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sequences related to those genes. Moreover, the cellular sequences related to the 3-kb AEV -specific RNA sequence have recently been shown to be distributed over a 15-kb DNA segment that includes AEV-related and AEV -unrelated sequences (J. M. Bishop, personal communication). Likewise, the cellular DNA sequence, related to the Abelson murine leukemia virus-specific RNA sequence of 3 kb (Shields et al. 1979), has been shown to be distributed over a 12-kb DNA segment that must include Abelson virus unrelated sequences (Goff et al. 1980). Hence in these cases proviral DNA and related cellular DNA sequences are not colinear. It follows that the genetic units of class I acute leukemia viruses that consist of gag-related and specific RNA sequences (Fig. 1) have no known counterparts in normal ceIls. It is conc1uded that viral onc genes of the RSV design and in particular those of the MC29 design are different from related sequences present in the cello The onc genes of the RSV design, like src and possibly amv (Fig. 1), may share most but possibly not aIl of their coding sequences with ceIlular homologs but differ from cellular relatives in essential regulatory elements. The onc genes of the MC29 design differ from ceIlular counterparts in coding (gag and pol-related sequences) as well as regulatory elements. Consequently, the cellular relatives of most viral onc genes are probably not present in the cell as functional onc genes as has been postulated (Huebner and Todaro 1969; Bishop et al. 1980) and hence are probably not directly relevant to transformation. Instead these ceIlular sequences may be relevant to the archaeology of viral onc genes. Viral onc genes probably have been generated by rare transductions of ceIlular sequences by nondefective viruses. To generate onc genes of the RSV design transduction must have involved illegitimate recombination with nondefective virus. In the case of Moloney MuSV specific deletions of the parental nondefective virus also had to occur (Dina et al. 1976; Donoghue et al. 1979; Chien et al. 1979; Blair et al. 1980). Until the ceIlular src-related sequence is characterized directly, it remains unclear whether in the case of RSV the coding sequence of src was transduced unchanged or after alteration when RSV was generated. Both transduction, involving again illegitimate recombination, as weIl as specific deletions of virion genes (see Fig. 1) must have been necessary to generate the onc genes of the MC29 design from cellular and viral genetic elements. Such events are much less likely to occur than, for example, the transduction by phage lambda of a functional galactosidase gene. It is noted that experimental evidence compatible with the transduction of cellular sequences has led to the hypo thesis that viral transformation is the product of enhancing the dosage of endogenous ceIlular onc genes by homologous equivalents from exogenous viruses (Bi shop et al. 1980). We submit that sequence transduction is not synonymous with the transduction of unaltered gene function which would be a necessary corollary of the gene dosage hypothesis. It would appear that viral onc genes are unique and more than the sum of their parts related to cellular DNA and replicative genes of retroviruses. H. Tbe RoJe 01 one Genes in Careinogenesis Highly oncogenic virus es with onc genes such as those described here have only been isolated in relatively few cases from animal tumors (reviewed in Gross 1970; Tooze 1973; Duesberg 1980). By contrast leukosis and lymphatic leukemia virus es have been isolated from many viral cancers, in particular from leukemias (see above) (Gross 1970; Tooze 1973). Thus paradoxically the lymphatic leukemia virus es which lack known onc genes appear to be more relevant to viral carcinogenesis than retroviruses with known onc genes. However, it has been argued that onc genes also play a role in carcinogenesis caused by lymphatic leukemia viruses (Duesberg 1980). These onc genes may derive from endogenous, defective retrovirus-like RNAs known to exist in some normal cells (Duesberg and Scolnick 1977; Scolnick et al. 1979) or from cellular genes acquired by processes involving illegitimate recombination and specific deletions (compare genetic structures shown in Fig. 1). The necessity for such a secondary event to occur would explain the poor correlation between the distribution of lymphatic leukemia viruses and cancers in animals (see above). The faHure to find onc genes in most retroviral cancers may then reflect technical difficulties. These include the lack of suitable probes to 393
