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References Cox DR (1972) Regression models and life-tables. J Stat Soc BuII 34: 187-220 - Cutler S, Ederer F (1958) Maximum utilisation of the life table method in analysing survivaI. J Chronic Dis 4: 699-712 - Dow LW, BoreIIa L, Sen L, Aur RJA, George SL, Mauer AM, Simone JV (1977) Initial prognostic factors and lymphoblast-erythroeyte rosette formation in 109 children with acute lymphoblastic leukemia. Blood 50:671-681 - Frei E III, SaIIan SE (1978) Aeute lymphoblastic leukemia: Treatment. Cancer 42: 828-838 - Henze G, Langermann HJ, Lampert F, Neidhardt M, Riehm H (1979) ALL therapy study 1971-1974 of the German Working Group for Leukemia Research and Therapy in childhood: Prognostie significance of initial features and different therapeutic modalities. Klin Paediat 191: 114-126 - Mathe G, Pouillart P, Sterescu M, Amiel JL, Schwarzenberg L, Schneider M, Hayat M, de Vassal F, Jasmin C, Lafleur M (1971) Subdivision of classical varieties of acute leukemia. Correlation with prognosis and eure expectancy. Eur J Clin Res 16: 1554-560 - Ortega JA, Nesbit ME, Donaldson MH, Weiner J, Hittle R, Karon M (1977) L-asparaginase, vincristine, and prednisone for induction of first remission in acute lymphocytic leukemia. Cancer Res 37 :535-540 - Riehm H, Gadner H, Henze G, Langermann HJ, Odenwald E (1980) The BerIin childhood acute lymphoblastic leukemia study, 1970-1976. Am J Pediatr Hematol Onco12 :299-306 - Robison LL, Sather HN, Coccia PF, Nesbit ME, Hammond GD (1980) Assessment of the interrelationship of prognostic factors in childhood acute lymphoblastie leukemia. Am J Pediatr Hematol Oneol 2: 5-13 - SaIIan SE, Camitta BM, Cassady JR, Nathan DG, Frei E III (1978) Intermittent eombination chemotherapy with adriamycin for childhood acute lymphoblastic leukemia: Clinical results. Blood 51 :425-433 - Simone JV, Verzosa MS, Rudy JA (1975) Initial features and prognosis in 363 children with acute lymphocytie leukemia. Cancer 36:2099-2108 - Wagner VM, Baehner RL (1979) Correlation of the F AB morphologie eriteria and prognosis in acute lymphocytic leukemia of ehiIdhood. Am J Pediatr Hematol Oneol 1: 103-106 - Working Party on Leukemia in Childhood (1978) Effects of varying radiation sehedule, eyclophosphamide treatment, and duration of treatment in aeute lymphoblastic leukemia. Br Med J II: 787-791 93
Haematology and Blood Transfusion Vol. 26 <strong>Modern</strong> Trends in Human Leukemia IV Edited by Neth, Gallo, Graf, Mannweiler, Winkler © Springer-Verlag Berlin Heidelberg 1981 Recurrent Childhood Lymphocytic Leukemia: Outcome 01 Marrow Relapses After Cessation 01 Therapy* G.Rivera A. Introduction Leukemia therapists have long agreed that relapse - particularly in the bone marrow - signals the end of opportunities to obtain long-Iasting remissions. This thinking can be traced to the emergence of drug-resistant lymphoblasts, the hallmark of leukemia in relapse, and to the lack of sufficient numbers of uniformly treated patients far analysis and comparison. It is becoming c1ear, however, that in patients with recurrent acute lymphocytic leukemia (ALL), treatment responses differ widely. Second hematologic remissions, for instance, are significantly longer in children who relapse after therapy is electively stopped than in those who relapse during therapy (Chessells and Cornbleet 1979; Ekert et al. 1979; Kearney et al. 1979; Rivera et al. 1976, 1978). Furthermore, in some patients, treatment can be stopped altogether far a second time with the possibility of continued diseasefree survival (Rivera et al. 1979). The purpose of this artic1e is to review the clinical course of 56 patients who were retreated for marrow relapses that developed after cessation of intensive initial treatment. B. Patients Studies From 1966 to 1978,288 of645 (0.44) children with ALL who were entered in Total-Therapy Studies I-VIII at St. Jude Children's Research Hospital (SJCRH) had aB therapy stopped. * Supported by Cancer Center Support (CO RE) Grant CA-21765, by Leukemia Program Project Grant CA-20180, and by ALSAC The details of each study group have been presented in earlier publications (Aur et al. 1978; Simone et al. 1972). Treatment was discontinued after 2-3 years of complete remission; thereafter, the patients had marrow and cerebrospinal fluid examinations at intervals ranging from every 2 months during the 1st year to annually after the 5th year off therapy. Of these 288 patients, 72 (0.25) have relapsed. Fifty-six children developed marrow relapses during unmaintained remissions ; in 43 only the marrow was involved, whereas in the remaining 13 the testes and central nervous system (CNS) were involved as weIl. Sixteen additional patients had isolated extrameduallary relapses: 11 testicular and 5 CNS (Table 1). This review inc1udes only the 56 patients who developed hematologic relapses with or without other sites of leukemic involvement. Table 1. Results of stopping therapy in childhood ALL: SJCRH Studies I-VIlla No. of patients entered 645 No. electively removed from treatment 288 No. still in remission (2-14 Yr) 216 No. relapsing 72 Sites of relapse in 72 patients 1. Bone marrow 2. Extramedullary BMalone 43 CNS 5 BM+CNS 5 Testicular 11 BM+T 6 BM+T+CNS 2 56 16 aAs of 1 lune 1980. BM, bone marrow; CNS, central nervous system; T, testicular 94
