. The combination of further cytogenetic-molecular dissection of ALL subtypes with the emergence of new and targeted therapies will thus continue to constitute the fundament upon which further progress will hopefully occur in adult ALL. 9.2 The General Treatment Outline of ALL Most of the initial therapeutic advances in adult ALL have arisen from successful adaptation of ALL treatment strategies in children. ALL therapy incorporates multiple drugs into regimen-specific sequences of dose and time intensity and is divided into several phases: (i) induction; (ii) a sequence of intensified consolidation; (iii) a prolonged maintenance phase; and (iv) CNS prophylaxis (Fig. 9.1). Intensive combination therapy in ALL following this pattern has resulted in complete remission (CR) rates of 80% to 90% and leukemia-free survival rates of between 30% and 40% [1–4]. Various groups in the USA and around the world are investigating modifications of these treatment blocks in an effort to improve upon the outcome. These strategies not only Fig. 9.1. Basic principle of ALL therapy.
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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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Page 79 and 80: Molecular Biology and Genetics Meir
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Page 85 and 86: a 6.5 · Molecular Aberrations 101
Page 87 and 88: a References 103 clear that homozyg
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Page 91 and 92: a References 107 122. Lennard L, Li
Page 93 and 94: Diagnosis of Acute Lymphoblastic Le
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Page 97 and 98: a 8.5 · Cytogenetic and Molecular
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Page 103 and 104: a References 129 47. Kita K, Shirak
Page 105 and 106: Acute Lymphoblastic Leukemia: Clini
Page 107 and 108: a 7.3 · Diagnosis 111 or neoplasti
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Page 117 and 118: a 9.3 · New Agents 133 dose methot
Page 119 and 120: a References 135 4. Gökbuget N, Ho
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Page 143 and 144: ALL Therapy: Review of the MD Ander
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Page 149 and 150: Treatment of Adult ALL According to
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Page 159 and 160: Philadelphia Chromosome-Positive Ac
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a 14.4 · Hematopoietic Stem Cell T
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a References 185 2. Kurzrock R, Sht
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a References 187 56. Mori T, Manabe
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a References 189 acute lymphoblasti
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192 Chapter 15 · Burkitt’s Acute
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204 Chapter 16 · Treatment of Lymp
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216 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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