detect viral RNA as the only characteristic viral structural component or nonstructural proteins as the only characteristic products of defective transforming viruses. Moreover, detection of a putative defective-transforming virus will be complicated by the fact that the ratio of defective-transforming to nondefective helper virus is low in typical stocks of defective helper virus complexes (Du es berg et al. 1977; Bister and Dues berg 1979; Duesberg et al. 1979; Lee et al. 1980). Thus, the analysis of viral onc genes may prove to be less academic than it appears at present - it may provide the tools and concepts necessary to und erstand all retroviral cancers. AcknowIedgments We thank L. Evans, M. Nunn, and G. S. Martin for a critical review of the manuscript and D. Baltimore, J. M. Bishop, and M. Essex for communicating results prior to publication. Supported by U .S. Public Health Grant CA 11426. References Beard JW, Langlois AJ, Beard D (1973) Etiological strain speeificities of the avian tumor virus. BibI Haematol 39:31-44 - Beemon K, Duesberg PH, Vogt PK (1974) Evidence for crossing over between avian tumor viruses based on analysis of viral RNAs. Proc Natl Acad Sci USA 71: 4254-4258 - Biggs PM, Milne BS, Graf T, Bauer H (1972) Oncogenieity of nontransforming mutants of avian sarcoma virus. J Gen ViroI18:399-403 - Bishop JM, Courtneidge SA, Levinson AD, Oppermann H, Quintrell N, Sheiness DK, Weiss SR, Varmus HE (1980) The origin and function of avian retrovirus transforming genes. Cold Spring Harbor Symp Quant Biol 44:919-930 - Bister K, Duesberg PH (1979) Structure and specific sequences of avian erythroblastosis virus RNA: Evidence for multiple classes of transforming genes among avian tumor viruses. Proc Natl Acad Sci USA 76:5023-5027 - Bister K, Duesberg PH (1980) Genetic structure of avian acute leukemia viruses. Cold Spring Harbor Symp Quant BioI44:801-822 - Bister K, Vogt PK (1978) Genetic analysis of the defectiveness in strain MC29 avian leukosis virus. Virology 88:213-221 - Bister K, Hayman MJ, Vogt PK (1977) Defectiveness of avian myelocytomatosis virus MC29: Isolation of long-term nonproducer cultures and analysis of virus-specific polypeptide synthesis. Virology 82: 431-448 - Bister K, Löliger H -C, Duesberg PH (1979) Oligoribonucleotide map and protein of CMII: Detection of conserved and nonconserved genetic elements in avian acute leukemia viruses CMII, MC29 andMH2. JViroI32:208-219-Bister K, Ramsay G, Hayman MJ, Duesberg PH (1980a) OKlO, an avian acute leukemia virus of the MC29 subgroup with a unique genetic structure. Proc Natl Acad Sei USA 77:7142-7146-Bister K, Lee W-H, Duesberg PH (1980b) Phosphorylation of the nonstructural proteins encoded by three avian acute leukemia viruses and by avian Fujinami sarcoma virus. J ViroI36:617-621-Blair DG, McClements WL, Oskarsson MK, Fischinger PJ, VandeWoude GF (1980) Biological activity of cloned Moloney sarcoma virus DNA: Terminally redundant sequences may enhance transformation effieiency. Proc Natl Acad Sei 77:3504-3508 - Brugge JS, Erikson RL (1977) Identification of a transformation-specific antigen induced by an avian sarcoma virus. Nature 269:346-348 - Chen A, EssexM, Shadduck JA, Niederkom JY, Albert D (1981) Retravirus encoded transformation-specific polyproteins : Expression coordinated with malignant phenotype in cells from different germ layers. PNAS, in press - Chien YS, Verma IM, Duesberg PH, Davidson N (1979) Heteroduplex analysis of the RNA of clone 3 Moloney murine sarcoma virus. J Virol 32: 1028-1032 - Cloyd MW, Hartley JW, Kene WP (1980) lymphomagenicty of recombinant mink cell focus - inducing murine leukemia viruses J Exp Med 151 :542-552 - Dina D, Beemon K, Duesberg PH (1976) The 30S Moloney sarcoma virus RNA contains leukemia virus nucleotide sequences. Cell 9:299-309 - Donoghue BJ, Sharp PA, Weinberg RA (1979) Comparative study of different isolates of murine sarcoma virus. J Virol 32: 1015-1027 - Duesberg PH (1980) Transforming genes of retroviruses. Cold Spring Harbor Symp Quant Biol 44: 13-29 - Duesberg PH, Scolnick EM (1977) Murine leukemia viruses containing a ",30S RNA subunit of unknown biological activity, in addition to the 38S subunit of the viral genome. Virology 83 :211-216 - Duesberg PH, Vogt PK (1970) Differences between the ribonucleic