Modern - Blog Science Connections

More documents

Recommendations

Info

induction in vivo by the RNA retroviruses. It is still a major puzzle that similar or identical genomes can induce quite different malignaneies, as observed for example in the induction of tumors as different as fibrosarcomas, melanomas, and glioblastomas by a single strain of Rous sarcoma virus, and that the same malignancy can be initiated by different viral genomes. I am sure that the pathogenicity of these diseases will be understood much better during the coming years, although this understanding will be achieved not only by analysis of the genomes down to the last base pair but more by examination of the total process of transformation, i.e., the virus, the route of infection, the type and physiologic state of the infected cells, and the response of the total organism to the emergence of transformed cell clones. There was relatively little discussion of DNA tumor viruses, except for an overview of the structure of the primate lymphotropic herpesviruses and discussions of the pathogenesis of Epstein - Barr virus (EBV) infections. The pathogenic events leading from primary lymphoproliferative EBV infections to complete recovery with a lifelong carrier state and the development later of monoclonal malignancies or an immediate progression of an acute monucleosis into a malignant fatallymphoproliferative disease are particularly interesting and deserve intensive study. The report of lytic activity of EBV is important for two reasons: it allows better study in vitro of EBV and it may explain the infection of epithelial cells in vivo. Of importance also is the demonstration of EBV genomes in normal parotic cells whieh may answer the old question of where EBV multiplies during the long periods of oral excretion. On reflecting generally on the viral studies I want to repeat a caution sounded often before : We must not ignore the fact that some of our virus models, and I am referring particularly to the avian and murine retroviruses, are highly artificial, using inbred selected animals and laboratory-propagated and perhaps laboratory-created viruses, whose rele \Wlnce to naturally occurring disease is at least in part questionable, although their value for a basic understanding of cell function and regulation is undisputed. Studies in outbred animal populations, such as cats and cattle, may be more comparable to reallife. Particularly intriguing is the situation of "virus-free" cat leukemias in which the virus might have acted as a "hit and run" villain, leaving either only a small part of itself behind or changing only the genes responsible for cell regulatory mechanisms without a need for persistence of any part of the viral genome, a mechanism which has also been considered for the transformation of cells by some DNA viruses, particularly the herpesviruses. In yesterday's sessions we heard about very exciting developments in cell biology and immunology. The differentiation of the cells of the hematopoietic and the immune systems into many highly specialized cell subpopulations has been analyzed in detail, thus allowing a much finer and detailed analysis of the immune mechanisms whieh play a role in the emergence of tumors and the defense of the organism against them. Use of monoclonal antibodies has alm ost revolutionized this field, and it will be most interesting to study not only the physiologie and immunologie functions and antigenie identities of the various cell types but also their susceptibility to exogenous viral infection, to activation of endogenous viral genes, and to chemical or physical carcinogens. The development of cell culture techniques and separation of various cell populations have progressed rapidly and already have improved our understanding of normal differentiation and of regulatory disturbances leading to malignant transformation, although this is another area in whieh we must remember that isolated cells in vitro may behave quite differently from cells in the intact organism with its multiple cell interactions and regulatory mechanisms, to which we should add Dr. Moore's new ly defined "oncgene" -mediated "pericrine" controls as well as still unidentified influences. The report of thymic nurse cells within which differentiation of other cells seems to occur is an intriguing observation, the general significance of which needs further exploration. In addition the nude thymusless, the spleenless, and the very special mice lacking both of these organs are now joined by the "beige mouse," astrain whieh is deficient for natural killer cells and wh ich will permit a further disseetion of the immune defenses against tumor development. The new perspective of the various, specific chromosomal aberrations in different diseases should stimulate furt her research to relate specific chromosomal to specific pathologie changes, and in this respect the studies on the X-linked lymphoproliferative syndrome (Duncan's disease) which is associated with 548
