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drug-resistant Chinese hamster celllines described by Biedler et al. (1976). When cells from these lines were exposed to methotrexate or methasquin, they developed extraordinarily high levels of dihydrofolate reductase (EC1.5.1.3-DHFR) in association with their drug resistance. Of the 13 independently derived drug-resistant cell lines, only those with greater than 100-fold increases in enzyme activity contained HSR-bearing chromosomes. In some cell lines, HSR represented as much as 6 % of the chromosome complement. In studies of various methotrexate-resistant mouse celliines, Alt et al. (1978) have shown that the relative number of DHFR gene copies is proportional to the cellular level of DHFR and DHFR mRNA sequences. Giemsa banding studies of a methotrexate-resistant murine lymphoblastoid cell line (Dolnick et al. 1979) showed a large HSR on chromosome No. 2. Molecular hybridization studies in situ indicate that the DHFR genes are localized in this HSR. Similar observations have been made in a methotrexate-resistant Chinese hamster ovary cellline (Nunberg et al. 1978). Evidence from other tumors suggests that amplification of genes coding for 18S and 28S ribosom al RNA may occur (Miller et al. 1979). All of these data taken together indicate that HSR and DM provide the chromosomal evidence of gene amplification which, in the case of these particular drug-resistant lines, represents amplification for the DHFR gene. The nature of the genes that are amplified in human neuroblastomas, in other human tumors, and in animal tumors is unknown. Recent technical advances provide the tools with which these significant questions can be answered. c. Conclusion The relatively consistent chromosome changes, especially specific translocations, that are dosely associated with particular neoplasms provide convincing evidence for the fundamental role of these changes in the transformation of anormal cell to a malignant cell. In some tumors these changes may be too small to be detected, and the cells would appear with present techniques to have anormal karyotype. When one considers the number of nonrandom changes that are seen in a ~alignancy such as ANLL, it is dear that not just one gene but rather a dass of genes is involved. Our knowledge of the human gene map has developed concurrently with our understanding of the consistent chromosome changes in malignancy (McKusick and Ruddle 1977).1t is now possible to try to correlate the chromosomes that are affected with the genes that they carry. Clearly, these efforts are preliminary, since relatively few genes have been mapped, and since some of the chromosomes that are most frequently abnormal have few genetic markers. In such a preliminary attempt in 1977 (Rowley 1977), I observed that chromosomes carrying genes related to nudeic acid biosynthesis and also the specific chromosome region associated with these genes were frequently involved in re arrangements associated with hematologic malignancies. More recently, Owerbach et al. (1978) reported that a gene for the large external transformation-sensitive (LETS) protein is located on chromosome No. 8. They noted that because LETS protein has been implicated in tumorigenicity and cellular transformation, its localization to a human chromosome associated with malignancies may prove to be a significant observation. In the future we will be able to determine the break points in translocations very precisely, to measure the function of genes at these break points, and to compare the activity of these genes in cells with translocations with their activity in normal cells. In other types of abnormalities such as HSR or DM we will be able to identify the genes involved in this process of gene amplification. Such information will be the basis for understanding how chromosome changes provide selected cells in certain individuals with a growth advantage that results in malignancy. References Alt FW, Kellems RE, Bertino JR, Schimke RT (1978) Selective multiplication of dihydrofolate reductase genes in methotrexateresistant variants of cultured murine cells. J Biol ehern 253: 1357-1370 - Balaban-Malenbaum G, Gilbert F (1977) Double minute chromosomes and the homogeneously staining regions in chromosomes of a human neuroblastoma cellline. Scierice 198: 739-741 - Biedler JL, Spengler BA (1976) Metaphase chromosome anomaly: Association with drug resistance and cellspecific products. Science 191: 185-187 - Biedler JL, Spengler BA (1977) Abnormally banded metaphase chromosome regions in cells with low levels of 154
