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that in addition to the LTR, MSV sequences immediatly preceeding V-mos are required for transformation (McClements et al. 1980). However, the data do not rule out the possibility that the mere removal of these cellular sequences allows transformation by C-mos. There may be controlling cellular sequences preceeding C-mos that block its expression. The activation of C-mos in clone pTS 1 is consistent with this interpretation if (1) the LTR sequences override the cellular control elements or (2) the putative controlling cellular sequences are more than approximately 600 bp before C-mos. The latter possibility suggests that removing normal cell sequences 5' to C-mos should activate its malignant potential in the transfection assay. Indeed, this is consistent with the model proposed by Cooper et al. (1980) to explain the transforming activity of normal cellular DNA after shearing. Because the LTR is directly repeated at both ends of the provirus it could be expected to allow transcription to occur from the 3' LTR into the cell genome. Thus, random integration of retroviruses into multiple sites in the host cell genome (see Weinberg 1980 for review) could result in the activation of normally quiescent cell genes. For example, 17 out of 19 tumors isolated from birds infected with avian leukosis virus show evidence for activation of expression of normal cell sequences by LTR sequerices (Hayward et al. this volume). The loss of almost all of the retrovirus genome in so me of the tumors, except for a residual LTR, could mean that LTR-promoted expression of normal cell sequences is responsible for the disease. Certainly in this case all other avian leukosis viral genes can be excluded. We have shown with pTS 1 (Table 3) that a single LTR which is linked 5' to C-mos activates transformation. This in vitro construction is analogous to a retrovirus integrating 5' (upstream) to anormal cell sequence (e.g., C-mos) in vivo, whereby the 3' LTR could activate expression of this sequence and cause transformation. This may be a useful model for other (nonviral) forms of transformation. Normal cellular sequences with functional properties of an LTR (e.g., an eukaryotic IS element) could become juxtaposed to quiescent cellular genes with transformation potential as a result of either chemically induced, radiation induced, or simply spontaneous genomic arrangements. References Aaronson S, Canaani E, Robbins K, Andersson P, Tronick S (to be published) Cellular origin of the transforming gene of Moloney murine sareoma virus. Cold Spring Harbor Symp Quant Biol 44 - Andersson P, Goldfarb MP, Weinberg (1979) A defined subgenomie fragment of in vitro synthesized Moloney sareoma virus DNA ean induee eell transformation upon transfeetion. Cell 16: 63-75 - Blair DG, MeClements W, Oskarrson M, Fisehinger P, Vande Woude GF (1980) The biological aetivity of c10ned Moloney sareoma virus DNA: terminally redundant sequenees may enhanee transformation efficieney. Proe Natl Aead Sei USA 77 :3504-3508-BukhariAI, ShapiroJA,AdhyaSL (eds) (1977) DNA insertion elements, plasmids and episomes. Cold Spring Harbor Laboratory, New York - Canaani E, Robbins KC, Aaronson SA (1979) The transforming gene of Moloney murine sareoma virus. Nature 282: 378-383 - Cooper GM, Okenquist S, Silverman L (1980) Transforming aetivity of DNA of ehemically transformed and normal eells. Nature 284:418-421 - Dhar R, MeClements W, Enquist LW, Vande Woude GF Nuc1eotide sequenees of integrated Moloney sareoma virus Long Terminal Repeats and their host and viral junetions. Proe N atl Aead Sei USA 77:3937-3941- GrahamFL, van der Eb AJ (1973) A new teehnique for the assay of infeetivity of human adenovirus 5 DNA. Virology 52: 456-467 - Lowy DR, Rands E, Seolniek EM (1977) Helper independent transformation by unintegrated Harvey sareoma virus DNA. J ViroI26:291-298 - MeClements WL, Blair DG, Oskarsson M, Vande Woude GF (1980) Two regions of the Moloney leukemia virus genome are required for effieient transformation by sre/sare. In: Fields B, Jaeniseh R, Fox C (eds) Animal virus geneties ICN-UCLA symposia on moleeular and eellular biology. Aeademic Press, New York - MeClements WL, Dhar R, Blair DG, Enquist LW, Oskarsson M, Vande Woude GF (to be published a) The terminal repeats of integrated Moloney sareoma provirus are like baeterial insertion sequenee (IS) elements. Cold Spring Harbor Symp Quant Biol 45 - MeClements