immunodeficiency, multic10nal lymphoproliferation, and finally lymphoma or lymphosarcoma are particular interesting. Better tools will be needed for a finer analysis of the human genetic material before we can understand the genetic influences on leukemias and lymphomas, as our current methods of chromosomal analysis are at best very crude. Another significant observation was the identification of la antigens on various tumor cells and the implication that they have not only immunologie functions but also play some role in differentiation and cell regulation. In closing, it must be said that we are still far from understanding the pathogenicity of leukemia, lymphoma, and related diseases but that our knowledge has rapidly increased and will continne to do so with the help of modern molecular, virologie, and immunologie techniques developed during the last years. I must, however, remind you that in the c1inical arena the battle against leukemia needs a better exchange and co-ordination between c1inidans, immunologists, molecular biologists, geneticists, and virologists. Only then can our potential be realized. 549
Page 1 and 2:
Haematology and Blood Transfusion 2
Page 3 and 4:
Dr. Rolf Neth, Universitäts-Kinder
Page 5 and 6:
Participants of the Meeting Aaronso
Page 7 and 8:
Kurth, R, Friedrich-Miescher-Labora
Page 9 and 10:
Wilsede Scholarship Holders (Grante
Page 11 and 12:
Preface Gut ist eine Lehrart, wo ma
Page 13 and 14:
Personal and scientific discussion
Page 15 and 16:
Acknowledgement We should like to t
Page 17 and 18:
Wilsede, June 21 1978 Memorial Trib
Page 19 and 20:
limiting benign lymphoproliferative
Page 21 and 22:
this most unlikely, however (for re
Page 23 and 24:
longer subject to the same control
Page 25 and 26:
Bregula U, Wiener F, Harris H (1971
Page 27 and 28:
fresh lymph node biopsies from ten
Page 29 and 30:
Fig. 3. Binucleate mitosis in an ob
Page 31 and 32:
y Fig. 4. Schematic diagram of post
Page 33 and 34:
than that among patients with Stage
Page 35 and 36:
Tests of binding affinity, agglutin
Page 37 and 38:
N Engl J Med 297: 963-968 - Green I
Page 39 and 40:
Clinical Aspects
Page 41 and 42:
"ring chromosome". "Mar" is marker,
Page 43 and 44:
191 chromosomally abnormal patients
Page 45 and 46:
tumors of both African and non-Afri
Page 47 and 48:
Haematology and Blood Transfusion V
Page 49 and 50:
Retrospective group 26/93 evolved l
Page 51 and 52:
Page 53 and 54:
Treatment
Page 55 and 56:
advantage in terms of duration of f
Page 57 and 58:
leukaemia. An analysis of 168 patie
Page 59 and 60:
11. Treatment Program Chemotherapy
Page 61 and 62:
efractory congestive heart failure
Page 63 and 64:
period (Sequence II) was gene rally
Page 65 and 66:
children with a multiple drug proto
Page 67 and 68:
DAYS 1 5 10 15 20 25 30 35 , I I I
Page 69 and 70:
Biologically Drug Outcome fit" sens
Page 71 and 72:
may counterbalance the potential be
Page 73 and 74:
Ht (0--0) 50 40 30 20 10 0 Platelet
Page 75 and 76:
10 7 ,-----------------------------
Page 77 and 78:
11. Haematological and Biochemical
Page 79 and 80:
0\ 0\ INTERFERON ... 10 3 rl E "'
Page 81 and 82:
Page 83 and 84:
("pre-B" phenotype) has been descri
Page 85 and 86:
human bone marrow cells exhibit the
Page 87 and 88:
10 9.,0 MBKCC .. .,4 B prot:oool 1'
Page 89 and 90:
demann W, Büehner T, Arlin Z, Gee
Page 91 and 92:
-...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:
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:
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 149 and 150:
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 and 160:
Page 161 and 162:
HS, HL- Heme >_ 40 0 HS I ;:. =====
Page 163 and 164:
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 179 and 180:
Page 181 and 182:
F. Transformation of Mouse Bone Mar
Page 183 and 184:
Page 185 and 186:
were carried out with 3H-MTX in the
Page 187 and 188:
Page 189 and 190:
the lysozyme cDNA prepared from ovi
Page 191 and 192:
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 203 and 204:
Page 205 and 206:
Dc;bt CT + i J.I9 Raji; 1. i .. 100
Page 207 and 208:
c. Discussion During infectious mon
Page 209 and 210:
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 219 and 220:
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:
Page 229 and 230:
Charaeteristie Morphologie maturati
Page 231 and 232:
