Chromosome Studies of a Contagious Reticulum Cell Sarcoma of the Syrian Hamster 1
HERBERT L. COOPER,2 CAROL M. MACKAY,B and
WILLIAM G. BANFIELO,B National Institute 01 Dental Re-
search and National Cancer Institute,4 Bethesda, Maryland
A CONTAGIOUS reticulum cell sarcoma (TM)
arising spontaneously in a Syrian hamster was
described by Brindley and Banfield (1). The
tumor had been carried by subcutaneous implantation in hamsters through 12 passages at the time of
their report, and through 80 passages at the present
writing. When tumor-free animals were caged
with tumor-inoculated animals, 9 of 10 uninoculated hamsters developed tumors histologically
identical to the original tumor. With cell-free
tumor extracts, no tumor-producing agent could
be demonstrated, but feeding of tumor tissue resulted in tumor development in 2 of 5 animals.
Brindley and Banfield suggested that gnawing of
ulcerated tumors and cannibalism, with direct
transfer of tumor cells from inoculated to uninocu-
lated animals, might be the mechanism of contagion. They emphasized that, while intact cells
seemed necessary to accomplish such contagion,
the possibility of a subcellular oncogenic agent
carried by the cells was not excluded.
In an effort to determine whether direct cell implantation might be involved in contagious
transmission of this tumor, detailed chromosome
studies of tumors transmitted by subcutaneous
Received April 16, 1964.
Human Genetics Branch, National Institute of Dental
Research.
3 Laboratory of Pathology, National Cancer Institute.
• National Institutes of Health, Public Health Service,
U.S. Department of Health, Education, and Welfare.
I
2
691
737-891--64----13
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SUMMARY-Chromosomes of a contagious reticulum cell sarcoma from the
Syrian hamster were studied. Tumors arising after subcutaneous implantation, after tumor fragments were fed, and in tumor-free animals, after they
were caged with tumor-bearing animals, were used. The stock tumor, maintained by serial subcutaneous passage in male hamsters, had a sharp modal
chromosome number of 51, with a unique karyotype including a minute
marker chromosome. Each tumor developing in either sex, after any mode
of passage, had a karyotype identical to that of the parent tumor, with one
exception. In that tumor, the modal chromosome number was 50, and the
karyotype was identical to that of the parent tumor except for the regular
absence of 1 chromosome in group #16-19. These findings support the
hypothesis of direct implantation of tumor cells as the mechanism of contagion.
This may be the mode of tumor transmission of some naturally occurring
neoplasms.-J Nat Cancer Inst 33: 691-706, 1964.
692
COOPER, MACKAY, AND BANFIELD
implantation, by feeding, and by cage contact
were undertaken.
MATERIALS AND METHODS
RESULTS
Table 1 summarizes data on the tumor passages
studied cytologically. The passages were designed
Tumor #60TM13
This specimen represents the continuously carried
tumor, passed serially by subcutaneous implantation in male hamsters. Table 1 shows that, of
the 30 cells examined, 27 had a chromosome
number of 51. In addition, all but 3 of these
modal-number cells had a minute chromosome
(fig. 2) which could serve as a marker.
Detailed karyotypes were prepared from 5 modal
cells. All were essentially identical and figure 3
shows a typical karyotype. All the modal cells
had 9 members of chromosome group #16-19,
5 members of group #20,2 members of group #21,
and 1 X chromosome. In addition, chromosome
group #1 4 had an extra chromosome; group
#6-9
Y was consistent with an XY sex-chromosome constitution; and in chromosome group #14,
2 extra chromosomes were present, as judged by
total length and median centromere placement.
There seems to be a high degree of karyotypic
consistency among modal cells and a marked
preponderance of such modal cells in this tumor.
In summary, the TM tumor has a vigorous and
karyotypically stable stem line, carrying a minute
marker chromosome and 7 chromosomes in addition to the normal Syrian hamster chromosome
number of 44. Morphologically, the extra chromosomes fall into group #1-4 (1 extra), group
#14 (2 extra), group #16-19 (1 extra), and group
#20 (3 extra). Groups #5-9
Y, 10-13, 15, and
+
+
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The tumor was carried by serial subcutaneous
injection of small fragments offreshly excised tumor
into male Syrian hamsters randomly bred at the
National Institutes of Health.
