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protein in the postribosomal supernatant of rabbit reticulocytes. This corresponds to less than a few thousand molecules of HS per reticulocyte. HS can be converted from an inactive form (HS i ) to an active species by he at or pressure. Activation of highly purified HS during a 5-min incubation at different temperatures is depicted in Fig. 2. Und er these conditions appreciable activation is seen at 37°C. It is likely that HS is stabilized by other components in intact cells. HS has the unusual property of reverting to an inactive form if it is held at ooe for 24-48 h. Table 1 shows the results of an experiment in which HS was cycled between the inactive and active form by repeated heating at 1000e for 3 min, followed by 24 h on ice. There is little or no loss of HS activity during this procedure. HS has little or no detectable inhibitory activity in the absence of the second factor, HL, which is a heat-labile protein of about 43,000 daltons. It appears that HS functions to inhibit protein synthesis by a catalytic, irreversible conversion of an inactive form of HL, HLi> to an active species. The reaction is ATP-dependent but phosphorylation does not appear to be involved (Henderson et al., 1979). The mechanism by which HS and HL inhibit protein synthesis appears to involve phospho- .., I 0 x ::E n. u z 0 ~ I- ~ 0:: 0 n. 0:: 0 U Z W Z U :::J W ...J '"0' .,. ~ 30 20 0 25 35 45 55 HS ACTIVATION TEMP., °C (5min. incubation) Fig. 2. Heat activation of HS. HS i was heated at the indicated temperature for 5 min, then inhibitory activity (100 fA.g HS protein/mI) was measured in the reticulocyte lysate system as described for Fig. 1 Table 1. Interconversion of HS j and HS by heating to 100°C followed by cold. A solution of purified HS similar to that used for the experiment of Fig. 1 was heated at 100°C for 3 min, then allowed to stand on ice for 24 h. The cycle of heating and standing in the cold was repeated as indicated. Aliquots containing 0.1 fA.g of HS protein were assayed in the reticulocyte lysate as described for Fig. 1 Cycle number 1 2 3 4 5 Leueine incorporation into protein, cpm X 10- 3 Unheated Heated 28 8.9 29 9.3 28 9.1 27 8.6 28 10.1 rylation of the smallest subunit of eIF-2, eIF-2a, by the specific protein kinase that is also activated in the absence of heme. This eIF-2a kinase appears to contain a peptide of about 100,000 daltons that is phosphorylated during activation by either HS-HL or by heme deficiency (Kramer et al. 1980). Antibodies against the eIF-2a kinase of the HeR system block inhibition by HS or HL. However, it should be emphasized that activation of this pro tein kin ase by HS and HL occurs in the presence of heme. Thus HS and HL appear to form the distal elements of a cascade-type sequence of reactions that lead to inhibition of protein synthesis by phosphorylation of eIF-2a. The relationship of the known components of the HS-HL and HeR systems that are involved in phosphorylation and dephosphorylation of eIF-2 is shown in Fig. 3. Also shown in Fig. 3 is the relation of the components of the interferon-dsRNA system that appear to lead to phosphorylation of the same three sites of eIF-2a that are phosphorylated by the 100,000 dalton protein kinase of the HS-HL and HeR system (SamueI1979). The protein kin ase of the interferon-dsRNA system involves a 67,000 dalton peptide that also is phosphorylated during activation of the kinase. This occurs in the presence of dsRNA. It is not established that the HS-HL system is activated during whole body or tissue hyperthermia. However, the biochemical studies indicated above considered with the effects of elevated temperature on pro tein synthesis apparatus of cells in culture make this seem likely. In turn, it appears that hyperthermia 147