esistance to antifolates. In Vitro 13 :200 - Boveri T (1914) Zur Frage der Entstehung maligner Tumoren. Fischer, Jena - Brynes RK, Golomb HM, Gelder F, Desser RK, Rowley JD (1978) The leukemic phase of histiocytic lymphoma. Am J Clin PathoI89:550-558-Comings DE (1973) Ageneral theory of careinogenesis. Proc Natl Acad Sei USA 70:3324-3328 - Dolnick BJ, Berenson RJ, Bertino JR, Kaufman RJ, Nunberg HH, Schimke RT (1979) Correlation of dihydrofolate reductase elevation with gene amplification in a homogeneously staining chromosomal region. J Cell Biol83 : 394-402 - German J (1972) Genes which increase chromosomal instability in somatic cells and predispose to cancer. Prog Med Genet 8:61-101-HendersonAS,Eicher EM, Yu MT, Atwood KC (1974) The chromosomal location of ribosomal DNA in the mouse. Chromosoma 49: 155-160 - Ihle JN, Joseph DR, Domofor 11 Jr (1979) Genetic linkage of C3H/HeJ and BALB/c endogenous extropic C-type viruses to phosphoglucomutase-1 on chromosome 5. Science 204:71-73 - Levan A, Levan G (1978) Have double minutes functioning centromeres? Hereditas 88:81-92 - Levan G, Mandahl N, Bengtsson BO, Levan A (1977) Experimental elimination and recovery of double minute chromosomes in malignant cell populations. Hereditas 86 :75-90 - Lilly F, Pincus T (1973) Genetic control of murine viral leukemogenesis. Adv Cancer Res 17: 231-277 - McKusick VA, Ruddle FH (1977) The status of the gene map of the human chromosomes. Science 196: 390-405 - Miller OJ, Tantravahi R, Miller DA, Yu L-C, Szabo P, Prensky W (1979) Marked increase in ribosom al RNA gene multiplieity in a rat hepatoma cell line. Chromosoma 71: 183-195 - Mitelman F, Levan G (1978) Clustering of aberrations to speeific chromosomes in human neoplasms. III. Ineidence and geographie distribution of chromosome aberrations in 856 cases. Hereditas 89:207-232 - Mulvihill 11, Miller RW, Fraumeni JF Jr (eds) (1977) Progress in cancer research and therapy. Genetics of human cancer, vol 3. Raven, National Cancer Institute, National Institute of Health, Bethesda, MD - Nowell PC (1976) The donal evolution of tumor cell poulations. Seience 194:23-28 - Nunberg JH, Kaufman RJ, Schimke RT, Urlaub G, Chasin LA (1978) Amplified dihydrofolate reductase genes are localized to a homogeneously staining region fo a single chromoso me in a methotrexate resistant chinese hamster ovary cell line. Proc Natl Acad Sei USA 75:5553-5556 - Owerbach D, Doyle D, Shows TB (1978) Genetics of the large, external, transformation sensitive (LETS) protein : Assignment of a gene co ding for expression of LETS to human chromosome 8. Proc Natl Acad Sei USA 75:5640-5644 - Rowe WP (1973) Genetic factors in the natural history of murine leukemia virus infection. GHA Clowes Memorial Lecture. Cancer Res 33:3061-3068 - Rowe WP, Kozak CA (1979) Genetic mapping of the ecotropic murine leukemia virus-inducing lccus of BALB/c mouse to chromosome 5. Seience 204:69-71 - Rowley JD (1977) Mapping of human chromosomal regions related to neoplasia: Evidence from chromosomes 1 and 17. Proc Natl Acad Sei USA 74:5729-5733 - Rowley JD A possible role for nonrandom chromosomal changes in human hematologic malignancies. In: De la Chapelle A, Sorsa M (eds) (1977) Chromosomes Today 6. Elsevier/North-Holland, Amsterdam, pp 345-359 - Rowley JD (1978) Chromosomes in leukemia and lymphoma. Semin Hematol 15 :301-319 - SachsL(1978) Controlofnormalcell differentiation and the phenotypic reversion of malignancy in myeloid leukemia. Nature 274: 535-539 - Sandberg AA (1980) Chromosomes in human cancer and leukemia. Elsevier/North-Holland, New York - Sugiyama T (1971) Speeific vulnerability of the largest telocentric chromosome of rat bone marrow cells to 7, 12-dimethylbenz(a)anthracene J Natl Cancer Inst 47:1267-1276 - Sugiyama T, Uenaka H, Ueda N, Fukuhara S, Maeda S (1978) Reprodueible chromosome changes of polycydic hydrocarbon-induced rat leukemia: Ineidence and chromosome banding pattern. J Natl Cancer Inst 60: 153-160 155
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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
Page 115 and 116: 1. 0 '--'1--" 0.9 e: o .- VI VI E C
Page 117 and 118: e: o e: 1. 0 ,.--...-- 1'"'\ ......
