Acute Leukemias - Republican Scientific Medical Library

More documents

Recommendations

Info

168 Chapter 13 · Treatment of Adult ALL According to Protocols of the German Multicenter Study Group for Adult ALL (GMALL) Table 13.1. Studies of the German Multicenter Study Group for Adult ALL Studies Period Aims Patients (~) 01/81 1978–1983 Application of a modified pediatric treatment protocol in adult ALL 384 13.2 Therapy for Younger (15–65 Years) Patients with B-Precursor and T-Lineage ALL 13.2.1 GMALL Trials 01/81–07/03 In the earlier trials (01/81–05/93), an 8-week induction therapy with two phases was scheduled with several minor modifications [1]. All patients received reinduction therapy, and maintenance therapy with methotrexate (M) and 6-mercaptopurine (MP) was scheduled for a total treatment duration of approximately 2 1/2 years. The overall treatment outline of GMALL studies 01/81–07/03 is given in Fig. 13.1. Central diagnosis review (morphology/cytochemistry, immunophenotyping) 02/84 1983–1987 Stratification to standard and high-risk patients Intensified consolidation therapy for high-risk patients B-NHL81 protocol for mature B-ALL 569 03/87 1987–1989 High-dose cytarabine/mitoxantrone as consolidation therapy in high-risk patients B-NHL84 protocol for mature B-ALL 350 04/89 1989–1993 Extended central diagnosis review (cytogenetics, molecular genetics) Randomized evaluation of high-dose consolidation therapy in high-risk patients Allogeneic stem cell transplantation in all high-risk patients in CR1 580 05/93 1993–1999 Risk-adapted, intensified consolidation therapy with 3 risk groups Randomized evaluation of conventional vs. intensified maintenance therapy Pilot study for evaluation of minimal residual disease B-NHL90 protocol for mature B-ALL and B-NHL 1200 06/99 1999–2003 Pilot study for GMALL 07/03 830 07/03 2003–ongoing Shortened and intensified induction therapy Evaluation of a combined risk stratification according to conventional risk factors and MRD Risk-adapted postremission therapy Stem cell transplantation (allogeneic sibling, unrelated, and autologous) in high-risk and very-high-risk patients 680 The results of earlier trials (01/81–04/89) have been summarized previously [1–4]. Major findings referred to identification of new prognostic factors, development of subgroup-specific and risk-adapted regimens, intensified consolidation and maintenance, and extended indications for stem cell transplantation (SCT). In study 03/87 it was shown that postponed (standard risk = SR patients) or omitted (high risk = HR patients) CNS irradiation was associated with inferior overall outcome and a higher rate of CNS relapse [1]. Complete remission (CR) rates, remission duration, and survival improved stepwise with significant differences between subgroups.
a 13.2 · Therapy for Younger (15–65 Years) Patients with B-Precursor and T-Lineage ALL 169 Fig. 13.1. Overview on treatment approaches in seven consecutive GMALL studies. SR, standard risk; T, T-ALL; HR, high risk; BMT, bone marrow transplantation; R, randomization. 13.2.2 Study 05/93 Based on improved knowledge of clinical and biological features as prognostic factors (PF) and specific effectiveness of distinct treatment elements in subtypes of ALL, a subgroup-specific consolidation therapy was initiated in study 05/93. The trial had four treatment arms: (1) SR B-precursor ALL (patients without adverse PF); (2) HR B-precursor ALL (at least one PF); (3) T- ALL; and (4) older patients above 50 years (Elderly) (PFs of the trial are listed in Fig. 13.4). The general principle was to intensify treatment with high-dose methotrexate (HDM) in SR B-lineage ALL, with cyclophosphamide (CP) and cytarabine (AC) in T-ALL, and with HDM and HDAC followed by SCT in HR B-lineage ALL. Furthermore, there was a randomized comparison of intensified versus conventional maintenance therapy in SR and T-ALL. Twelve hundred patients with a median age of 35 (15–65) years were included. The CR rate was 83% with Fig. 13.2. Induction therapy in GMALL Study 07/03. DEXA, dexamethasone; CP, cyclophosphamide; VCR, vincristine; DNR, daunorubicine; PEG-ASP, PEG-L-asparaginase; MTX, methotrexate; i.th., intrathecal; CNS 24 Gy, CNS irradiation; 6-MP, mercaptopurine; ARAC, cytarabine. a range of 70% in older patients to 87% in SR B-lineage ALL (Table 13.2). In T-ALL, immunologic subtypes had a substantial impact on outcome, with a rate of continuous complete remission (CCR) of 63% for thymic, 28% for mature, and 25% for early T-ALL, and ruled out the prognostic impact of WBC and time to CR.
Page 1 and 2:
E.H. Estey · S.H. Faderl · H. M.
Page 3 and 4:
E. H. Estey Department of Leukemia
Page 5 and 6:
VI Table of Contents 14 Philadelphi
Page 7 and 8:
VIII Contributors S. H. Faderl Depa
Page 9 and 10:
X Contributors D. Wartenberg Depart
