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should not have become resistant to therapy. Moreover, previous experience had shown that patients in good clinical condition and with good blood cell values at the time of transplantation had a much better chance of surviving the transplantation procedure. nonlymphoblastic leukemia in first remission have been confirmed by reports from the marrow transplant teams at the City of Hope in Duarte, California (Blume et al. 1980) and at the Royal Marsden Hospital in Sutton, Surrey, England (Powies et al. 1980a). A. Acute Nonlymphoblastic Leukemia in First or Subsequent Remission Patients with acute nonlymphoblastic leukemia have a poor prognosis with chemotherapy. The median duration of the first remission is approximately one year and onyl15 %-20% of the patients are alive at 3 years. A Kaplan Meier plot of survival with a logarithmic ordinate for the fraction of patients surviving usually shows no evidence of a plateau (Powies et al. 1980b). Our past observation that marrow transplantation could lead to an operational cure of 13 % of end stage refractory patients made it ethically acceptable to consider marrow grafting for acute nonlymphoblastic leukemia in first remission. The first 19 patients were transplanted between March 1976 and March 1978 at a median of4months following initial treatment or 21/2 months following the achievement of the first complete remission (Thomas et al. 1979b). Of the 19 patients, 12 are alive in continued unmaintained remission with a functioning marrow graft between 27 and 48 months after transplantation. Nine of the twelve are entirely weIl, while three have mild chronic graft-vs-host disease with Karnofsky performance scores of 80%-90%. A Kaplan-Meier plot of the probability of survival shows a plateau at 65 % with the long-term survivors far out on the plateau and presumably cured of their disease. Six of the nineteen patients died from graft-vshost disease and/or interstitial pneumonia. Of particular interest is the fact that only 1 of the 19 patients has had a recurrence of leukemia. Forty-eight patients have now been transplanted in first remission, and again recurrence has been limited to that single patient. Evidently the chemo-radiotherapy regimen used is capable of eradicating the leukemic cell population in most of these patients. In contrast, patients grafted in second remission have a leukemic recurrence rate of 35%. More recently, the Seattle results in acute B. Acute Lymphoblastic Leukemia in Second or Subsequent Remission Approximately 50% of the patients with acute lymphoblastic leukemia, particularly children, can be cured by combination chemotherapy. However, once marrow relapse has occurred, only 5 % of the patients treated with conventional chemotherapy are alive at 2 years after relapse (Chessels and Cornbleet 1979). Transplantation of patients with this disease in second or subsequent remission would entail the risk of losing some of them early after grafting due to grafts-vs-host disease and/or infections. However, this risk seemed acceptable if other patients could be "cured" of their disease. The first 22 patients were graf ted between April 1976 and December 1977 (Thomas et al. 1979a). Three patients died of interstitial pneumonia within three months of transplantation. Eleven patients died of recurrent leukemia within 27 months of grafting. The latest relapse was in the central nervous system of a patient who had active central nervous system leukemia at the time of grafting. The median survival of this group of transplanted patients was 1 year compared to the 6-8 months usually observed after combination chemotherapy. Eight patients are surviving between 32-41 months after transplantation in unmaintained remission. Seven of the eight are without problems and one has moderately severe chronic graft-vs-host disease with a Karnofsky performance score of 70%. It is clear that recurrent leukemia was the major problem in patients with acute lymphoblastic leukemia transplanted in second or subsequent remission. These recurrences were in cells of host type indicating that the conditioning regimen was ineffective in eradicating residual leukemic cells in approximately 50% of the patients. Further improvement in survival in patients with acute lymphoblastic leukemia hinges on the development of new preparative regimens. 137
C. Chronic Myelogenous Leukemia The Seattle team has carried out six marrow grafts from monozygous twins for chronic myelogenous leukemic in blast crisis and one of these patients continues to be in unmaintained remission with disappearance of the Philadelphia chromosome 53 months after transplantation. Four of 22 patients with chronic myelogenous leukemia in blast crisis treated by marrow grafts from HLA identical siblings are alive in unmaintained remission 8, 15,27, and 31 months after grafting, while the remainder died either of transplantation associated complications of recurrent blast crisis. In an attempt to improve the results in patients with chronic mye1ogenous leukemia, a study was initiated during the chronic phase of the disease for those patients who had a healthy monozygous twin (Fefer et al. 1977). The objective was to eradicate the Philadelphia chromosome positive clone by chemotherapy and total body irradiation and, thus, to prevent the transformation into blast crisis and cure the disease. An initial group of four patients was treated with a combination of dimethylbusulfan, cyclophosphamide, and total body irradiation followed by marrow infusion. Complete hematologic and cytogenetic remissions were induced in all four. One patient has relapsed 30 months after transplantation and is now back in the original state of chronic myelogenous leukemia. The other three are clinically, hematologically, and cytogenetically normal 36, 39, and 44 months after transplantation. It is possible that the Philadelphia chromosome positive clone has been eradicated. Obviously a longer follow-up of these three patients and of seven similar patients grafted since the initial report is in order. References Blume KG, Beutler E, Bross KJ, Chillar RK, Ellington OB, Fahey JL, Farbstein MJ, Farman SJ, Sehmidt GM, Seott EP, Spruee WE, Turner MA, Wolf JL (1980) Bone marrow ablation and allogeneic marrow transplantation in aeute leukemia. N Engl J Med 302: 1041-1046 - Chessels JM, Cornbleet M (1979) Combination ehemotherapy for bone marrow relapse in ehildhood lymphoblastie