For chromosome studies, tumors were passed
from the line of male carriers to animals of both
sexes, by subcutaneous implantation and also by
feeding freshly excised tumor tissue. Tumor was
also passed after healthy males and tumor-bearing
males were caged together. When a tumor arose
in the head, neck, or larynx in a tumor-fed or cageexposed animal, it was killed. The tumor w~s
then excised and implanted subcutaneously III
hamsters of the same sex as the experimental
animal. The resulting tumor was studied
cytologically.
Animals bearing rapidly enlarging tumors were
given 1.4 mg per kg of Vinblastin sulfate (Lilly)
intra peritoneally to produce mitotic arrest. Mter
6 hours the animals were killed and tumors excised.
Becaus~ of its lymphomatous nature, teasing of
tumor fragments in isotonic saline produced a
fairly uniform single-cell suspension. SUc? suspensions were centrifuged at 225 X g for 5 mIllutes,
the supernatant was removed, and the cells were
resuspended in 1 percent sodium citrate. Mter 10
minutes, the cells were spun down at 150 X g for 5
minutes and the supernatants were discarded.
Three to 5 ml of freshly mixed cold acetic-methanol
(1: 3) was added drop by drop with gentle agitation
and the cells were allowed to fix for 10 minutes.
Mter centrifugation, the fixed cells were resuspended in enough fresh acetic-methanol to m.ake a
faintly cloudy suspension. Small drops of this cell
suspension were applied to chilled coverslips and
dried rapidly by blowing. When thoroughly dry,
coverslips were inverted onto a drop of 1 percent
lactic-acetic-orcein (2) on a slide, the excess stain was
removed by blotting, and the preparations were
examined with phase-contrast microscopy.
to utilize the prominent X chromosome of the
Syrian hamster (fig. 1) as a cytogenetic marker.
Table 1 shows the chromosome number distributions for 30 clear metaphase plates from each tumor.
Metaphase figures were chosen under low magnification for chromosomal clarity and apparent completeness (absence of obvious cell breakage).
Karyotypes were made from suitably clear modalnumber cells by photographic enlargement and
identification of chromosomes according to the
groups indicated in the normal Syrian hamster
karyotype (fig. 1), which contains 44 chromosomes.
In the interest of uniformity in the literature, the
chromosome numbering in figure 1 was changed
from that used in our previous publication (3) to
conform with the equally convenient system
adopted by Lehman et at. (4).
693
CHROMOSOME STUDY OF CONTAGIOUS HAMSTER TUMOR
T ABLE I.-Summary of tumor passages studied and chromosome number distribution of 30 clear metaphases from
each tumor*
Chromosome numbert
Tumor designation
Type of
passaget
Sex of
host
60TM13 (carrier)
60TM12
67TM25
68TM14
65TM18
77TM7
SC
SC
F§
F
F
C
d'
45
'?
49
50
:~
1
'?
d'
48
2
2
2
9
1
d'
d'
:1
2
19(18)
3
51
27(24)
25(23)
20(20)
26(26)
-
52
4
3
1
27(27)
21 are indistinguishable from the same groups in
the normal karyotype. The sex-chromosome constitution appears to be XV.
Tumor #60TM12
This tumor arose from the stock tumor implanted
subcutaneously in a female hamster. Of 30 metaphases examined, all had a single X chromosome,
25 had a chromosome number of 51, and 23 of the
25 carried the minute marker (table 1). Microscopic and karyotypic analysis of the modal cells
again revealed a high degree of uniformity. A
representative metaphase and karyotype are shown
in figures 4 and 5. The karyotype was indistinguishable from that of the parent line. In addition
to the details already mentioned for this specimen,
the extra members of groups #1-4, #14, #16-19,
and #20 were present, as in the parent tumor.
Despite its passage in a female animal, the sexchromosome constitution of the tumor cells
appeared to have remained XV. The implanted
tumor cells apparently grew successfully after
transplantation and remained karyotypically
unchanged.
