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le co operative study (CALGB Protocol 7111) (Jones et al. 1977). Furthermore, our objective to dispense with the need for cranial RT now appears even more important that when the study was designed in 1974. Arecent study of children treated with prophylactic cranial RT and IT MTX or IT cytosine arabinoside showed that 53 % developed abnormal findings as detected by computerized tomography (CT) (Peylan-Ramu et al. 1978). These findings included dilated ventricles, intracerebral calcifications, demyelination, and dilation of subarachnoid space. Signs of endocrinologic long-range effects have been reported as evidenced by a reduction in growth hormone secretion in children treated with prophylactic cranial RT (Shalet et al. 1976). A comparable CT scan study has been undertaken in our 43 patients (Ochs et al. 1978). Only 19 % showed abnormal changes, and furthermore, these findings were much less marked than those reported by Peylan-Ramu et al. No calcifications and no patients with decreased attenuation coefficient were seen in any of the 43 cases. In a similar study from Norway, the investigators found only 1 child out of 19 with an abnormal CT scan. These patients had been treated with IDM similar to the schedule described in this report (Kolmannskog et al. 1979). The possible effect of prophylactic cranial RT on psychological, neurologic, and intellectual development is the subject of studies now in progress. The overall relapse rate in this study is 20/52 and the CNS relapse rate as the initial site of failure is 10/52. Thus, 10/20 relapses occurred first in the CNS. In arecent comparison by Green et al. it was demonstrated that patients treated at RPMI (standard risk) with IDM (Fig. 2) were maintained in complete remission significantly longer than two other groups of patients. One group consisted of those treated with prophylactic IT MTX (Children's Cancer Study Group CCG-101) and the other of those who received IT MTX and prophylactic RT (Sidney Farber Cancer Institute SFCI-73-01). This was in spite of the fact that CNS relapse rate was high er in the IDM-treated group (Fig. 4) compared to the irradiated group (Green et al., to be published). In this same comparison the increased risk group of patients did better in terms of CNS relapse and complete remission when treated with IT MTX and cranial irradiation. Another large study (CALGB Protocoll 7111) recently reported by Jones et al. (1977) has demonstrated a protective value of cranial RT and IT MTX alone in preventing CNS leukemia but not benefit in the overall complete remission rate. This was the result of an increased incidence of hematological relapse in the patients who received cranial RT. The British Medical Research Council also has observed a higher rate of hematologic relapse in these patients receiving prophylactic craniospinal radiation than in those without CNS prophylaxis (Medical Research Council1973). In the British study the radiated group, either cranial or craniospinal, had a greater lymphopenia, which may reflect a pertubation of the immune surveillance system and thus lead to a greater systemic relapse (Medical Research Counci11975, 1978). Moe and Seip (1978) patterned their study in Norway closely after the one reported here; their results are preliminary, but to date there have been only 5 of 69 patients relapsing. Seventy-eight percent of the children have been followed for 18 months or more and are in complete remission. It appears reasonable on the basis of present information to advance the conclusion that the treatment of children with ALL who fall into the standard risk category (age and WBC) can effectively be treated by IDM plus IT MTX in terms of better overall control of disease. Furthermore, the long-term risks and complications of cranial irradiation (Peylan-Ramu et al. 1978; Medical Research Council 1975; Fishman et al. 1976; Freeman et al. 1973; McIntosh et al. 1977) can be avoided with this type of therapy. Children who are at increased risk appear to be protected by the use of cranial irradiation, but the way is clear to improve upon the present schedule of IDM in terms of dose escalation and pulse dose administration through the 1st year of remission. Such studies are currently under way in a number of centers. The second objective, i.e., to intensify systemic treatment (Fig. 3) and thus to prevent other sanctuary site infiltration, has also been reasonably achieved. Only one male child (26 males) developed testicular relapse. We attribute this to effective serum levels of MTX which presumably can eradicate disease in sanctuary sites such as the liver, spleen, and gonads. 105
