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Fig. la,b. Survey of myeloid dysplasia in semit hin seetions of plastic embedded trephine biopsies. a Low magnification with patchy edema of the stroma (Ed), a macrocytic/ megaloblastoid erythropoiesis (E), abnormal megakaryopoiesis (M) and dispersed neutrophilic granulopoesis (G). b The higher magnification shows the prominent megaloblastoid differentiation of erythropoiesis (E). a X 234, bX256 Statistical evaluation of principle hematological data showed that median values of the retrospective group - regardless wether AML or CML was the evolving disease - and the prospective group showed no significant differences (for details see Thiele et al. , to be published b). Median values of these data accompanying MD of 75 patients (retrospective and prospective group) are listed in Table 2. Our results demonstrate that common morphological alterations exist in the bone marrow before onset of AML and CML and that they are associated with a normochromic anemia and a slight to moderate pancytopenia of the peripheral blood count. The clinical as weIl as statistical evaluation of our retrospective and prospective groups of patients confirms this statement (Thiele et al. , to be published b). The term "preleukemia" should therefore be replaced by MD, which does not necessarily imply evolution towards leukemia in every case but refers also to CML. Hemopoietic dysplasia as proposed by Linman and Bagby (1978) only pertains to the hematopoietic cells and does not include the changes of the mesenchymal cells and stroma nor the development of chronic myeloproliferative disorders such as CML. The maturation defects of erythro- and granulopoiesis are in agreement with the megaloblastoid differention observed in aplastic or so-called iron refractory anemia or preleukemia (Saarni and Linman 1973; 35
Retrospective group 26/93 evolved leukemia with the following histological categories: AML CML CML with blastic crisis 11 9 6 26 Prospective group 0 / 67 Deadline of this study was 1 February 1980; no leukemia among the 67 patients observed so far - Table 1. 93 patients who showed myeloid dysplasia (MD) in the first and initial biopsy of the bone marrow Fig. 2a-c. Conspicuous abnormalities in myeloid dysplasia. a Megaloblasts with linear deployment along a sinus wall and a so-called Pelger form of neutrophils (arrow head, see below). b Atypia of neutrophilic granulopoesis with hyposegmentation of nuc1ei associated with mature cytoplasm (pseudo Pelgerforms, arrow heads). Megakaryopoiesis (M) with immature forms and micromegakaryocytes (mM). There is also also a patchy edema of the stroma (Ed). c Perivascular plasmacytosis along a marrow capillary with lumen (L) and prominent endothelial cells surrounded by edema (Ed). a-cx792 36
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: Haematology and Blood Transfusion V
Page 51 and 52: Haematology and Blood Transfusion V
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
Page 101 and 102:
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
Page 109 and 110:
me nt indicated that additional the
Page 111 and 112:
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
Page 173 and 174:
Table 1. Subdivision of 1827 Myelo-
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NORMAL CELL ®
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some change of the primary type, in
Page 179 and 180:
Page 181 and 182:
F. Transformation of Mouse Bone Mar
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were carried out with 3H-MTX in the
Page 187 and 188:
Page 189 and 190:
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
Page 197 and 198:
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
Page 241 and 242:
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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
Page 257 and 258:
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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
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
Page 297 and 298:
The cobblestone areas were often no
Page 299 and 300:
L (1976) Induction of colony format
Page 301 and 302:
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
Page 311 and 312:
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
Page 323 and 324:
Functional studies of UCHT1 separat
Page 325 and 326:
Page 327 and 328:
40 ,...... (5 L.. C o u 30 .9 ~ .~
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with immunohistochemieal methods (L
Page 331 and 332:
Page 333 and 334:
can be dissected by cloning. Utiliz
Page 335 and 336:
Table 1. Origin and marker profile
Page 337 and 338:
Page 339 and 340:
complete identity of gp 100 from no
Page 341 and 342:
Table 1. Reaction of single anti se
Page 343 and 344:
Page 345 and 346:
media. Following 24-h incubation, c
Page 347 and 348:
nonleukemic eells (Greaves 1979). L
Page 349 and 350:
Page 351 and 352:
Fig. 2. Cytocentrifuged smears of b
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Modification of amino-groups of hum
Page 355 and 356:
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
Page 367 and 368:
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
Page 377 and 378:
Reverse Infectious ASC/2X1Q6 transc
Page 379 and 380:
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munized animals to 1316 tumor cells
Page 383 and 384:
Page 385 and 386:
Fig. 3. Expression of retroviral gp
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pg70. J Exp Med 143: 151-166 - McGr
Page 389 and 390:
Table 1. Expression of tumor antige
Page 391 and 392:
Virological and Molecularbiological
Page 393 and 394:
Table 1. Oncogenic properties of re
Page 395 and 396:
also Fig. 1). It followed that the
Page 397 and 398:
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
Page 409 and 410:
.. 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
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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 .
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
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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
Page 453 and 454:
~ ..................... ~ 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
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
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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:
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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
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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
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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
Page 547 and 548:
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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