after TPA-induction (Table 3). The
Page 233 and 234:
PA (1978) Reactivity of a rabbit an
Page 235 and 236:
Blood Monocyte. B lood Monocytes 1-
Page 237 and 238:
Page 239 and 240:
and nonhistone proteins can serve a
Page 241 and 242:
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 257 and 258:
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
Page 279 and 280:
Page 281 and 282:
the macrophage series in which the
Page 283 and 284:
Page 285 and 286:
Table 1. Production of factor depen
Page 287 and 288:
Page 289 and 290:
Table 1. Characteristics of the adh
Page 291 and 292:
Fig. 3. A human marrow culture at 6
Page 293 and 294:
300 250 • HYPERPROLIFERATIVE PATT
Page 295 and 296:
Fig. 9. Nonadherent population from
Page 297 and 298:
The cobblestone areas were often no
Page 299 and 300:
L (1976) Induction of colony format
Page 301 and 302:
B. Materials and Methods J. Tissue
Page 303 and 304:
Fig. 2. Ultrastructural appearance
Page 305 and 306:
Page 307 and 308:
Page 309 and 310:
Table 1. Monoclonal antibody reacti
Page 311 and 312:
al. 1979; Janossy et al. 1979) is e
Page 313 and 314:
to which this is an exact replica o
Page 315 and 316:
inger JL (1976) Distribution of la-
Page 317 and 318:
I region antigens were found to be
Page 319 and 320:
have been reported to be present on
Page 321 and 322:
V. FunctionalAssays Assays for PHA
Page 323 and 324:
Functional studies of UCHT1 separat
Page 325 and 326:
Page 327 and 328:
40 ,...... (5 L.. C o u 30 .9 ~ .~
Page 329 and 330:
with immunohistochemieal methods (L
Page 331 and 332:
Page 333 and 334:
can be dissected by cloning. Utiliz
Page 335 and 336:
Table 1. Origin and marker profile
Page 337 and 338:
Page 339 and 340:
complete identity of gp 100 from no
Page 341 and 342:
Table 1. Reaction of single anti se
Page 343 and 344:
Page 345 and 346:
media. Following 24-h incubation, c
Page 347 and 348:
nonleukemic eells (Greaves 1979). L
Page 349 and 350:
Page 351 and 352:
Fig. 2. Cytocentrifuged smears of b
Page 353 and 354:
Modification of amino-groups of hum
Page 355 and 356:
disturb this balance in the directi
Page 357 and 358:
The majority of human blood lymphoc
Page 359 and 360:
of the EBV infected B cells. Howeve
Page 361 and 362:
and immunoglobulins. J Immunol 120:
Page 363 and 364:
" K 10 • j ~ ALL RNlL AL wtfh les
Page 365 and 366:
tion akuter Leukämiezellen in "spo
Page 367 and 368:
D. Results and Discussion J. Acute
Page 369 and 370:
selectively responsive to different
Page 371 and 372:
Page 373 and 374:
l1J ~ 100 ~ Q. ::) l1J Z 0 ~ z >- .
Page 375 and 376:
Table 2. Growth inhibition of S49 e
Page 377 and 378:
Reverse Infectious ASC/2X1Q6 transc
Page 379 and 380:
Page 381 and 382:
munized animals to 1316 tumor cells
Page 383 and 384:
Page 385 and 386:
Fig. 3. Expression of retroviral gp
Page 387 and 388:
pg70. J Exp Med 143: 151-166 - McGr
Page 389 and 390:
Table 1. Expression of tumor antige
Page 391 and 392:
Virological and Molecularbiological
Page 393 and 394:
Table 1. Oncogenic properties of re
Page 395 and 396:
also Fig. 1). It followed that the
Page 397 and 398:
whether this sequence is related to
Page 399 and 400:
zed in infected cells argue that th
Page 401 and 402:
a specific viral transforming prote
Page 403 and 404:
detect viral RNA as the only charac
Page 405 and 406:
Eisen H (1980) Myeloproliferate vir
Page 407 and 408:
p,60- -34K - 1 2 3 4 Fig. 1. In vit
Page 409 and 410:
.. p - • a'T ... I .t'l Fig. 4. D
Page 411 and 412:
Page 413 and 414:
Fig. 2. Photomicrographs of NY68 in
Page 415 and 416:
DEAE (o(lJmn 'liI GI -2 2 o e s 1
Page 417 and 418:
vity was deterrnined. For endogenou
Page 419 and 420:
pr 180 - - - P 12/15 - A B c D E F
Page 421 and 422:
85,- 66- -27 - -66 40- 27- -1'9 19-
Page 423 and 424:
Page 425 and 426:
= 0.5 o E Q. o ILI 0.4 (J) « ILI .
Page 427 and 428:
Table 1. Oncogenic potential of avi
Page 429 and 430:
100 III GI c: o "8 80 > w
Page 431 and 432:
Expt. No. Infecting virus Proportio
Page 433 and 434:
Haematology and Blood 'fransfusion
Page 435 and 436:
sequences, provided its gag portion
Page 437 and 438:
77:3009-3013 - Hu SSF, Moscoviei C,
Page 439 and 440:
RI 2.2 md and Hind III 2.6 md leuke
Page 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
Page 455 and 456:
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: Haematology and Blood Transfusion V
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 531 and 532: SSV TrS-gp labeled effectively with
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: Haematology and Blood Transfusion V
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
show all

Modern - Blog Science Connections

Create successful ePaper yourself

Delete template?

Save as template?