In conclusion, we can state that the use of a systemic form of therapy, as opposed to a local form (RT to cranium), appears to confer greater protection to standard risk children with ALL than the use of cranial RT. In addition, we can avoid the long-range complications of cranial RT. In the high risk patients, cranial RT and IT MTX appears superior to the systemic form (IDM); however, manipulation of this form of therapy (increasing dose and pulse therapy) may overco me this disadvantage. Acknowledgment Thanks to E. S. Henderson for his comments and help in preparing this manuscript. We gratefully acknowledge the statistical assistance provided by J. Coombs, Ph. D., Assistant Professor, Division of Biostatistics and Epidemiology, Vincent T. Lombardi Cancer Research Center, Georgetown University Hospital. References Aur RJA, Simone JV, Hustu HO, Walters T, Borella L, Pratt L, Pinkel D (1971) Central nervous system therapy and combination chemotherapy of childhood lymphocytic leukemia. Blood 37:272-281 - Aur RJA, Simone JV, Hustu HO, Verzosa MS (1972) A comparative study of central nervous system irradiation and intensive chemotherapy early in remission of childhood acute lymphocytic leukemia. Cancer 29:381-391 - Aur RJA, Hustu HO, Verzosa MS, Wood A, Simone JS (1973) Comparison of two methods of preventing central nervous system leukemia. Blood 42/3: 349-357 - Baum E, Sather H, Nachman J, Seinfeld J, Drivit W, Leikin S, Miller D, Joo P, Hammond D (1979) Relapse rates following cessation of chemotherapy during complete remission of acute lymphocytie leukemia. Med Pediatr Oncol 7: 25-34 - Bourke RS, West CR, Chheda G, Tower DB (1973) Kineties of entry and distribution of 5-fluoruracil in cerebrospinal fluid and brain foIIowing intravenous injection in a primate. Cancer Res 33 : 1735-1747 - Djerassi I, Farber S, Abir E, Neikirk W (1967) Continous infusion of methotrexate in children with acute leukemia. Cancer 20:233-242 - Ellison RR, Holland JF, Weil M, Jacquillat C, Boiron M, Bernard J et al. (1968) Arabinosyl cytosine: A useful agent in the treatment of acute leukemia in adults. Blood 32:507-523 - Evans AE, Gilbert ES, Zandstra A (1970) The increasing incidence of central nervous system leukemia in children (Children's cancer study group A). Cancer 26: 404-409 - Fishman ML, Bear SC, Cogan DG (1976) Opticatrophy following prophylactic chemotherapy and cranial radiation for acute lymphocytie leukemia. Am J OpthalmoI82/4:571-576 - Freeman JE, Johnson PGB, Volre JM (1973) Somnolence after prophylactic cranial irradiation in children with acute lymphocytic leukemia. Br Med J 4: 523-525 - Freeman AI, Wang JJ, Sinks LF (1977) High-dose methotrexate in acute lymphocytic leukemia. Cancer Treat Rep 61/4:727-731 - Green DM, Sather HN, Sallan SE, Nesbit ME Jr, Freeman AI, Cassady JR, Sinks LF, Hammond D, Frei E (1980) A comparison of four methods of central nervous system prophylaxis in childhood acute lymphoblastie leukemia. Lancet 1398-1402 - Haghbin M, Tan CTC, Clarkson BD et al. (1975) Treatment of acute lymphocytic leukemia in children with prophylactic intrathecal methotrexate and intensive systemic chemotherapy. Cancer Res 35:807-811 - Holland JF (1976) Oncologists reply. N Engl J Med 294: 440 - Hustu HO, Aur RJA, Verzosa MS, Simone JV, Pinkel D (1973) Prevention of central nervous system leukemia by irradiation. Cancer 32:585-597 - Jones B, Holland JF, Glidewell 0, Jacquillat C, Weil M, Pochedly C, Sinks LF, Chevalier L, et al. (1977) Optimal use of L-Asparaginase (NSC-109229) in acute lymphocytic leukemia. Med Pediatr Oncol 3: 387-400 - Kay HEM, Knapton PJ, O'SulIivan JP, Wells DG, Harris RF, Innes EM, Surart J, Schwartz FCM, Thompson EN (1972) Encephalopathy in acute leukemia associated with methotrexate therapy. Arch Dis Child 47 :344-354 - Kolmannskog S, Moe PJ, Anke IM (1979) Computed tomographie findings of the brain in children with acute lymphocytic leukemia after central nervous system prophylaxis without cranial irradiation. Acta Paediatr Scand 68: 254-256 - Land VJ, Berry DH, Herson J, Miale T, Reid H, Silva-Sosa M, Starling K (1979) Long-term survival in childhood acute leukemia: "Late" relapses. Med Pediatr Oncol 7:19-24 - Mclntosh S, Fisher D, Rothman SG, Rosenfeld N, Lebel JF, O'Brien RT (1977) Intracranial calcifications in childhood leukemia. J Pediatr 91 :909-913 - Medieal Research Council: Working party on leukemia in childhood: Treatment of acute lymphocytic leukemia: Effect of "prophylactic" therapy against central nervous leukemia. Br Med J 2:381-384 - Medieal Research Council: Working party on leukemia in chiIdhood: Analysis of treatment in childhood leukemia 1. Prolonged predisposition to drug induced neu tropenia foIIowing craniospinal irradiation. Br Med J 244: 563-566 - Medical Research Council: Working party on leukemia in childhood: Analysis of treatment in childhood leukemia IV. The critical association between dose fractionation and immunosuppression induced by cranial irradiaton. Cancer 41:108-111 - Moe PJ, Seip M (1978) High dose methotrexate in acute lymphocytic leukemia in childhood. Acta Paediatr Scan 67: 265-268 - Ochs JJ, Berger PE, Brecher ML, Sinks LF, Freeman AI (1978) Computed tomography (CT) scans in child- 106
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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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Page 53 and 54:
Treatment
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advantage in terms of duration of f
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leukaemia. An analysis of 168 patie
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11. Treatment Program Chemotherapy
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efractory congestive heart failure
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period (Sequence II) was gene rally
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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 and 106: 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: e: o e: 1. 0 ,.--...-- 1'"'\ ......