Page 11 and 12:
Therapy of AML Elihu Estey Contents
Page 13 and 14:
a 1.2 · Standard Therapy 3 Table 1
Page 15 and 16:
a 1.2 · Standard Therapy 5 Table 1
Page 17 and 18:
a 1.2 · Standard Therapy 7 tween G
Page 19 and 20:
a 1.2 · Standard Therapy 9 Fig. 1.
Page 21 and 22:
a 1.2 · Standard Therapy 11 of tre
Page 23 and 24:
a 1.2 · Standard Therapy 13 Table
Page 25 and 26:
a 1.2 · Standard Therapy 15 permit
Page 27 and 28:
a References 17 19. Care RS, Valk P
Page 29 and 30:
a References 19 6-thioguanine in th
Page 31 and 32:
Acute Myeloid Leukemia: Epidemiolog
Page 33 and 34:
a 3.1 · Epidemiology 49 3.1.4 Gend
Page 35 and 36:
a 3.2 · Etiology 51 part of the in
Page 37 and 38:
a 3.2 · Etiology 53 for the develo
Page 39 and 40:
a References 55 38. Crane MM, Stom
Page 41 and 42:
Relapsed and Refractory Acute Myelo
Page 43 and 44:
a 4.2 · Prognostic Factors in Pati
Page 45 and 46:
a 4.3 · Treatment of Relapsed and
Page 47 and 48:
a 4.4 · Hematopoietic Stem Cell Tr
Page 49 and 50:
a 4.6 · Gemtuzumab Ozogamicin 65 T
Page 51 and 52:
a 4.7 · Relapsed and Refractory Ac
Page 53 and 54:
a 4.7 · Relapsed and Refractory Ac
Page 55 and 56:
a References 71 The ability of immu
Page 57 and 58:
a References 73 39. Vogler WR, McCa
Page 59 and 60:
a References 75 95. Sievers EL, Lar
Page 61 and 62:
Part II - Acute Lymphoblastic Leuke
Page 63 and 64:
78 Chapter 5 · Acute Lymphoblastic
Page 65 and 66:
Page 67 and 68:
Page 69 and 70:
Page 71 and 72:
Page 73 and 74:
Page 75 and 76:
Page 77 and 78:
Page 79 and 80:
Molecular Biology and Genetics Meir
Page 81 and 82:
a 6.3 · Structural Aberrations 97
Page 83 and 84:
a 6.3 · Structural Aberrations 99
Page 85 and 86:
a 6.5 · Molecular Aberrations 101
Page 87 and 88:
a References 103 clear that homozyg
Page 89 and 90:
a References 105 53. Chim CS, Tam C
Page 91 and 92:
a References 107 122. Lennard L, Li
Page 93 and 94:
Diagnosis of Acute Lymphoblastic Le
Page 95 and 96:
a 8.3 · Cytochemistry and Immunoph
Page 97 and 98:
a 8.5 · Cytogenetic and Molecular
Page 99 and 100: a 8.5 · Cytogenetic and Molecular
Page 101 and 102: a References 127 including the reti
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
Page 109 and 110: a 7.3 · Diagnosis 113 Fig. 7.2. Hi
Page 111 and 112: a 7.3 · Diagnosis 115 The vast maj
Page 113 and 114: a References 117 dren: Biologic bas
Page 115 and 116: General Approach to the Therapy of
Page 117 and 118: a 9.3 · New Agents 133 dose methot
Page 119 and 120: a References 135 4. Gökbuget N, Ho
Page 121 and 122: 138 Chapter 10 · Recent Clinical T
Page 129 and 130: 146 Chapter 11 · Conventional Ther
Page 143 and 144: ALL Therapy: Review of the MD Ander
Page 145 and 146: a 12.2 · The Hyper-CVAD Regimen in
Page 147 and 148: a 12.3 · Subset-Specific Approache
Page 149: Treatment of Adult ALL According to
Page 153 and 154: a 13.3 · Therapy of Ph/BCR-ABL-Pos
Page 155 and 156: a 13.5 · Prognostic Factors 173 13
Page 157 and 158: a References 175 Only patients with
Page 159 and 160: Philadelphia Chromosome-Positive Ac
Page 161 and 162: a 14.2 · Molecular Biology of the
Page 163 and 164: a 14.3 · Treatment of Ph+ ALL 181
Page 165 and 166: a 14.4 · Hematopoietic Stem Cell T
Page 167 and 168: a References 185 2. Kurzrock R, Sht
Page 169 and 170: a References 187 56. Mori T, Manabe
Page 171 and 172: a References 189 acute lymphoblasti
Page 173 and 174: 192 Chapter 15 · Burkitt’s Acute
Page 185 and 186: 204 Chapter 16 · Treatment of Lymp
Page 197 and 198: 216 Chapter 17 · The Role of Allog
Page 199 and 200: 218 Chapter 17 · The Role of Allog
Page 201 and 202:
220 Chapter 17 · The Role of Allog
Page 203 and 204:
Page 205 and 206:
Page 207 and 208:
Page 209 and 210:
Page 211 and 212:
230 Chapter 18 · The Role of Autol
Page 213 and 214:
Page 215 and 216:
Page 217 and 218:
Page 219 and 220:
238 Chapter 19 · Novel Therapies i
Page 221 and 222:
Page 223 and 224:
Page 225 and 226:
Page 227 and 228:
Page 229 and 230:
248 Chapter 20 · Minimal Residual
Page 231 and 232:
Page 233 and 234:
Page 235 and 236:
Page 237 and 238:
Page 239 and 240:
Page 241 and 242:
Page 243 and 244:
Page 245 and 246:
264 Chapter 21 · Central Nervous S
Page 247 and 248:
Page 249 and 250:
Page 251 and 252:
Page 253 and 254:
Page 255 and 256:
Page 257 and 258:
276 Chapter 22 · Relapsed Acute Ly
Page 259 and 260:
278 Chapter 22 · Relapsed Acute Ly
Page 261 and 262:
Emergencies in Acute Lymphoblastic
Page 263 and 264:
a 23.5 · Hyperleukocytosis 283 LA
Page 265 and 266:
a 23.9 · Neurological Complication
Page 267 and 268:
a References 287 29. Hingorani AD,
Page 269 and 270:
Subject Index A aberrant methylatio
Page 271 and 272:
a Subject Index 291 CREB, see enhan
Page 273 and 274:
a Subject Index 293 MUD, see matche
show all

Acute Leukemias - Republican Scientific Medical Library

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?