acids of transforming and nontransforming avian tumor viruses. Proc Natl Acad Sei USA 67: 1673-1680 - Duesberg PH, Vogt PK (1973) RNA speeies obtained from clonallines of avian sarcoma and from avian leukosis virus. Virology 54:207-219 - Duesberg PH, Vogt PK (1979) Avian acute leukemia viruses MC29 and MH2 share specific RNA sequences: Evidence for a second class of transforming genes. Proc Natl Acad Sei 76:1633-1637 - Duesberg PH, Bister K, Vogt PK (1977) The RNA of avian acute leukemia virus MC29. Proc Natl Acad Sei 74:4320-4324 - Duesberg PH, Bister K, Moscovici C (1979) Avian acute leukemia virus MC29: Conserved and variable RNA sequences and recombination with helper virus. Virology 99:121-134 - Duesberg P, Bister K, Moscovici C (1980) Genetic structure of avian myeloblastosis virus released as defective virus particle from transformed myeloblasts. Proc Natl 394
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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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Page 109 and 110:
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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Haematology and Blood Transfnsion V
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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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Page 351 and 352: Fig. 2. Cytocentrifuged smears of b
Page 353 and 354: Modification of amino-groups of hum
Page 355 and 356: disturb this balance in the directi
Page 357 and 358: The majority of human blood lymphoc
Page 359 and 360: of the EBV infected B cells. Howeve
Page 361 and 362: and immunoglobulins. J Immunol 120:
Page 363 and 364: " K 10 • j ~ ALL RNlL AL wtfh les
Page 365 and 366: 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: Haematology and Blood Transfusion V
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 381 and 382: munized animals to 1316 tumor cells
Page 383 and 384: Haematology and Blood Transfnsion V
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: a specific viral transforming prote
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 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 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
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~ ..................... ~ Cell 3' 5
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a :Sa,C! + . ~ 111 i' ( " '~ .J. b
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Table 1 Sampie Tissue TS fragment"
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a b Sac I / rep ._-_.-_ K J nl rep
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Haematology and Blood 'fiansfusion
Page 463 and 464:
Osteopetrosis and osteosarcomas occ
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Lymphoma cellline Table 1. T and B
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Table 2. In vivo growth and oneogen
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Table 1. Transforming aetivity of c
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Table 3. Transformation aetivity of
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- Shoemaker C, Goff S, Gilboa E, Pa
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indieate a shifting of target eell
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Table 2. Expression of Jl and Sourc
Page 481 and 482:
Page 483 and 484:
~ i ,..1---------,,':::::::::::::::
Page 485 and 486:
fragment of pBR322 DNA, a 3.0-kbp S
Page 487 and 488:
Mak TW (1979) Proc Natl Acad Sci US
Page 489 and 490:
Table 1. Transformation of 3T3 cell
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inserts in the genome of rapidly tr
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pulations, it seemed likely that th
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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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Page 503 and 504:
gic approach. In: Hiatt HH, Watson
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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
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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
Page 521 and 522:
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
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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
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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