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
Page 157 and 158: followed by dialysis against isoton
Page 161 and 162: HS, HL- Heme >_ 40 0 HS I ;:. =====
Page 165 and 166: knowing at present. These genes may
Page 167 and 168: 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)
Page 271 and 272:
References Biermann E, Neth R, Gros
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ehambers, the growth pattern observ
Page 275 and 276:
References Anderssen LC, 10kinen M,
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REH CELL UNE TO CALLb~Ö ~q~ V.M. c
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Page 281 and 282:
the macrophage series in which the
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Page 285 and 286:
Table 1. Production of factor depen
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Page 289 and 290:
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
Page 299 and 300:
L (1976) Induction of colony format
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B. Materials and Methods J. Tissue
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Fig. 2. Ultrastructural appearance
Page 305 and 306:
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
Page 315 and 316:
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
Page 321 and 322:
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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Page 333 and 334:
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
Page 341 and 342:
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
Page 369 and 370:
selectively responsive to different
Page 371 and 372:
Page 373 and 374:
l1J ~ 100 ~ Q. ::) l1J Z 0 ~ z >- .
Page 375 and 376:
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
Page 383 and 384:
Haematology and Blood Transfnsion V
Page 385 and 386:
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
Page 401 and 402:
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
Page 411 and 412:
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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
Page 417 and 418:
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-
Page 423 and 424:
Page 425 and 426:
= 0.5 o E Q. o ILI 0.4 (J) « ILI .
Page 427 and 428:
Table 1. Oncogenic potential of avi
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100 III GI c: o "8 80 > w
Page 431 and 432:
Expt. No. Infecting virus Proportio
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Haematology and Blood 'fransfusion
Page 435 and 436:
sequences, provided its gag portion
Page 437 and 438:
77:3009-3013 - Hu SSF, Moscoviei C,
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RI 2.2 md and Hind III 2.6 md leuke
Page 441 and 442:
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
Page 453 and 454:
~ ..................... ~ Cell 3' 5
Page 455 and 456:
a :Sa,C! + . ~ 111 i' ( " '~ .J. b
Page 457 and 458:
Table 1 Sampie Tissue TS fragment"
Page 459 and 460:
a b Sac I / rep ._-_.-_ K J nl rep
Page 461 and 462:
Haematology and Blood 'fiansfusion
Page 463 and 464:
Osteopetrosis and osteosarcomas occ
Page 465 and 466:
Lymphoma cellline Table 1. T and B
Page 467 and 468:
Table 2. In vivo growth and oneogen
Page 469 and 470:
Page 471 and 472:
Table 1. Transforming aetivity of c
Page 473 and 474:
Table 3. Transformation aetivity of
Page 475 and 476:
- Shoemaker C, Goff S, Gilboa E, Pa
Page 477 and 478:
indieate a shifting of target eell
Page 479 and 480:
Table 2. Expression of Jl and Sourc
Page 481 and 482:
Page 483 and 484:
~ 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
Page 491 and 492:
inserts in the genome of rapidly tr
Page 493 and 494:
pulations, it seemed likely that th
Page 495 and 496:
contains antigens which react with
Page 497 and 498:
Page 499 and 500:
le of reacting in sensitive radioim
Page 501 and 502:
Page 503 and 504:
gic approach. In: Hiatt HH, Watson
Page 505 and 506:
12 Eco R [ Fig. 1. Hybridization pa
Page 507 and 508:
Page 509 and 510:
10 - '1~ )( -~ S:! E A U I o 1 2
Page 511 and 512:
Haematology and Blood 'fransfusion
Page 513 and 514:
cultures. These cells did not conta
Page 515 and 516:
indication of malignant T-cells in
Page 517 and 518:
Fig. 3. Thin-section electron micro
Page 519 and 520:
Table 3. Lack of detectable related
Page 521 and 522:
J. HTLV Was Present in the Primary
Page 523 and 524:
specific signals into nonspecific s
Page 525 and 526:
Table 2. Distribution of HTLV-relat
Page 527 and 528:
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
Page 533 and 534:
Page 535 and 536:
60 HFF/SSV cDNA CELL RNAs: 0 HF/SSV
Page 537 and 538:
Antisera a Table 1. Immunofluoresce
Page 539 and 540:
Haematology and Blood 'ftansfusion
Page 541 and 542:
y competition RIA yielded virtually
Page 543 and 544:
SiS'V' gp70: ANTIGEN, ANTI BODY, IM
Page 545 and 546:
type-C virus p30 antigen in cells f
Page 547 and 548:
c. Results The fractionated whole-b
Page 549 and 550:
induced antibodies as well as exper
Page 551 and 552:
- Fig. la-f. Retravirus particles p
Page 553 and 554:
eplication of infecting murine leuk
Page 555 and 556:
Page 557 and 558:
immunodeficiency, multic10nal lymph
Page 559 and 560:
Bovine leukemia --, proteins of 499
Page 561 and 562:
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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