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found in RSV or in avian acute leukemia virus es AEV, MC29, or MH2. Cells transformed by PRell were labeled with [3 2 P]orthophosphate (1 mCi/ml) and followed by analysis by immunoprecipitation with anti-virion sera. Electrophoresis and autoradiography indicated that p105 was heavily phosphorylated. This degree of phosphorylation was greater than could be accounted for by the presence of the phosphorylated gagprotein p 19 in p 1 05. The most abundant phosphoamino acid in p 1 05 was tyrosine. These observations suggest that p105 is phosphorylated in its non-gag portion, probably at one or several tyrosine residues. In order to test for phosphokinase activity associated with p105, immunoprecipitates were incubated with [3 2 p]ATP according to published procedures before immunoprecipitation, electrophoresis, and autoradiography. Under these conditions both p105 and the heavy chain of IgG were phosphorylated. We suggest that p105 is a phosphoprotein with associated kinase activity capable of autophosphorylation and of phosphorylating homologous IgG. et al. 1981). Since the latter sequences have been detected in normal feline cells where they code for a eellular protein homologue (Barbaeid et al. 1981) one ean expect [ps to be also cell derived. The transformation-specifie polyproteins of FSV, Y73, PRell, and feHne sarcoma virus are all phosphorylated and show phosphokinase aetivity. The predominant phosphoacceptor for these polyproteins is tyrosine (Hanafusa et al. 1980; Kawai et al. 1980; Neil et al.1981; Barbacid et al. 1980). For PRell and the Snyder-Theilen strain of feHne sareoma virus it has also been shown that phosphotyrosine levels in transformed eells are substantially inereased over normal eells (Barbacid et al. 1980; K. Beemon 1980, personal eommunication). Phosphorylation and kin ase activity are also charaeteristic of p60 src , and cells transformed by RSV contain elevated levels of phosphotyrosine (Collett and Erikson 1978; Levinson et al. 1978; Hunter and Sefton 1980). These paralleis suggest that even though sarcoma viruses may carry different transforming genes, the meehanisms of viral sarcomagenesis could share common elements in protein function and eellular targets. D. Discussion PRell is a representative of a new dass of avian sarcoma viruses that lack src, have a genetic structure similar to avian acute leukemia viruses, and code for a transformation-specific gag-related polyprotein. Other members of this dass are FSV and avian sarcoma virus Y73 (Hanafusa et al. 1980; Kawai et al. 1980; Lee et al. 1980). FSV and Y73 have been shown to contain a small (26 S) RNA genome. Our preliminary data suggest that the genome of PRCII has also a size of about 26 S. PRell and FSV habe some common transformation-specific sequences as detected by nudeic acid hybridization (Shibuya et al. 1980), and the proposal has been made to refer to these sequences as [ps (FSV, PRClI Sarcoma) (J. Coffin et al. to be published). Y73 appears to have no appreciable sequence relations hip in its transformation-specific information to either PRell, FSV, or RSV (Shibuya et al. 1980; M. Yoshida et al. 1980, personal communications). The transformation-specific sequences of FSV have also been found to be related to those of the Snyder Theilen and Gardner-Arnstein strains of feline sarcoma virus (Shibuya et al. 1980; Barbacid Acknowledgment Supported by U.S. Public Health Service Research Grants No. CA 13213 and 19725 awarded by the National Cancer Institute. References Barbaeid M, Beemon K, Devare SG (1980) Proc Natl Acad Sei USA 77:5158-5162 - Barbaeid M, Lauver AV, Devare SG (1980) J Viro133: 196-207 - Barbacid M, Breitmann ML, Lauver A V, Long LK, Vogt PK (1981) Virology 110:411-419-Bister K, Hayman MJ, Vogt PK (1977) Virology 82:431-448 - Bister K, Vogt PK (1978) Virology 88:213-221 - Breitman ML, Neil JC, Moscoviei C, Vogt PK (1981) Virology 108:1-12 - Brugge JS, Erikson RL (1977) Nature 269:346-348 -Carr JG, Campbell JG (1958) Brit J Cancer 12:631-635 - Collett MS, Erikson RL (1978) ProcNatlAcadSci USA 75: 2021-2024 - Duesberg PH, Vogt PK (1970) Proc Natl Acad Sei USA 67:1673-1680 -Duff R, Vogt PK (1969) Virology 39: 18-30-Graf T (1975) Z Naturforsch 30:847-849 -Hanafusa T, Wang L-H, Anderson SM, Karess RE, Hayward W, Hanafusa H (1980) Proc Natl Acad Sei USA 427
