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Haematology and Blood Transfusion Vol. 26 <strong>Modern</strong> Trends in Human Leukemia IV Edited by Neth, Gallo, Graf, Mannweiler, Winkler © Springer-Verlag Berlin Heidelberg 1981 Enzyme Polymorphism as a Biochemical Cell Marker: Application to the Cellular Origin and Homogeneity of Human Macrophages and to the Classification of Malignant Lymphomas * H. J. Radzun, M. R. Parwareseh, and K. Lennert The polymorphism of enzyme systems can be ascribed to four different mechanisms. Physicochemical heterogeneity ensues from free combination of subunits constituting the quaternary structure of enzyme proteins. The so-called microheterogeneity is caused by the presence of nonpeptide groups in the enzyme molecules. Furthermore, genetic activity leads to the appearance of molecular enzyme variants called isoenzymes. Finally, the phenotypical expression of genetic variations is usually obscured by the inductive and repressive influences exerted during ontogenesis and differentiation. This is referred to as balanced polymorphism (Ford 1940). There is ample evidence that the pattern of enzyme variants remains constant within a homogeneous cell population and reveals a stable feature specific to this cell co hort (Li et al. 1970). We have used isoelectric focusing on poly acryl amide gels for investigation of the lysosomal acid esterase (BC 3.1.1.6) and lysosomal acid phosphatase (EC3.1.3.2) polymorphism in purified human blood cell types (Radzun et al. 1980, to be published). It could be shown that clear differences in the pattern of enzyme variants were detectable between platelets, red blood cells, granulocytes, monocytes, and T and B lymphocytes. The unique distribution pattern of acid esterase in human blood monocytes with four minor and one major anodic band within a pH range of 6.25-5.70 was used to detect the homogeneity and cellular origin of human peritoneal macrophages. Purified unstimulated sessile peritoneal macrophages, obtained * This work was supported by the Deutsche Forschungsgemeinschaft, programs CL3 and CN2 from noninflammatory peritoneal cavity, showed in addition- to the five isoenzymes of acid esterase which are specific for blood monocytes, two further enzyme variants (Fig. 1). Exposure of blood monocytes to an uncoated glass surface led to the appearance of these two bands on the third day of culture. From these results we deduce that sessile peritoneal macrophages, like exudate peritoneal macrophages, represent a monocytic cell cohort. Thus, all macrophages of the peritoneal cavity constitute a homogeneous cell population. This contradicts the opinion of other authors, who hold the view that sessile peritoneal macrophages are self-sustaining (Daems et al. 1973). Another example for the application of cell-specific polymorphism of enzymes is its employment in the characterization of tumor cells. On the basis of morphological conventions and enzyme cytochemical and immunocytochemical methods, human malignant lymphomas have been successfully classified (Lennert et al. 1978). It has been shown that the four lymphoma entities - chronic lymphocytic leukemia of B-cell type, follicular lymphoma, lymphoplasmacytic/lymphoplasmacytoid lymphoma, and plasmacytoma - represent B lymphocyte neoplasias, imitating various stages of activity and differentiation of normal B lymphocytes. In line with these considerations all four lymphoma entities shared the isoenzyme pattern of lysosomal acid phosphatase observed in normal human B lymphocytes (Fig. 2). Furthermore, the stepwise rise in enzyme activity from one lymphoma entity to the next was at least partly due to the appearance of additional isoenzymes (Schmidt et al. , to be published). These results show that it is possible to classify a tumor as B lymphocytic in origin on the basis of its typical isoenzyme 222
Blood Monocyte. B lood Monocytes 1-4 days after gla •• exposure Peritoneal Macrophoge. - - pI /'6.45 --....,/26.30 --36.25 ----4 6.10 =~5 6.00 _",6 5.95 7 5.90-5.70 Fig. 1. Polymorphism of lysosomal acid esterase in normal human blood monocytes and sessile peritoneal - - macrophages. Prolonged exposure of blood monocytes to uncoated glass surface showed a gradual transition of the monocytic pattern of acid esterase into that of peritoneal macrophages. pI, isoelectric point pH B-CLL CB/CC IC PC B-Ly 60 -- 6.1 --6.1 --6.1 --6.1 ]A[- 6.1 - 5.85 - 58S - 5.85 - 5.8 1-- 1-- 2-- 2-- -- 5.45 --5.45 --5.5 --5.5 -- 5.45 B 5.0 -- 4.95 --495 --4.95 -- 4.95 3 -- --4.6 --4.6 --4.6 5 4 7 === 6 -- 4.55 C --4.6 4.0 --3.95 --3.95 --3.9 --3.9 --3.9 Fig. 2. Polymorphism of lysosom al acid phosphatase in chronic lymphocytic leukemia of B-cell type (B-CLL), follicular lymphoma (CB/CC), lymphoplasmacytic/lymphoplasmacytoid lymphoma (IC), and