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Culture system Effect a 1. Reactivity on blood cell populations (Complement fixation) Table 6. Properties of anti-human-T -cell globulin used for Cells Titer clinical bone marrow transplantation. For details see: Cells Rodt et al., Experimental Hematology Today, Springer Thymocytes 1 :1064 Peripher al blood lymphocytes 1: 512 1979 Bone Marrow cells 1: 32 B-Iymphocytes (CLL) Granulocytes neg. neg. 2. Reactivity on hemopoietic progenitors AHTCG-incubated bone marrow cells 3. Cross reactions Antigen CFU-C diffusion chamber Reaction No reduction of CFU No reduction of cell numbers and normal differentiation Erythrocytes Glomerulo-basalmembrane Plasmaproteins No No No 4. Sterility, absence of pyrogenic substances, and no general toxicity a Compared with normal globulin incubated controls. Five patients had the common type of acute lymphoblastic leukemia (cALL) and six had acute myelogeneous leukemia. Three other patients suffered from ALL of the T -cell type, an erythroleukemia, and an acute undifferentiated leukemia (AUL), respectively (Table 7). Treatment of bone marrow with ATCG was preceeded by a concentration of the collected bone marrow to about 300 ml (Fig. 5). The recovery of CFUc was more than 80%. The use of a cell separator permitted the recovery of red cells for retransfusion into the bone marrow donor, a particular advantage when the donor is a child. Separation of red cells from the bone marrow is also advantageous in ABO-incompatible patients where hemolysis of donor red cells by preformed antibodies of the patient must be avoided. The final dilution of ATCG of 1: 200 of apreparation of 10 mg/mI was derived from our studies in dogs. Injection of the ATCG-pretreated bone marrow over aperiod of about 20 min caused no immediate symptoms. Transient fever and chills were occasionally observed after bone marrow transfusion with or without ATCG. In general, engraftment and recovery of bone marrow functions after incubation treatment did not differ from that of earlier transplantations without ATCG. Engraftment was documented by bone marrow cellularity and the rise of peripheral blood cell counts. Of 14 patients, 12 showed an engraftment between day 13 and day 26 after transplantation, which was indicated by a rise in the peripheral granulocyte counts to va lues between SOO-1000/mm 3 . This range does not markedly differ from other groups performing BMT without any marrow incubation treatment. Thomas et al. (1977) reported bone marrow engraftment after an average time of 16 days after transplantation in 91 cases with acute leukemia. Seven of the twelve patients were sex mismatched, three showed ABO blood group incompatibility, and in one patient sex and blood group and ,in another HLA-D and blood group were different. Two patients did not show substantial engraftment. One of these patients was one-way HLA-D different and died very early on day 21 with septicemia. In the other case the HLA-D compatibility could not be clearly documented. This patient in addition showed persisting leukemia at 131
...... w N Table 7. Clinical results in 14 patients with akute leukemias undergoing bone marrow transplantation. For prevention of GvHD the marrow was preincubated with ATCG Patient Donor-recipient-diff. Conditioning' Leukemia, Marrow treatment Clinic d Hospital f Relapse HLA Sex ABO Separat. ATCG incub b No. of cells c Take GvHD Survival time Outcome BAC cALL B.V. no + no TBI -I OOOrad 3. Relapse + + 3,3 + no >872 Alive in remission U-K-KI BAC T-ALL Died on inter- K.G. no + no TBI-lOOOrad 2. Relapse no + 4,0 + no 38 stitial pneumonitis M-KI-TU AdAC AML Died on sepsis after 2. BMT B.S. HLA-D? no AlB TB! - 1000rad 2. Relapse + + 8,0 no no 34 without incubation K-P-KI diff. BAC cALL Died on leukemic S.A. no + A/O TBI-lOOOrad 2. Relapse + + 6,0 + no 190 relapse U-K-KI diff. BAC cALL skin Died on leukemic A.G. no no no TBI-IOOOrad 2. Relapse + + 6,0 + (I-lI) 215 relapse U-K-KI AdAC AML B.K. no + no TBI - 1000rad I. Relapse + + 9,5 + no >424 Alive in remission K-P-KI AdAC Ery-L T.G. HLA-D? + no TBI-IOOOrad 2. Relapse + + 6,2 no no 19 Died on pneumonitis K-P-KI Cy AML A.E. no no no TBI-lOOOrad e 2. Remission + + 11,1 + no >220 Alive in remission M-KI-UT BAC AML Died on inter- H.G. no + no TBI-lOOOrad I. Relapse + + 4,3 + no 49 stitial pneumonitis M-KI-GH Cy AUL Died on inter- D.S. no + no TBI-IOOOrad e 1. Remission + + 3,4 + no 64 stitial pneumonitis M-KI-UT BAC cALL Died on MU.H. no no AB/O TBI-IOOOrad 2. Relapse + + 9,1 + no 98 leukemic relapse U-K-KI HLA-D diff. Cy AML skin Kr.G. HLA-DR no O/B TBI-lOOOrad e I. Remission + + 3,4 + (11) > 95 Alive in remission M-KI-UT ident. diff. BAC ALL H.J. no + no TBI-IOOOrad I. Relapse + + 7,7 + no > 53 Alive in remission U-K-KI Cy AML skin M.l. no no no TBI-IOOOrad e I. Remission + + 1,8 + (11) > 52 Alive in remission M-KI-UT a BAC=BCNU, Ara C, Cy I Ad AC=Adriblastin, Ara C, Cy b Final concentration 1:200, incubation at 4° C for 30' C cells X 10 8 per kg body weight d Methotrexate prophylaxis post BMT in all patients e Lungs shielded to 800 rad f U-K-KI = Universitätskinderklinik München; K-P-KI=Kinderpoliklinik der Universität München; M-KI-TU=I. Medizinische Klinik der TU München; M-KI-GH=III. Medizinische Klinik, Klinikum Großhadem; M-KI-UT=Med. Klinik, Universität Tübingen