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Haematology and Blood Transfusion 2
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Dr. Rolf Neth, Universitäts-Kinder
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Participants of the Meeting Aaronso
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Kurth, R, Friedrich-Miescher-Labora
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Wilsede Scholarship Holders (Grante
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Preface Gut ist eine Lehrart, wo ma
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Personal and scientific discussion
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Acknowledgement We should like to t
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Wilsede, June 21 1978 Memorial Trib
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limiting benign lymphoproliferative
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this most unlikely, however (for re
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longer subject to the same control
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Bregula U, Wiener F, Harris H (1971
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fresh lymph node biopsies from ten
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Fig. 3. Binucleate mitosis in an ob
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y Fig. 4. Schematic diagram of post
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than that among patients with Stage
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Tests of binding affinity, agglutin
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N Engl J Med 297: 963-968 - Green I
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Clinical Aspects
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"ring chromosome". "Mar" is marker,
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191 chromosomally abnormal patients
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tumors of both African and non-Afri
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Haematology and Blood Transfusion V
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Retrospective group 26/93 evolved l
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Treatment
Page 55 and 56: advantage in terms of duration of f
Page 57 and 58: leukaemia. An analysis of 168 patie
Page 59 and 60: 11. Treatment Program Chemotherapy
Page 61 and 62: efractory congestive heart failure
Page 63 and 64: period (Sequence II) was gene rally
Page 65 and 66: children with a multiple drug proto
Page 67 and 68: DAYS 1 5 10 15 20 25 30 35 , I I I
Page 69 and 70: Biologically Drug Outcome fit" sens
Page 71 and 72: may counterbalance the potential be
Page 73 and 74: Ht (0--0) 50 40 30 20 10 0 Platelet
Page 75 and 76: 10 7 ,-----------------------------
Page 77 and 78: 11. Haematological and Biochemical
Page 79 and 80: 0\ 0\ INTERFERON ... 10 3 rl E "'
Page 81 and 82: Haematology and Blood Transfusion V
Page 83 and 84: ("pre-B" phenotype) has been descri
Page 85 and 86: human bone marrow cells exhibit the
Page 87 and 88: 10 9.,0 MBKCC .. .,4 B prot:oool 1'
Page 89 and 90: demann W, Büehner T, Arlin Z, Gee
Page 91 and 92: -...l 00 a-tLDRENS CAt«:ER S TU>Y
Page 93 and 94: prognostic characteristics under in
Page 95 and 96: significantly higher in HR} (14.5%,
Page 97 and 98: normal or elevated immunoglobulin l
Page 99 and 100: References Andreeff M, Darzynkiewic
Page 101 and 102: R GROUP 1 ( 1970 - 1971 ) 17 PTS. R
Page 103 and 104: Table 3. Influence of initial featu
Page 105: LIJ (f) a.. < -1 LIJ Q: u. 0 >- I-
Page 109 and 110: me nt indicated that additional the
Page 111 and 112: 42:2123-2134 - Chessells JM, Cornbl
Page 113 and 114: Baum et al. 1979). This study was b
Page 115 and 116: 1. 0 '--'1--" 0.9 e: o .- VI VI E C
Page 117 and 118: e: o e: 1. 0 ,.--...-- 1'"'\ ......
Page 119 and 120: In conclusion, we can state that th
Page 121 and 122: Haematology and Blood Transfnsion V
Page 123 and 124: INDUCTION VCR + PRED + ASNASE (wk 3
Page 125 and 126: SCHED.INT 1 MTX • ! Adria MTX •
Page 127 and 128: ~ looh---------ooooc>----o---c>----
Page 129 and 130: Consoll- Irra .tlon t) .tlon Indu
Page 131 and 132: Highrisk Standard risk Table 1. Cli
Page 133 and 134: Cumulo/ive comp/el9 remission 1.0 .
