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anemic WW" and SI /S 1 d mice was defective in vitro, and long-term bone marrow cultures could not be established (Dexter and Moore 1977). However, the addition of S1/S1 d marrow (with normal stern cell function) to adhere nt bone marrow monolayers of WWV (with anormal hemopoietic environment) resulted in normal long term hemopoeisis. Coculture studies were undertaken involving NZB bone marrow with either WW" or S1/S1 d marrow. The results c1early indicated that coculture of NZB and S1/S1 d marrow did not augment the in vitro replication of stern cells of either genotype, whereas coculture of NZB with WWv marrow showed long-term maintenance of stern cell production and myelopoiesis significantly in excess of that observed with marrow from either strain when cultured alone. These results point to a defect in a regulatory cell population in NZB marrow, and a defect in macrophage function has been proposed (Warner 1978). D. Conclusion The linked production of a wide spectrum of hemopoietic growth regulatory factors, as displayed by the WEHI-3 cell line, can be duplicated by pokeweed mitogen stimulation of murine spleen cells (Metcalf et al. 1978). A mitogenic stimulus, T lymphocytes, and adherent cells are required for multifactor production by spleen cells suggesting that induced lymphokines may in turn induce macrophages to elaborate the growth factors. The feature of the WEHI-3 myelomonocytic cells is their ability to produce factors constitutively and thus circumvent control networks implied by mitogen-Iymphocyte-macrophage interactions. A second feature is that the leukemic cells produce factors (G-, GM-, M CSF) to which the leukemic cells can respond by proliferation and differentiation (Metcalf and Moore 1970; Metcalf 1979). Under normal conditions the myelomonocytic progenitor cells respond to GM-CSF but do not produce it; in contrast the neoplastic myelomonocytic CFU-c of WEHI-3 (50%-100% cloning efficiency) both produce and respond to GM-CSF. In this context normal monocytes and macrophages can be induced to produce CSF and can be shown to possess receptors for CSF, since macrophage proliferation and prostaglandin synthesis can be induced by exposure of the cells to exogenous CSF (Kur land et al. 1979. Pelus et al. 1979). Individual WEHI-3 leukemic cells would appear to possess a combination of features possessed by the earliest committed progenitor cells (CFU -c) and their differentiated progeny. The association of growth factor production with the presence of growth factor receptors on the cell surface is rare among tumor cells but has been reported in the case of nerve growth factor and human melanoma cells (Sherwin et al, 1979). It is possible that this represents an opportunity for "autostimulation" of tumor cells by growth factors and may be more universally applicable as we better understand the characteristics of specific growth factors required for different tissues. The model developed by Todaro and De Larco (1978) to explain the mechanism of sarcoma virus transformation mediated by endogenous polypeptide growth stimulatory factors may equally be applicable to leukemogenesis. In this model growth factors are produced by cells that normally do not respond to their own product. Inappropriate production by a target cell of an active factor for which it also has receptors may be sufficient to stimulate cell division, and the persistent production of a growth factor may serve as a continuous endogenous stimulus leading to continued inappropriate cell growth. The inability of CFU-c from certain mouse strains to respond to G-CSF of a WEHI-3 origin may involve a defect in the CSF molecule, i.e., WEHI-3 G-CSF is a leukemic product similar but not identical to normal G-CSF. Alternatively, or perhaps in addition, an impaired G-CSF response reveals a broader defect involving growth factor receptors back as far as the pluripotential stern cello Certainly the associated abnormality of NZB, NZC, and C58 mice involving impaired stern cell replicati on in long term marrow culture would suggest a broader defect. This is supported by the in vivo evidence of multiple defects in G-CSFunresponsive mouse strains variously involving autoimmunity, endogenous xenotropic virus expression, and high leukemia incidence. References Bodel P (1978) Spontaneaus pyrogen production by mouse histiocytic and myelomonocytic tumor cell lines in vitro. J Exp Med 147:1503 - Broxmeyer HE, Ralph P (1977) Regulation of a mouse myelo- 241