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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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Page 53 and 54:
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
Page 93 and 94: prognostic characteristics under in
Page 95 and 96: significantly higher in HR} (14.5%,
Page 97 and 98: normal or elevated immunoglobulin l
Page 99 and 100: References Andreeff M, Darzynkiewic
Page 101 and 102: R GROUP 1 ( 1970 - 1971 ) 17 PTS. R
Page 103 and 104: Table 3. Influence of initial featu
Page 105 and 106: LIJ (f) a.. < -1 LIJ Q: u. 0 >- I-
Page 107 and 108: Haematology and Blood Transfusion V
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 139 and 140: % SURVIVAL 100 ~ ~II 0 80 60 40 - -
Page 141 and 142: a) Percentage of donor cell mitoses
Page 143: Table 5. Results of bone marrow tra
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 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
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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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Page 307 and 308:
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Table 1. Monoclonal antibody reacti
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al. 1979; Janossy et al. 1979) is e
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to which this is an exact replica o
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inger JL (1976) Distribution of la-
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I region antigens were found to be
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have been reported to be present on
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V. FunctionalAssays Assays for PHA
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Functional studies of UCHT1 separat
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40 ,...... (5 L.. C o u 30 .9 ~ .~
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with immunohistochemieal methods (L
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can be dissected by cloning. Utiliz
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Table 1. Origin and marker profile
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complete identity of gp 100 from no
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Table 1. Reaction of single anti se
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media. Following 24-h incubation, c
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nonleukemic eells (Greaves 1979). L
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Fig. 2. Cytocentrifuged smears of b
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Modification of amino-groups of hum
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disturb this balance in the directi
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The majority of human blood lymphoc
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of the EBV infected B cells. Howeve
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and immunoglobulins. J Immunol 120:
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" K 10 • j ~ ALL RNlL AL wtfh les
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tion akuter Leukämiezellen in "spo
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D. Results and Discussion J. Acute
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selectively responsive to different
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l1J ~ 100 ~ Q. ::) l1J Z 0 ~ z >- .
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Table 2. Growth inhibition of S49 e
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Reverse Infectious ASC/2X1Q6 transc
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munized animals to 1316 tumor cells
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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
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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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Page 443 and 444:
RELATIONSHIP OF ENDOGENOUS AND EXOG
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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
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
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
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Table 3. Transformation aetivity of
Page 475 and 476:
- 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
Page 491 and 492:
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:
Page 499 and 500:
le of reacting in sensitive radioim
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gic approach. In: Hiatt HH, Watson
Page 505 and 506:
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
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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:
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immunodeficiency, multic10nal lymph
Page 559 and 560:
Bovine leukemia --, proteins of 499
Page 561 and 562:
Human T- cell - -, characterization
Page 563 and 564:
RNA -, of tumor virus 439 Rous sarc
Page 565 and 566:
Haematology andBlood Transfusion Su
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