Acute Leukemias - Republican Scientific Medical Library

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a 15.7 ·L 3ALL in Adults Positive for the Human Immunodeficiency Virus (HIV) 199 none of the patients who relapsed could be durably salvaged [17–19]. Those patients generally had failure, only PR, or had rapid relapse after salvage treatment, and rarely achieved sufficient tumor reduction to envisage subsequent intensification by allogeneic or autologous SCT. Outcome of adult L3ALL patients who had PR or relapsed after first-line, more optimal intensive protocols (SFOP, BFM or German ALL trials) also appeared dismal. In the French experience [35], four of the six adult L 3ALL patients refractory or who relapsed after first line treatment were refractory to salvage treatment. The remaining two patients, who had sufficient tumor response with salvage chemotherapy, could be intensified by allo (one case) or auto (one case) SCT. However, they also rapidly died from relapse. Only two patients in the report of Soussain et al. [35] on adult BL and L 3ALL could be salvaged after a relapse, but they initially had stage I and stage II E BL. Outcome of relapses was not detailed in Hoelzer’s et al. study [9], but none of the patients who relapsed appeared to have obtained subsequent disease cure. The EBMT recently assessed the benefit of allogeneic bone marrow transplant when compared to high-dose therapy and autologous stem cell reinjection in lymphomas including Burkitt lymphomas [45]. No benefit was observed with allogeneic bone marrow transplant when compared to autologous bone marrow transplant in this series including 71 patients who received an allograft compared to 416 patients who received an autograft. Most of the patients were intensified when their disease remained chemosensitive, but results with allogeneic or autologous bone marrow transplant were disappointing. Allogeneic bone marrow transplant gave similar results to autologous bone marrow transplant, with a median survival of 4.7 months from the date of transplant and a progression-free survival of 2.5 months [37]. 15.7 L3ALL in Adults Positive for the Human Immunodeficiency Virus (HIV) Although the number of HIV-associated NHL is now decreasing with improvement of treatment of HIV infection in industrialized countries, this virus has led to a major increase in BL cases. For example, the National Cancer Institute of Italy recently reported, during an 8-year period, 131 cases of HIV-associated NHL, of which 46 (35%) were BL. During the same time, only 29 of the 1004 (2.8%) negative NHL diagnosed at the same institution were BL [48]. Large studies have shown that, in HIV-positive patients, BL tended to develop at a stage when immune functions are still relatively preserved, whereas other types of HIV-associated NHL (including large cell NHL, immunoblastic NHL, and Burkitt-like NHL), tend to develop at a stage of profound immunodeficiency. EBV infection is also found less often in HIV-associated BL than in HIV-associated immunoblastic NHL [49]. Bone marrow involvement is reported in 20–60% of HIV-associated BL. However, it is unclear from most published series how many of those patients fulfilled criteria for L3ALL [49]. Only occasional cases clearly described as HIV-associated L3ALL have been reported [17–19]. The outcome of HIV-associated NHL is generally poorer than that of NHL occurring in HIV-negative patients, due both to greater aggressiveness of the disease and to the underlying poor general condition and immune deficiency. In HIV-associated BL, CR rates of 20–45%, and median survival of 3–6 months have generally been reported with chemotherapy [19, 50–51]. Details regarding patients with bone marrow involvement were not available in those reports, however. In the report of the Italian NCI [48], treatment results in HIVpositive adult BL, regardless of disease stage, were less favorable than in HIV-negative BL: CR rate of 40% vs. 65% (p = 0.03). The difference was due to a higher incidence of deaths from opportunistic infections in HIV-associated BL, but also to the fact that HIV-positive cases were generally treated less intensively. Survival was also poorer in HIV-positive BL (median 7 months) as compared to HIV-negative BL (median not reached). DFS at 4 years was, however, identical in the two groups (74 vs. 73%). The French BL study group also reported 18 cases of BL, among 103 cases of HIV-positive NHL [52]. Only two of the 18 patients met criteria for AIDS before the diagnosis of NHL. Bone marrow involvement was reported in seven of them, but the degree of marrow infiltration was not known. Those seven patients received high-dose CHOP plus CNS prophylaxis. Only two of them achieved CR, and they both had prolonged response. Treatment results in the rare cases of precisely described L3ALL in HIV-positive patients were uniformly poor [17–19]. The possible impact of highly active antiretroviral therapy (HAART) in combinations with intensive Burkitt protocols has recently been investigated