Page 135 and 136: 10° 8 = 6 ö 4 Non T Cell .~ :ö
Page 139 and 140: % SURVIVAL 100 ~ ~II 0 80 60 40 - -
Page 141 and 142: a) Percentage of donor cell mitoses
Page 143 and 144: Table 5. Results of bone marrow tra
Page 145 and 146: ...... w N Table 7. Clinical result
Page 147 and 148: agent had to be added and that in t
Page 151 and 152: C. Chronic Myelogenous Leukemia The
Page 153 and 154: Patients with a suitable donor rece
Page 155 and 156: No. Recurrent Leukaemia Other death
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followed by dialysis against isoton
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HS, HL- Heme >_ 40 0 HS I ;:. =====
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knowing at present. These genes may
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esistance to antifolates. In Vitro
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a DNA probe specific for the gene t
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translocation between chromosomes 9
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Table 1. Subdivision of 1827 Myelo-
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NORMAL CELL ®
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some change of the primary type, in
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F. Transformation of Mouse Bone Mar
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were carried out with 3H-MTX in the
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the lysozyme cDNA prepared from ovi
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et al. 1976). The BJAB cellline in
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dalton bands corresponding to light
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1979). The EBV-carrying cell lines
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producer lines (DAUDI and P3HR-1),
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G, Giovanella B, Westman A, Stehlin
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Dc;bt CT + i J.I9 Raji; 1. i .. 100
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c. Discussion During infectious mon
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C. Nonepisomal Viral DNA We have us
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A 260 3.0 A B 1670 70 N2 2.0 c: E .
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vivo. Nature 260:302-306 - Kirk JTO
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Fig. 1. a Polyacrylamide gelelectro
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1979). The lymphocyte subpopulation
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lysin 0 antigens are found, and mix
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Pope JH (1978) Long-term T cell-med
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Haematology and Blood Transfnsion V
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Charaeteristie Morphologie maturati
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after TPA-induction (Table 3). The
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PA (1978) Reactivity of a rabbit an
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Blood Monocyte. B lood Monocytes 1-
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and nonhistone proteins can serve a
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The findings of the evaluation of s
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Fig. 3. Tumor grawth of L 428 cells
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Cell biological and Immunological A
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consideration. Sanel (1973) obtaine
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endotoxin serum, were used. A parti
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monocytic leukemia cell line in cul
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B. Isolation, Characterization and
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don al hemopathies generally displa
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nitors. Blood Cells 6:595-607 - Min
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\I) ....I ....I IU Jl 200 r 100 90
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their haemopoietic cells' ability t
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normal normal ALL ALL ALL persons p
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64.5 { V)
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References Biermann E, Neth R, Gros
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ehambers, the growth pattern observ
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References Anderssen LC, 10kinen M,
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REH CELL UNE TO CALLb~Ö ~q~ V.M. c
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the macrophage series in which the
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Table 1. Production of factor depen
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Table 1. Characteristics of the adh
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Fig. 3. A human marrow culture at 6
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300 250 • HYPERPROLIFERATIVE PATT
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Fig. 9. Nonadherent population from
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The cobblestone areas were often no
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L (1976) Induction of colony format
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B. Materials and Methods J. Tissue
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Fig. 2. Ultrastructural appearance
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Page 307 and 308:
Page 309 and 310:
Table 1. Monoclonal antibody reacti
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al. 1979; Janossy et al. 1979) is e
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to which this is an exact replica o
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inger JL (1976) Distribution of la-
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I region antigens were found to be
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have been reported to be present on
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V. FunctionalAssays Assays for PHA
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Functional studies of UCHT1 separat
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40 ,...... (5 L.. C o u 30 .9 ~ .~
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with immunohistochemieal methods (L
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can be dissected by cloning. Utiliz
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Table 1. Origin and marker profile
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Page 339 and 340:
complete identity of gp 100 from no
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Table 1. Reaction of single anti se
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media. Following 24-h incubation, c
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nonleukemic eells (Greaves 1979). L
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Fig. 2. Cytocentrifuged smears of b
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Modification of amino-groups of hum
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disturb this balance in the directi
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The majority of human blood lymphoc
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of the EBV infected B cells. Howeve
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and immunoglobulins. J Immunol 120:
Page 363 and 364:
" K 10 • j ~ ALL RNlL AL wtfh les
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tion akuter Leukämiezellen in "spo
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D. Results and Discussion J. Acute
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selectively responsive to different
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l1J ~ 100 ~ Q. ::) l1J Z 0 ~ z >- .
