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Total 75 Hb E 30.3pg Sex 33M/42F Leukocytes 3.9 X 10 3 fll age 66 years Neutrophils 47% ESR 28/89 (Westergren) Monocytes 3% Erythrocytes 3.0 X 10 6 /fll Platelets 141 X 10 3 fll Hemoglobin 9.1g/dl Table 2. Clinical findings in 75 patients with myeloid dysplasia (MD) at the time of their first biopsy (median values) Maldonado et al. 1976) as weH as the frequent pseudo-Pelger forms (Linman and Bagby 1978), results which in the majority are derived from aspirates of the bone marrow. These morphological atypia account for the functional disturbances of colony formation and iron metabolism as demonstrated in "preleukemic" states by several authors (Golde and Gline 1973; Senn et al. 1976; Hast and Reizenstein 1977; Koeffler 1978). Cytogenetic studies may be of a major value to establish or confirm the diagnosis of a possible preleukemic conditi on as shown by Pierre (1978) and our findings of a Philadelphia-chromosome occurring before obvious CML in four cases (Thiele et al., 1979). References Dreyfus B (1976) Preleukemic states. 1. Definition and classification. H. Refractory anemia with a excess of myeloblasts in the bone marrow (smoldering acute leukemia). Blood Cells 2: 33-55 - Fisher WB, Armentrout SA, Weisman R, Graham RC (1973) "Preleukemia" A myelodysplastic syndrome often terminating in acute leukemia. Arch Intern Med 132:226-232 - GeorgiiA (1979) Histopathologyof bone marrow in human chronic leukemias. In: Neth, R (eds) <strong>Modern</strong> trends in human leukemias IH. Berlin Heidelberg New York, Springer, pp 60-70 - Golde DW, Cline MJ (1973) Human preleukemia. Identification of a maturation defect in vitro. N Engl J Med 28821: 1083-1086 - Hast R, Reizenstein P (1977) Studies on human preleukaemia. 1. Erythroblast and iron kinetics in aregenerative anaemia with hypercellular bone marrow. Scand J Haematol 19:347-354 - Koeffler HP, Golde DW (1978) Cellular maturation in human preleukemia. Blood 52:355-361-LinmanJW,BagbyGC (1978) Preleukemic syndrome (hemopoietic dysplasia). Cancer 42: 854-864 - Maldonado JE, Maigne J, Lecoq D (1976) Comparative electronmicroscopic study of the erythrocytic line in refractory anemia (preuleukemia) and myelomonocytic leukemia. Blood Cells 2: 167-185 - Pierre RV (1978) Preleukemic syndromes Virchows Arch [Cell Pathol] 29:29-37 -Saarni, MI, Linman, JW (1973) Preleukemia. The hematologic syndrome preceding acute leukemia. Am J Med 55 :38-48 -SennJS, Price GB, Mak TW, McCulloch EA (1976) An approach to human preleukemia using cell culture studies. Blood Cells 2: 161-166 - Thiele J, Vykoupil KF, Georgii A (1979) Präleukämien : Knochenmarks- und Chromosomenbefunde zum Versuch einer Definition. Verh. Dtsch Ges Path f 63:372-379 - Thiele J, Vykoupil KF, Georgii A (1980a) Myeloid dysplasia (MD): A hematological disorder preceding acute and chronic myeloid leukemia. A morphological study on sequential core biopsies of the bone marrow in 27 patients. Virchows Arch, A, [Pathol Anat] 389:343-367 - Thiele J, Vykoupil KF, Perschke B, Babilas J, Török M, Krmpotic E, Bodenstein H, Georgii A (to be published b) Preleukaemic lesions of the bone marrow or myeloid dysplasia (MD): Morphological and clinical features in a combined retro- and prospective study of 93 patients. 37
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 Progress in Acute Myeologenous Leukemia T. A. Lister, S. A. N. Johnson, R. Bell, G. Henry, andJ. S. Malpas A. Introduction Experimental and potentially life threatening combination ehemotherapy has been used for the induetion of remission of aeute myelogenous leukaemia (AML) for a little over 10 years. During that time the proportion of patients ente ring remission has risen from less than a quarter to approaehing three-quarters. Furthermore, there is now evidence to suggest that about one-fifth of those now entering remission will remain disease free for more than 3 years and be "at risk for eure". Between 1969 and 1980 588 eonseeutive adults with AML were treated at St. Bartholomew's Hospital, 443 of them in prospeetive trials. Selected data from these studies, which have been reported in part elsewhere (Crowther et al. 1973; Powles et al. 1977; Lister et al. 1980) are presented to illustrate what has been learnt during the last deeade and to provide a new base line, instead of the natural history of the disease, with whieh to compare future studies. 11. Treatment Programmes Three generations of combination chemotherapy experiments have been undertaken since 1969: in each of them cytosine arabinoside and an anthracycline antibiotic have been the central component of the treatment. At the outset, adults of all ages were treated the same (Trials I, II, III). For the duration of Trials IVA-VIII patients of more than 60 years of age were treated in a separate programme (Trial IVB). This policy was reversed in 1978 at the beginning of Trial IX, since which time adults of all ages have received the same initial therapy. Antibio- Table 1. Patient details. n = 443; Sex M: F = 243: 200 Age Range 14-77years Mean 49years Median 53years Platelet count Range 5-704 Mean 69.89 Median 45 Blast count Range 0-495.0 Mean 29.76 Median 3.8 B. Materials and Methods Table 2. Morphological variants I. Patients Five hundred and eighty-eight consecutive adults were treated for AML at St. Bartholomew's Hospital between June 1969 and July 1980. Four hundred and forty-three were treated on prospective trials of combination chemotherapy. Exclusions from the trials were made because of advanced age and extensive prior chemotherapy. No patient under the age of 60 years who had not received therapy was excluded. Clinical details of the patients entered in to the different trials are shown in Tables 1-3. 38 FAB classification MI M2 M3 M4 M5 M6 Total No. of patients 108 109 27 138 39 22 443