HS, HL- Heme >_ 40 0 HS I ;:. ======~~ HS (Inaetlve) co Id (aetlve) lATP HLj---"·HL (inaetlve) (aetlve) I I Trypsin Inhibitor -....ll'-llr--.. ~ + ~ 90K Peptide I I -Heme I ~! lOOK eIF-2q -.--~ Kinase-P04 Kinase Phosphatase (aetlve) (inaetlve) 1 elF - 2 _. ------:-1-- (aetlve) Phosphatase :!"==:::;. Phosphatase (aetlvl1ted) t Activators Interferon - dsRNA Interferon :-..... 56K 2 1 ,5 1 _ oligoA Synthetase I (lnaetlvel tl dsRNA I I ! Synthetase (aetlvel 67K eIF-2q Kinase dsRNA jr ATP ~ 2'.5 1 -oligoA I : Phosphatase 1 l ~: endonuclease~endonuclease PO (lnae'ive) (aetive) (aetlve) + K· mase- 4 I 1 mRNA t RNA Breakdown Fig. 3. Comparison of protein synthesis inhibition by HS-HL and by interferon-dsRNA. Dashed lines indicated unknown or uncertain relationship and interferon may function by equivalent biochemical mechanisms to reduce the rate of peptide initiation. A change in this rate may not only slow the rate of cell growth but may also alter the relative proportion of proteins formed from different competing mRNA speeies (Kramer et al. 1980), thus alte ring the basic composition and physiology of the cello Such a change brought on by activation of HS during high fever may constitute a basic defense mechanism for limiting translation of viral mRNA during viral infections and might be exploited for the treatment of cancer by hyperthermia. References Ardenne M von, Krüger W (1980) Ann NY Acad Sei 335:356-361 - Bonanou-Tzedaki SA, Smith KE, Sheeran BA, Arnstein HRV (197 8a) Eur J Biochem 84:591-600 - Bonanou-Tzedaki SA, Smith KE, Sheeran BA, Arnstein HRV (1978b) Eur J Biochem 84:601-610 - Conference on Hyperthermia in Cancer Treatment (1979) Cancer Res 39:2231-2340 - Goldstein ES, Penman S (1973) J Mol Biol 80: 243-254 - Henderson AB, Hardesty B (1978) Biochem Biophys Res Commun 83 : 715-723 - Henderson AB, Miller AH, Hardesty B (1979) Proc Natl Acad Sei USA 76:2605-2609 - Kramer G, Henderson AB, Grankowski N, Hardesty B (1980). In: Chamblis G, Craven G, Davies J, Davis K, Kahan L, Nomura M (eds) RIBOSOMES: Structure, function and genetics; University Park Press, Baltimore, pp 825-845 - Overgaard J (1978) Cancer 39:2637-2646 - Samuel CE (1979) Proc Natl Acad Sei USA 76:600-604 - Schochetman G, Perry RP (1972) J Mol Biol 63:577-590 -Thermal Characteristics of Thmors: Applications in Detection and Treatment (1980) Jain RK, Gullino PM (eds) Ann NY Acad Sei 335 :542 148
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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
Page 111 and 112: 42:2123-2134 - Chessells JM, Cornbl
Page 113 and 114: 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 159: Haematology and Blood Transfusion V
Page 165 and 166: knowing at present. These genes may
Page 167 and 168: esistance to antifolates. In Vitro
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
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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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Page 243 and 244:
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)
Page 271 and 272:
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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Page 281 and 282:
the macrophage series in which the
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Page 285 and 286:
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
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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Page 425 and 426:
= 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
Page 437 and 438:
77:3009-3013 - Hu SSF, Moscoviei C,
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RI 2.2 md and Hind III 2.6 md leuke
Page 441 and 442:
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
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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 469 and 470:
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 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
Page 491 and 492:
inserts in the genome of rapidly tr
Page 493 and 494:
pulations, it seemed likely that th
Page 495 and 496:
contains antigens which react with
Page 497 and 498:
Page 499 and 500:
le of reacting in sensitive radioim
Page 501 and 502:
Page 503 and 504:
gic approach. In: Hiatt HH, Watson
Page 505 and 506:
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
Page 513 and 514:
cultures. These cells did not conta
Page 515 and 516:
indication of malignant T-cells in
Page 517 and 518:
Fig. 3. Thin-section electron micro
Page 519 and 520:
Table 3. Lack of detectable related
Page 521 and 522:
J. HTLV Was Present in the Primary
Page 523 and 524:
specific signals into nonspecific s
Page 525 and 526:
Table 2. Distribution of HTLV-relat
Page 527 and 528:
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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