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Table 2. Growth inhibition of S49 e
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Reverse Infectious ASC/2X1Q6 transc
Page 379 and 380:
Page 381 and 382:
munized animals to 1316 tumor cells
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Haematology and Blood Transfnsion V
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Fig. 3. Expression of retroviral gp
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pg70. J Exp Med 143: 151-166 - McGr
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Table 1. Expression of tumor antige
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Virological and Molecularbiological
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Table 1. Oncogenic properties of re
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also Fig. 1). It followed that the
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whether this sequence is related to
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zed in infected cells argue that th
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a specific viral transforming prote
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detect viral RNA as the only charac
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Eisen H (1980) Myeloproliferate vir
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p,60- -34K - 1 2 3 4 Fig. 1. In vit
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.. p - • a'T ... I .t'l Fig. 4. D
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Fig. 2. Photomicrographs of NY68 in
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DEAE (o(lJmn 'liI GI -2 2 o e s 1
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vity was deterrnined. For endogenou
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pr 180 - - - P 12/15 - A B c D E F
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85,- 66- -27 - -66 40- 27- -1'9 19-
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= 0.5 o E Q. o ILI 0.4 (J) « ILI .
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Table 1. Oncogenic potential of avi
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100 III GI c: o "8 80 > w
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Expt. No. Infecting virus Proportio
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Haematology and Blood 'fransfusion
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sequences, provided its gag portion
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77:3009-3013 - Hu SSF, Moscoviei C,
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RI 2.2 md and Hind III 2.6 md leuke
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Page 443 and 444:
RELATIONSHIP OF ENDOGENOUS AND EXOG
Page 445 and 446:
E ........ E Cl. U E :::l .... Q) (
Page 447 and 448:
References Astrin S (1978) Endogeno
Page 449 and 450:
the same animal were examined (e.g.
Page 451 and 452:
I) 'IQ a \0 - CL -- Fig. 2. Restrie
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~ ..................... ~ Cell 3' 5
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a :Sa,C! + . ~ 111 i' ( " '~ .J. b
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Table 1 Sampie Tissue TS fragment"
Page 459 and 460:
a b Sac I / rep ._-_.-_ K J nl rep
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Haematology and Blood 'fiansfusion
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Osteopetrosis and osteosarcomas occ
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Lymphoma cellline Table 1. T and B
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Table 2. In vivo growth and oneogen
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Table 1. Transforming aetivity of c
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Table 3. Transformation aetivity of
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- Shoemaker C, Goff S, Gilboa E, Pa
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indieate a shifting of target eell
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Table 2. Expression of Jl and Sourc
Page 481 and 482:
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~ i ,..1---------,,':::::::::::::::
Page 485 and 486:
fragment of pBR322 DNA, a 3.0-kbp S
Page 487 and 488:
Mak TW (1979) Proc Natl Acad Sci US
Page 489 and 490:
Table 1. Transformation of 3T3 cell
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inserts in the genome of rapidly tr
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pulations, it seemed likely that th
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contains antigens which react with
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le of reacting in sensitive radioim
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gic approach. In: Hiatt HH, Watson
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12 Eco R [ Fig. 1. Hybridization pa
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10 - '1~ )( -~ S:! E A U I o 1 2
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Haematology and Blood 'fransfusion
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cultures. These cells did not conta
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indication of malignant T-cells in
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Fig. 3. Thin-section electron micro
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Table 3. Lack of detectable related
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J. HTLV Was Present in the Primary
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specific signals into nonspecific s
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Table 2. Distribution of HTLV-relat
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u 10 ~ 20 ~ :c 30 a 40 o Fig. 1. Ki
Page 529 and 530:
Page 531 and 532:
SSV TrS-gp labeled effectively with
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60 HFF/SSV cDNA CELL RNAs: 0 HF/SSV
Page 537 and 538:
Antisera a Table 1. Immunofluoresce
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Haematology and Blood 'ftansfusion
Page 541 and 542:
y competition RIA yielded virtually
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SiS'V' gp70: ANTIGEN, ANTI BODY, IM
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type-C virus p30 antigen in cells f
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c. Results The fractionated whole-b
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induced antibodies as well as exper
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- Fig. la-f. Retravirus particles p
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eplication of infecting murine leuk
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immunodeficiency, multic10nal lymph
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Bovine leukemia --, proteins of 499
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Human T- cell - -, characterization
Page 563 and 564:
RNA -, of tumor virus 439 Rous sarc
Page 565 and 566:
Haematology andBlood Transfusion Su
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