Page 1 and 2: Haematology and Blood Transfusion 2
Page 3 and 4: Dr. Rolf Neth, Universitäts-Kinder
Page 5 and 6: Participants of the Meeting Aaronso
Page 7 and 8: Kurth, R, Friedrich-Miescher-Labora
Page 9 and 10: Wilsede Scholarship Holders (Grante
Page 11 and 12: Preface Gut ist eine Lehrart, wo ma
Page 13 and 14: Personal and scientific discussion
Page 15 and 16: Acknowledgement We should like to t
Page 17 and 18: Wilsede, June 21 1978 Memorial Trib
Page 19 and 20: limiting benign lymphoproliferative
Page 21 and 22: this most unlikely, however (for re
Page 23 and 24: longer subject to the same control
Page 25 and 26: Bregula U, Wiener F, Harris H (1971
Page 27 and 28: fresh lymph node biopsies from ten
Page 29 and 30: Fig. 3. Binucleate mitosis in an ob
Page 31 and 32: y Fig. 4. Schematic diagram of post
Page 33 and 34: than that among patients with Stage
Page 35 and 36: Tests of binding affinity, agglutin
Page 37 and 38: N Engl J Med 297: 963-968 - Green I
Page 39 and 40: Clinical Aspects
Page 41 and 42: "ring chromosome". "Mar" is marker,
Page 43 and 44: 191 chromosomally abnormal patients
Page 45 and 46: tumors of both African and non-Afri
Page 47 and 48: Haematology and Blood Transfusion V
Page 49: Retrospective group 26/93 evolved l
Page 53 and 54: 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
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R GROUP 1 ( 1970 - 1971 ) 17 PTS. R
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Table 3. Influence of initial featu
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LIJ (f) a.. < -1 LIJ Q: u. 0 >- I-
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Haematology and Blood Transfusion V
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me nt indicated that additional the
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42:2123-2134 - Chessells JM, Cornbl
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Baum et al. 1979). This study was b
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1. 0 '--'1--" 0.9 e: o .- VI VI E C
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e: o e: 1. 0 ,.--...-- 1'"'\ ......
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In conclusion, we can state that th
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Haematology and Blood Transfnsion V
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INDUCTION VCR + PRED + ASNASE (wk 3
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SCHED.INT 1 MTX • ! Adria MTX •
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~ looh---------ooooc>----o---c>----
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Consoll- Irra .tlon t) .tlon Indu
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Highrisk Standard risk Table 1. Cli
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Cumulo/ive comp/el9 remission 1.0 .
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10° 8 = 6 ö 4 Non T Cell .~ :ö
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% SURVIVAL 100 ~ ~II 0 80 60 40 - -
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a) Percentage of donor cell mitoses
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Table 5. Results of bone marrow tra
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...... w N Table 7. Clinical result
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agent had to be added and that in t
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C. Chronic Myelogenous Leukemia The
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Patients with a suitable donor rece
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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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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
Page 297 and 298:
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
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
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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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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
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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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Page 373 and 374:
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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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
Page 435 and 436:
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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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
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"
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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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Page 471 and 472:
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:
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
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inserts in the genome of rapidly tr
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pulations, it seemed likely that th
Page 495 and 496:
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
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SSV TrS-gp labeled effectively with
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60 HFF/SSV cDNA CELL RNAs: 0 HF/SSV
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Antisera a Table 1. Immunofluoresce
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Haematology and Blood 'ftansfusion
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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
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Haematology andBlood Transfusion Su
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