monocytic leukemia cell line in culture. Cancer Res 37:3578 - Dexter M, Moore MAS (1977) In vitro duplication and "cure" of hemopoietic defects in genetieally anemic mice. Nature 269:412 - Dexter TM, Allen TD, Lajtha LG (1977) Conditions controlling the proliferation of hemopoietie stern cells in vitro. J Cell Physiol 91: 335 - Horland AA, McMarrow L, Wolman SR (1980) Growth of granulopoietie bone marrow cells of RF miee. Exp Hematol 8:1024 - Kincade PW (to be published) Hemopoietie abnormalities in New Zealand Black and Motheaten mice. In: Gershwin ME, Merchant B (eds) Laboratory animals. Plenum, New York - Kincade PW, Lee G, Fernandes G, Moore MAS, Williams N, Good RA (1979) Abnormalities in clonable B lymphocytes and myeloid progenitors in autoimmune NZB mice. Proc Natl Acad Sci USA 76:3464 - Kurland J, Moore MAS (1977) Modulation of hemopoiesis by prostaglandins. Exp Hematol 5:357 - Kurland J, Pelus L, Bockman R, Ralph P, Moore MAS (1979) Synthesis of prostagiandin E by normal and neoplastic macorohages is dependent upon colony stimulating factors (CSF). Proc Natl Acad Sei USA 76:2326-LachmanLB,HackerMP, Blyden GT, Handschumacher T (1977) Preparation of lymphocyte-activating factor from continuous murine macrophage celliines. Cell Immunol 34: 416 - Metcalf D (1979) Clon al analysis of the action of GM-CSF on the proliferation and differentiation of myelomonocytic leukemie cells. Int J Cancer 24: 616 - Metcalf D, Moore MAS (1970) Factors modifying stern cell proliferation of myelomonocytic leukemic cells in vitro and in vivo. J Natl Cancer Inst 44: 801 - Metcalf D, Moore MAS, Warner N (1969 Colony formation in vitro by myelomonocytic leukemic cells. J Natl Cancer Inst 43: 983 - Metcalf D, Parker J, Chester HM, Kincade PW (1974) Formation of eosinophiliclike granulocyte colonies by mouse bone marrow cells in vitro. J Cell Physiol84: 275 - Metcalf D, Russell S, Burgess AW (1978) Production of hemopoietic stimulating factors by pokeweed-mitogen stimulated spleen cells. Transplant Proc 10: 91 - Pelus LM, Broxmeyer HE, Kurland JI, Moore MAS (1979) Regulation of macrophage and granulocyte proliferation. J Exp Med 150:277 - Ralph P, Nakoinz I (1977) Direct toxic effects of immunopotentiators on monocytic, myelomonocytic and histiocytie or macrophage tumor cells in culture. Cancer Res 37:546 - Ralph P, Moore MAS, Nilsson K (1976) Lysozyme synthesis by human and murine histiocytie lymphoma cell lines. J Exp Med 143: 1528 - Ralph P, Nakoinz I, Broxmeyer HE, Schrader S (1977) Immunologie functions and in vitro activation of cultured macrophage tumor lines. Natl Cancer Inst Monogr 48: 303 - Ralph P, Broxmeyer HE, Moore MAS, Nakoinz I (1978) Induction of myeloid colony-stimulating activity in murine monocyte tumor cell lines by macrophage activators and in a T-cell line by concanavalin A. Cancer Res 38: 1414 - Sanel Fr (1973) Studies of neoplastic myelomonocytie cells in Balb/c mice produeing infectious C-type virus. Cancer Res 33:671 - Shah RG, Green S, Moore MAS (1978) Colony-stimulating and inhibiting activities in mouse serum after corynebacterium Parvum-endotoxin treatment. J Reticuloendothel Soc 23: 29 - Sherwin SA, Sliski AH, Todaro GJ (1979) Human melanoma cells have both nerve growth factor and nerve growth factor-speeific receptors on their cell surface. Proc N atl Acad Sci USA 76: 1288 - Todaro GJ de Larco JE (1978) Cancer Res 38:4147 - Warner NL (1978) Genetic aspects of immunologic abnormalities in New Zealand mouse strains. Arthritis Rheum 21 :5106 - Warner NL, Moore MAS (1971) Defects in hematopoietic differentiation in NZB and NZC mice. J Exp Med 134: 313 - Warner N, Moore MAS, Metcalf D (1969) A transplantable myelomonocytic leukemia in BALB/c mice: Cytology, karyotype and muramidase content. J Natl Cancer Inst 43: 963 - Williams N, Eger RR, Moore MAS, Mendelsohn N (1978) Differentiation of mouse bone marrow precursor cells into neutrophil granulocytes by an activity separated from WEHI-3 cell-conditioned medium. Differentiation 11 :59 - Williams N, Jackson HM, Eger RR, Long MW (to be published) The separate roles of factors in murine megakaryocyte colony formation. In: Levine R, Williams N, Evatt B (eds) Megakaryocytes in vitro. Elsevier North Holland, New York Oxford - Yung YP, Eger R, Tertian G, Moore MAS (1981) Long term culture of mouse mast cells. H. Purification of mast cell growth factor and its dissociation from T cell growth factor. J Imunol, in press 242