plasmacytoma (PC) in comparison with normal human B lymphocytes (B-Ly) pattern as long as pure populations of tumor cells are provided. The examples mentioned above document the new perspectives of using enzyme polymorphism as a biochemical marker for the characterization of maturational stages, functional derivatives, and neoplastic variants of a certain cellline. References Daems WT, Poelman RE, Brederoo P (1973) Peroxidatic activity in resident peritoneal macrophages and exudate monocytes of the guinea pig after ingestion of latex partic1es. J. Histochem Cytochem 21 :93-95 - Ford EB (1940) In: Huxley J (ed) The new systematics. Clarendon, Oxford, pp 493-513 - Lennert K, Stein H, Mohri N, Kaiserling E, Mueller-Hermelink KH (1978) Malignant lymphomas other than Hodgkin's disease. Springer, New York Berlin Heidelberg - Li CY, Yam LT, Lam KW (1970) Studies of acid phosphat ase isoenzymes in human leucocytes. Demonstration of isoenzyme cell specificity. J Histochem Cytochem 18:901-910 - Radzun HJ, Parwaresch MR, Kulenkampff C Staudinger M, Stein H (1980) Lysosomal acid esterase : Activity and isoenzymes in separated normal human blood cells. Blood 55: 891-897 - Radzun HJ, Parwaresch MR, Kulenkampff C, 223
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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
Page 183 and 184: Haematology and Blood Transfusion V
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
Page 217 and 218: Fig. 1. a Polyacrylamide gelelectro
Page 221 and 222: 1979). The lymphocyte subpopulation
Page 223 and 224: lysin 0 antigens are found, and mix
Page 225 and 226: Pope JH (1978) Long-term T cell-med
Page 227 and 228: Haematology and Blood Transfnsion V
Page 229 and 230: Charaeteristie Morphologie maturati
Page 231 and 232: after TPA-induction (Table 3). The
Page 233: PA (1978) Reactivity of a rabbit an
Page 239 and 240: and nonhistone proteins can serve a
Page 243 and 244: The findings of the evaluation of s
Page 245 and 246: Fig. 3. Tumor grawth of L 428 cells
Page 247 and 248: Cell biological and Immunological A
Page 249 and 250: consideration. Sanel (1973) obtaine
Page 251 and 252: endotoxin serum, were used. A parti
Page 253 and 254: monocytic leukemia cell line in cul
Page 255 and 256: B. Isolation, Characterization and
Page 259 and 260: don al hemopathies generally displa
Page 261 and 262: nitors. Blood Cells 6:595-607 - Min
Page 263 and 264: \I) ....I ....I IU Jl 200 r 100 90
Page 265 and 266: their haemopoietic cells' ability t
Page 267 and 268: normal normal ALL ALL ALL persons p
Page 269 and 270: 64.5 { V)
Page 271 and 272: References Biermann E, Neth R, Gros
Page 273 and 274: ehambers, the growth pattern observ
Page 275 and 276: References Anderssen LC, 10kinen M,
Page 277 and 278: REH CELL UNE TO CALLb~Ö ~q~ V.M. c
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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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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
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Expt. No. Infecting virus Proportio
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Haematology and Blood 'fransfusion
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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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RELATIONSHIP OF ENDOGENOUS AND EXOG
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E ........ E Cl. U E :::l .... Q) (
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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
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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
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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
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~ i ,..1---------,,':::::::::::::::
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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
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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
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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
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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
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immunodeficiency, multic10nal lymph
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Bovine leukemia --, proteins of 499
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Human T- cell - -, characterization
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RNA -, of tumor virus 439 Rous sarc
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Haematology andBlood Transfusion Su
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