leukemia (ALL). Med Pediatr Oneol 6: 359-365 - Fefer A, Buekner CD, Thomas ED, Cheever MA, Clift RA, Glueksberg H, Neiman PE, Storb R (1977) Cure of hematologic neoplasia with transplantation of marrow from identieal twins. N Engl J Med 297:146-148 - Fefer A, Cheever MA, Thomas ED, Boyd C, Ramberg R, Glueksberg H, Buekner CD, Storb R (1979) Disappearanee of PhI-positive eells in four patients with ehronie granuloeytie leukemia after chemotherapy, irradiation and marrow transplantation from an identieal twin. N Engl J Med 300:333-337 - Powles RL, Morgenstern G, Clink HM, Hedley D, Bandini G, Lumley H, Watson JG, Lawson D, Spenee D, Barrett A, Jameson B, Lawler S, Kay HEM, MeElwain TJ (1980a) The place of bone-marrow transplantation in aeute myelogenous leukemia. Lancet I: 1047-1050 - Powles RL, Palu G, Raghavan D (1980b) The eurability of acute leukemia. In: Roath S (ed) Topical review of haematology. Wright, London, pp 186-219 - Thomas ED, Buekner CD, Banaji M, Clift RA, Fefer A, Flournoy N, Goodell BW, Hickman RO, Lerner KG, Neiman PE, Sale GE, Sanders JE, Singer J, Stevens M, Storb R, Weiden PL (1977a) One hundred patients with acute leukemia treated by chemotherapy, total body irradiation, and allogeneic marrow transplantation. Blood 49:511-533 - Thomas ED, Flournoy N, Buekner CD, Clift RA, Fefer A, Neiman PE, Storb R (1977b) Cure of leukemia by marrow transplantation. Leuk Res 1: 67-70 - Thomas ED, Sanders JE, Flournoy N, Johnson FL, Buekner CD, Clift RA, Fefer A, Goodell BW, Storb R, Weiden PL (1979a) Marrow transplantation for patients with acute lymphoblastie leukemia in remission. Blood 54:468-476 - Thomas ED, Buckner CD, Clift RA, Fefer A, Johnson FL, Neiman PE, Sale GE, Sanders JE, Singer JW, Shulman H, Storb R, Weiden PL (1979b) Marrow transplantation for aeute nonlymphoblastic leukemia in first remission. N Engl J Med 301:597-599 - Weiden PL, Flournoy N, Thomas ED, Prentice R, Fefer A, Buekner CD, Starb R (1979) Antileukemie effeet of graft-versus-host disease in human recipients of allogeneie marrow grafts. N Engl J Med 300: 1068-1073 138
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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
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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
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DAYS 1 5 10 15 20 25 30 35 , I I I
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Biologically Drug Outcome fit" sens
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may counterbalance the potential be
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Ht (0--0) 50 40 30 20 10 0 Platelet
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10 7 ,-----------------------------
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11. Haematological and Biochemical
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0\ 0\ INTERFERON ... 10 3 rl E "'
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("pre-B" phenotype) has been descri
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human bone marrow cells exhibit the
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10 9.,0 MBKCC .. .,4 B prot:oool 1'
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demann W, Büehner T, Arlin Z, Gee
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-...l 00 a-tLDRENS CAt«:ER S TU>Y
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prognostic characteristics under in
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significantly higher in HR} (14.5%,
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normal or elevated immunoglobulin l
Page 99 and 100: References Andreeff M, Darzynkiewic
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Page 103 and 104: Table 3. Influence of initial featu
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Page 107 and 108: Haematology and Blood Transfusion V
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
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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
Page 169 and 170: a DNA probe specific for the gene t
Page 171 and 172: translocation between chromosomes 9
Page 173 and 174: Table 1. Subdivision of 1827 Myelo-
Page 175 and 176: NORMAL CELL ®
Page 177 and 178: some change of the primary type, in
Page 181 and 182: F. Transformation of Mouse Bone Mar
Page 185 and 186: were carried out with 3H-MTX in the
Page 189 and 190: the lysozyme cDNA prepared from ovi
Page 193 and 194: et al. 1976). The BJAB cellline in
Page 195 and 196: dalton bands corresponding to light
Page 197 and 198: 1979). The EBV-carrying cell lines
Page 199 and 200: 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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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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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:
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" 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
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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
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E ........ E Cl. U E :::l .... Q) (
Page 447 and 448:
References Astrin S (1978) Endogeno
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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"
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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---------,,':::::::::::::::
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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
Page 507 and 508:
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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
Page 519 and 520:
Table 3. Lack of detectable related
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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
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u 10 ~ 20 ~ :c 30 a 40 o Fig. 1. Ki
Page 529 and 530:
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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
Page 539 and 540:
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
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:
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immunodeficiency, multic10nal lymph
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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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