200 Chapter 15 · Burkitt’s Acute Lymphoblastic Leukemia (L 3ALL) in Adults in HIV-positive Burkitt lymphomas and leukemias [53, 54]. The combination of HAART and intensive chemotherapy was feasible and resulted in long-term survivors in both series, which suggests that HAART should be combined with chemotherapy in L 3ALL patients. However those patients had generally received “classical” ALL protocols, and it is difficult to determine if underlying HIV infection worsened prognosis. The impact of intensive protocols now applied to non-HIV related cases of disseminated BL and L 3ALL on the prognosis of HIV-related cases is also difficult to determine. Such protocols should probably be applied whenever possible, i.e., in patients without advanced AIDS symptoms and without very low CD4 counts. 15.8 Conclusion L3ALL is a rare type of adult ALL, probably difficult to distinguish from disseminated BL involving the bone marrow. This tumor is highly proliferative, and tends to involve the CNS at diagnosis or rapidly during the disease course. It shows rapid chemosensitivity, initially leading to the risk of severe acute tumor lysis syndrome. Principles of its treatment, by comparison to the other types of ALL, include (i) a low-dose chemotherapy “prephase” to prevent acute tumor lysis syndrome; (ii) multiagent chemotherapy using high-dose cyclophosphamide, an anthracycline, high-dose MTX, high-dose Ara C and probably VP16. A short and intensive treatment (6–8 months) without maintenance, is indicated; (iii) early, intensive CNS treatment, with multiple triple intrathecal injections, high-dose MTX and high-dose Ara C, and possibly cranial irradiation. Autologous or allogeneic stem cell transplantation do not appear to be useful in first CR. Using such approaches, recent results suggest that about two thirds of L 3ALL in adults can be cured, i.e., more than in any other type of adult ALL. References 1. Bennett JM, Catovsky D, Daniel MT, et al. (1976) Proposals for the classification of the acute leukaemias. French-American-British (FAB) co-operative group. Br J Haematol 33(4):451 2. Bloomfield CD, Goldman AI, Alimena G, et al. (1986) Chromosomal abnormalities identify high-risk and low-risk patients with acute lymphoblastic leukemia. Blood 67(2):415 3. Flandrin G, Brouet JC, Daniel MT, Preudhomme JL (1975) Acute leukemia with Burkitt’s tumor cells: A study of six cases with special reference to lymphocyte surface markers. Blood 45:183 4. Berger R, Bernheim A (1982) Cytogenetic studies on Burkitt’s lymphoma-leukemia. Cancer Genet Cytogenet 7(3):231 5. Dalla-Favera R, Gregni M, Erikson J, et al. (1982) Human C-myc oncogene is located on the region of chromosome 8 that is translocated in Burkitt’s lymphoma cells. Proc Natl Acad Sci 79:7824 6. Jaffe ES, Harris NL, Stein H, Vardiman JW (2001) World Health Organization Classification of Tumours. Pathology and genetics. Tumours of hematopoietic and lymphoid tissues. IARC Press, Lyon, pp 181–184 7. Vassal G, Leverger G, Schaison G, Castaigne S (1986) Leucémies aiguës lymphoblastiques á cellules de Burkitt. Aspects cliniques, thérapeutiques et évolutifs. Nouv Rev Fr Hematol 28(3):141 8. Massey EW, Moore J, Schold SC, Jr (1981) Mental neuropathy from systemic cancer. Neurology 31(10):1277 9. Hoelzer D, Ludwig WD, Thiel E, et al. (1996) Improved outcome in adult B-cell acute lymphoblastic leukemia. Blood 87(2):495 10. Navid F, Mosijczuk AD, Head DR, et al. (1999) Acute lymphoblastic leukemia with the (8;14)(q24;q32) translocation and FAB L3 morphology associated with a B-precursor immunophenotype: The Pediatric Oncology Group experience. Leukemia 13(1):135 11. Hammami A, Chan WC, Michels SD, Nassar VH (1991) Mature B-cell acute leukemia: A clinical, morphological, immunological, and cytogenetic study of nine cases. Hematol Pathol 5(3):109 12. Sullivan MP, Pullen DJ, Crist WM, et al. (1990) Clinical and biological heterogeneity of childhood B cell acute lymphocytic leukemia: Implications for clinical trials. Leukemia 4(1):6 13. Lee EJ, Petroni GR, Schiffer CA, Freter CE, Johnson JL, Barcos M, Frizzera G, Bloomfield CD, Peterson BA (2001) Brief-duration high-intensity chemotherapy for patients with small noncleaved-cell lymphoma or FAB L3 acute lymphocytic leukemia: Results of cancer and leukemia group B study 9251. J Clin Oncol 19:4014–4022 14. Rizzieri DA, Johnson JL, Niedzwiecki D, Lee EJ, Vardiman JW, Powell BL, Barcos M, Bloomfield CD, Schiffer CA, Peterson BA, et al. (2004) Intensive chemotherapy with and without cranial radiation for Burkitt leukemia and lymphoma: Final results of Cancer and Leukemia Group B Study 9251.Cancer 100(7): 1438–1448 15. Thomas DA, Cortes J, O‘Brien S, Pierce S, Faderl S, Albitar M, Hagemeister FB, Cabanillas FF, Murphy S, Keating MJ, et al. (1999) Hyper-CVAD program in Burkitt’s-type adult acute lymphoblastic leukemia. J Clin Oncol. 17:2461–2470 16. Garcia JL, Hernandez JM, Gutierrez NC, Flores T, Gonzalez D, Calasanz MJ, Martinez-Climent JA, Piris MA, Lopez-Capitan C, Gonzalez MB, et al. (2003) Abnormalities on 1q and 7q are associated with poor outcome in sporadic Burkitt’s lymphoma. A cytogenetic and comparative genomic hybridization study. Leukemia 17: 2016–2024 17. Bernasconi C, Brusamolino E, Pagnucco G, Bernasconi P, Orlandi E, Lazzarino M (1991) Burkitt’s lymphoma/leukemia: A clinicopathologic study on 24 adult patients. Leukemia 5(Suppl 1):90 18. Fenaux P, Lai JL, Miaux O, Zandecki M, Jouet JP, Bauters F (1989) Burkitt cell acute leukaemia (L3 ALL) in adults: A report of 18 cases [see comments]. Br J Haematol 71(3):371
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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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a 7.3 · Diagnosis 111 or neoplasti
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a 7.3 · Diagnosis 113 Fig. 7.2. Hi
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a 7.3 · Diagnosis 115 The vast maj
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a References 117 dren: Biologic bas
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General Approach to the Therapy of
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a 9.3 · New Agents 133 dose methot
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a References 135 4. Gökbuget N, Ho
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138 Chapter 10 · Recent Clinical T
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250 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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