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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
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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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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),
Page 201 and 202: G, Giovanella B, Westman A, Stehlin
Page 203 and 204: Haematology and Blood Transfusion V
Page 205 and 206: Dc;bt CT + i J.I9 Raji; 1. i .. 100
Page 207 and 208: c. Discussion During infectious mon
Page 211 and 212: C. Nonepisomal Viral DNA We have us
Page 213 and 214: A 260 3.0 A B 1670 70 N2 2.0 c: E .
Page 215 and 216: vivo. Nature 260:302-306 - Kirk JTO
Page 217 and 218: Fig. 1. a Polyacrylamide gelelectro
Page 221 and 222: 1979). The lymphocyte subpopulation
Page 223 and 224: lysin 0 antigens are found, and mix
Page 225 and 226: Pope JH (1978) Long-term T cell-med
Page 227 and 228: Haematology and Blood Transfnsion V
Page 229 and 230: Charaeteristie Morphologie maturati
Page 231 and 232: after TPA-induction (Table 3). The
Page 233 and 234: PA (1978) Reactivity of a rabbit an
Page 235 and 236: Blood Monocyte. B lood Monocytes 1-
Page 239 and 240: and nonhistone proteins can serve a
Page 243 and 244: The findings of the evaluation of s
Page 245 and 246: Fig. 3. Tumor grawth of L 428 cells
Page 247 and 248: Cell biological and Immunological A
Page 249 and 250: consideration. Sanel (1973) obtaine
Page 251: endotoxin serum, were used. A parti
Page 255 and 256: B. Isolation, Characterization and
Page 259 and 260: don al hemopathies generally displa
Page 261 and 262: nitors. Blood Cells 6:595-607 - Min
Page 263 and 264: \I) ....I ....I IU Jl 200 r 100 90
Page 265 and 266: their haemopoietic cells' ability t
Page 267 and 268: normal normal ALL ALL ALL persons p
Page 269 and 270: 64.5 { V)
Page 271 and 272: References Biermann E, Neth R, Gros
Page 273 and 274: ehambers, the growth pattern observ
Page 275 and 276: References Anderssen LC, 10kinen M,
Page 277 and 278: REH CELL UNE TO CALLb~Ö ~q~ V.M. c
Page 281 and 282: the macrophage series in which the
Page 285 and 286: Table 1. Production of factor depen
Page 289 and 290: Table 1. Characteristics of the adh
Page 291 and 292: Fig. 3. A human marrow culture at 6
Page 293 and 294: 300 250 • HYPERPROLIFERATIVE PATT
Page 295 and 296: 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
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Page 307 and 308:
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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
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
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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 .
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
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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
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
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~ ..................... ~ Cell 3' 5
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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
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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:
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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
Page 479 and 480:
Table 2. Expression of Jl and Sourc
Page 481 and 482:
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~ i ,..1---------,,':::::::::::::::
Page 485 and 486:
fragment of pBR322 DNA, a 3.0-kbp S
Page 487 and 488:
Mak TW (1979) Proc Natl Acad Sci US
Page 489 and 490:
Table 1. Transformation of 3T3 cell
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inserts in the genome of rapidly tr
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pulations, it seemed likely that th
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contains antigens which react with
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Page 499 and 500:
le of reacting in sensitive radioim
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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
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
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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
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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