WL, Enquist LW, Oskarsson M, Sullivan M, Vande Woude GF (to be published b) Frequent site-speeifie deletion of eoliphage ?.murine sareoma virus recombinants and its use in the identifieation of a retrovirus integration site. J Virol 35 - Oskarsson M, MeClements WL, Blair DG, Maizel JV, Vande Woude GF (1980) Properties of a normal mouse eell DNA sequenee (sare) homologous to the sre sequenee of Moloney sareoma virus. Scienee 207: 1222-1224 - Sherr CJ, Fedele LA, Oskarsson M, Maizel J, Vande Woude GF (1980) Moleeular cloning of Snyder-Theilen feline leukemia and sareoma viruses: eomparative studies of feline sarcoma virus with its natural helper and Moloney sareoma virus. J Virol 24:200-212 465
- Shoemaker C, Goff S, Gilboa E, Paskind M, Mitra SW, Baltimore D (to be published) Structure of a cloned eircular Moloney murine leukemia virus DNA moleeule containing an inverted segment: implications for retrovirus integration. Proc Natl Acad Sei USA 77 - Vande Woude GF, Oskarsson M, Enquist LW, Nomura S, Sullivan M, Fischinger PJ (1979) Cloning of integrated Moloney sarcoma virus proviral DNA sequences in bacteriophage A. Proc Natl Acad Sei USA 76:4464-4468 - Vande Woude GF, Oskarsson M, McClements WL, Enquist LW, Blair DG, Fischinger PJ, Maizel J, Sullivan M (to be published) Characterization of integrated Moloney sarcoma proviruses and flanking host sequences c10ned in bacteriophage A. Cold Spring Harbor Symp Quant Biol 44 - Weinberg RA (1980) Integrated genomes of animal viruses. Ann Rev Biochem 49:197-226 466
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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),
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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
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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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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-
Page 423 and 424: Haematology and Blood Transfusion V
Page 425 and 426: = 0.5 o E Q. o ILI 0.4 (J) « ILI .
Page 427 and 428: Table 1. Oncogenic potential of avi
Page 429 and 430: 100 III GI c: o "8 80 > w
Page 431 and 432: Expt. No. Infecting virus Proportio
Page 433 and 434: Haematology and Blood 'fransfusion
Page 435 and 436: sequences, provided its gag portion
Page 437 and 438: 77:3009-3013 - Hu SSF, Moscoviei C,
Page 439 and 440: RI 2.2 md and Hind III 2.6 md leuke
Page 443 and 444: RELATIONSHIP OF ENDOGENOUS AND EXOG
Page 445 and 446: E ........ E Cl. U E :::l .... Q) (
Page 447 and 448: References Astrin S (1978) Endogeno
Page 449 and 450: the same animal were examined (e.g.
Page 451 and 452: I) 'IQ a \0 - CL -- Fig. 2. Restrie
Page 453 and 454: ~ ..................... ~ Cell 3' 5
Page 455 and 456: a :Sa,C! + . ~ 111 i' ( " '~ .J. b
Page 457 and 458: Table 1 Sampie Tissue TS fragment"
Page 459 and 460: a b Sac I / rep ._-_.-_ K J nl rep
Page 461 and 462: Haematology and Blood 'fiansfusion
Page 463 and 464: Osteopetrosis and osteosarcomas occ
Page 465 and 466: Lymphoma cellline Table 1. T and B
Page 467 and 468: Table 2. In vivo growth and oneogen
Page 471 and 472: Table 1. Transforming aetivity of c
Page 473: Table 3. Transformation aetivity of
Page 477 and 478: indieate a shifting of target eell
Page 479 and 480: Table 2. Expression of Jl and Sourc
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 499 and 500: le of reacting in sensitive radioim
Page 503 and 504: gic approach. In: Hiatt HH, Watson
Page 505 and 506: 12 Eco R [ Fig. 1. Hybridization pa
Page 509 and 510: 10 - '1~ )( -~ S:! E A U I o 1 2
Page 511 and 512: Haematology and Blood 'fransfusion
Page 513 and 514: cultures. These cells did not conta
Page 515 and 516: indication of malignant T-cells in
Page 517 and 518: Fig. 3. Thin-section electron micro
Page 519 and 520: Table 3. Lack of detectable related
Page 521 and 522: J. HTLV Was Present in the Primary
Page 523 and 524: specific signals into nonspecific s
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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
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
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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
Page 555 and 556:
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immunodeficiency, multic10nal lymph
Page 559 and 560:
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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