77:3009-3013 - Hu SSF, Moscoviei C, Vogt PK (1978) Virology 89:162-178 - Hu SSF, Vogt PK (1979) Virology 92:278-284 - Ishizaki R, Shimizu T (1970) Cancer Res 30:2827-2831 - Hunter T, Sefton BM (1980) Proc Natl Acad Sei USA 77:1311-1315 - Kawai S, Yoshida M, Segawa K, Sugiyama H, Ishizaki R, Toyoshima K (1980) Proc Natl Acad Sei USA 77:6199-6203 -LaiMMC, Hu SSF, Vogt PK (1979) Virology 97:366-377 - Lee WH, Bister K, Pawson A, Robins T, Moscoviei C, Duesberg PH (1980) Proc Natl Acad Sei USA 77:2018-2022 - Levinson AD, Oppermann H, Levintow L, Varmus HE, Bishop JM (1978) Cell 15:561-572 - Manteuil-Brutlag S, Liu SI, Kaplan HS (1980) Cell 19:643-652 - Neil JC, Breitman ML, Vogt PK (1981) Virology 108:98-110-Payne LN, Biggs PM (1966) Virology29: 190-198-RousseI M, Saule S, Lagrou C, Rommens C, Beug H, Graf T, Stehelin D (1979) Nature 281 :452-455 - Shealy DJ, Mosser AG, Rueckert RR (1980) J Virol 34:431-437 - Sheiness D, Bishop JM (1979) J Virol 31 :514-521 - Sheiness D, Bister K, Moscovici C, Fanshier L, Gonda T, Bishop JM (1980) J Virol 33:962-968 - Sherr CJ, Fedele LA, Oskarsson M, Maizel J, Vande Woude G (1980) J Virol 34: 200-212 - Shibuya M, Hanafusa T, Hanafusa H, Stephenson JR (1980) 77: 6536-6540 - Spector D, Varmus HE, Bishop 1M (1978) Proc Natl Acad Sei USA 75:4102-4106 - Stehelin D, Varmus HE, Bishop 1M, Vogt PK (1976) Nature 260: 170-173 - Van de Yen WJM, Khan AS, Reynolds FH jr, Mason KT, Stephenson JR (1980) J Virol 33: 1034-1045 - Wang L-H, Duesberg PH, Beemon K, Vogt PK (1975) J ViroI16:1051-1070 - Witte ON, Rosenberg N, Paskind M, Shields A, Baltimore D (1978) Proc Natl Acad Sei USA 75 :2488-2492 428
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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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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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Page 385 and 386: Fig. 3. Expression of retroviral gp
Page 387 and 388: 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
Page 399 and 400: zed in infected cells argue that th
Page 401 and 402: a specific viral transforming prote
Page 403 and 404: detect viral RNA as the only charac
Page 405 and 406: Eisen H (1980) Myeloproliferate vir
Page 407 and 408: 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: Haematology and Blood Transfusion V
Page 413 and 414: Fig. 2. Photomicrographs of NY68 in
Page 415 and 416: DEAE (o(lJmn 'liI GI -2 2 o e s 1
Page 417 and 418: vity was deterrnined. For endogenou
Page 419 and 420: pr 180 - - - P 12/15 - A B c D E F
Page 421 and 422: 85,- 66- -27 - -66 40- 27- -1'9 19-
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: sequences, provided its gag portion
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 and 474: Table 3. Transformation aetivity of
Page 475 and 476: - Shoemaker C, Goff S, Gilboa E, Pa
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
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Table 1. Transformation of 3T3 cell
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inserts in the genome of rapidly tr
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pulations, it seemed likely that th
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contains antigens which react with
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le of reacting in sensitive radioim
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gic approach. In: Hiatt HH, Watson
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12 Eco R [ Fig. 1. Hybridization pa
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10 - '1~ )( -~ S:! E A U I o 1 2
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Haematology and Blood 'fransfusion
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cultures. These cells did not conta
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indication of malignant T-cells in
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Fig. 3. Thin-section electron micro
Page 519 and 520:
Table 3. Lack of detectable related
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J. HTLV Was Present in the Primary
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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
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
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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
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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