Page 119 and 120: In conclusion, we can state that th
Page 121 and 122: Haematology and Blood Transfnsion V
Page 123 and 124: INDUCTION VCR + PRED + ASNASE (wk 3
Page 125 and 126: SCHED.INT 1 MTX • ! Adria MTX •
Page 127 and 128: ~ looh---------ooooc>----o---c>----
Page 129 and 130: Consoll- Irra .tlon t) .tlon Indu
Page 131 and 132: Highrisk Standard risk Table 1. Cli
Page 133 and 134: Cumulo/ive comp/el9 remission 1.0 .
Page 135 and 136: 10° 8 = 6 ö 4 Non T Cell .~ :ö
Page 137 and 138: Haematology and Blood Transfusion V
Page 139 and 140: % SURVIVAL 100 ~ ~II 0 80 60 40 - -
Page 141 and 142: a) Percentage of donor cell mitoses
Page 143 and 144: Table 5. Results of bone marrow tra
Page 145 and 146: ...... w N Table 7. Clinical result
Page 147 and 148: agent had to be added and that in t
Page 151 and 152: C. Chronic Myelogenous Leukemia The
Page 153 and 154: Patients with a suitable donor rece
Page 155 and 156: No. Recurrent Leukaemia Other death
Page 157 and 158: followed by dialysis against isoton
Page 161 and 162: HS, HL- Heme >_ 40 0 HS I ;:. =====
Page 165: knowing at present. These genes may
Page 169 and 170: a DNA probe specific for the gene t
Page 171 and 172: translocation between chromosomes 9
Page 173 and 174: Table 1. Subdivision of 1827 Myelo-
Page 175 and 176: NORMAL CELL ®
Page 177 and 178: some change of the primary type, in
Page 181 and 182: F. Transformation of Mouse Bone Mar
Page 185 and 186: were carried out with 3H-MTX in the
Page 189 and 190: the lysozyme cDNA prepared from ovi
Page 193 and 194: et al. 1976). The BJAB cellline in
Page 195 and 196: dalton bands corresponding to light
Page 197 and 198: 1979). The EBV-carrying cell lines
Page 199 and 200: producer lines (DAUDI and P3HR-1),
Page 201 and 202: G, Giovanella B, Westman A, Stehlin
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
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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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Page 307 and 308:
Page 309 and 310:
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
Page 379 and 380:
Page 381 and 382:
munized animals to 1316 tumor cells
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Haematology and Blood Transfnsion V
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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-
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= 0.5 o E Q. o ILI 0.4 (J) « ILI .
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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
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Page 443 and 444:
RELATIONSHIP OF ENDOGENOUS AND EXOG
Page 445 and 446:
E ........ E Cl. U E :::l .... Q) (
Page 447 and 448:
References Astrin S (1978) Endogeno
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the same animal were examined (e.g.
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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"
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a b Sac I / rep ._-_.-_ K J nl rep
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Haematology and Blood 'fiansfusion
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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:
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
Page 495 and 496:
contains antigens which react with
Page 497 and 498:
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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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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
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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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