Tumor #67TM25
This tumor arose in the larynx of a male hamster
after the first feeding of tumor tissue from the stock
line. It was excised, implanted subcutaneously in
a male hamster, and then studied: Of 30 metaphases, 20 had a chromosome number of 51 (table
1), and all cells carried a single X chromosome
VOL. 33, NO.4, OCTOBER 1964
and the minute marker. Microscopic and karyotypic examination (11gs. 6 and 7) revealed the
modal cells to be karyotypically homogeneous and
cytogenetically indistinguishable from the parent
tumor line. Table 1 shows that a wider spread of
chromosome numbers was found in this tumor than
in those previously studied. This may be due to
a combination of technical factors and possible
greater selective pressures of tumor production by
tissue feeding. Cells best adapted for survival on
subcutaneous inoculation may not possess such a
strong advantage over some karyotypically altered
members of the cell population in the feeding situation. As in any heteroploid cell line, despite the
presence of a predominant modal karyotype, nonmodal cells are probably always present and, under
altered growth conditions, may enjoy favorable
selection.
Tumor #68TM 14
This tumor developed In the submaxillary
salivary gland of a female hamster 29 days after
the first feeding of tumor tissue from the stock line.
After subcutaneous passage in a female hamster it
was studied chromosomally: Of 30 cells examined,
26 had a chromosome number of 51, and all carried a single X chromosome and the minute
marker (table 1). The karyotypes of these cells
were homogeneous and showed no apparent difference from the stock tumor line (figs. 8 and 9).
Despite having arisen in a female hamster after
feeding, the sex-chromosome constitution is consistent with an XY pattern.
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• All tl.:rr:ors were passed (rom carriers in whom the tumor was maintained by serial subcutaneous inoculation.
tSC = subcutaneous; F = (eeding; C - cage contact.
tNot including minute marker chromooome. Number of modal cells with minute marker shown in parenthe..es.
iAII tumors arising after leeding or cage contact wore passed once subcutaneously in animals of the sarno sex as tbe original host.
694
COOPER, MACKAY, AND BANFIELD
Tumor #65TM18
Tumor #77TM 7
This tumor was first detected in the submaxillary
salivary gland of a male hamster 30 days after it
was caged with carrier animals bearing subcutaneous tumors. On several occasions this animal had
cannibalized his tumor-bearing cage mates. The
original tumor was transplanted subcutaneously
in male animals and studied chromosomally.
Table 1 shows that #77TM7 also had a markedly
predominant modal chromosome number of 51.
All cells examined carried the minute marker
chromosome (fig. 14). These cells were karyo-
DISCUSSION
When the TM hamster reticulum cell sarcoma
was transferred from one hamster to another,
either by subcutaneous implantation, by feeding,
or by cage contact, the resulting tumor was karyotypically indistinguishahle from the parent tumor
in every case but one. The karotype of the parent
tumor was uniquely altered from that of the
normal hamster and contained 7 extra chromosomes and a minute marker chromosome. The 7
extra chromosomes were distributed among the
various chromogomal groups of the hamster karyotype in characteristic fashion. The altered karyotype of this tumor was therefore easily recognized
and deviations from it were readily detectable.
In the one tumor transferred by feeding, in which
a karyotypic difference was observed, a single
chromosome was absent. The remainder of the
karyotype had all the characteristic features of the
parent tumor, including the marker chromosome.
Further, whether the tumor was grown in male or
female animals, only 1 X chromosome could be
identified, and the karyotype was always consistent
with an XY sex-chromosome constitution.
This study was undertaken to clarify whether
contagion in this tumor (1) was mediated by direct
implantation of malignant cells or by transmission
of some subcellular oncogenic agent by intact cells
which newly induced the tumor in each host. The
results strongly support the direct implantation and
growth of malignant cells as the mechanism of contagion. A subcellular agent would have to induce
a highly specific set of karyotypic changes, resulting in the repeated production of a unique and
unusual karyotype, including a marker chromosome, loss or alteration of 1 X chromosome in
female animals, and specific increases in the number of members in certain chromosome groups.
No known oncogenic agent produces cytogenetic
effects even faintly approaching such a degree of
specificity. The simian vacuolating virus (SV40),
when producing in vitro transformation of human
cell cultures, has been reported to induce nonrandom loss of certain chromosomes (5, 6). However, that phenomenon does not involve the degree
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This tumor developed in the soft tissues of the
jaw of a male hamster 59 days after the first feeding of samples of the stock tumor. It was studied
after subcutaneous passage in another male
animal. The modal chromosome number was 50
rather than 51, as in the previous tumors examined
(table 1), but 18 of 19 modal cells carried the
minute marker chromosome (fig. 10). When these
cells were karyotyped, it became apparent that
the difference between the modal cells of this tumor
and those of the previous tumors examined was due
to the presence of only 8 members of group #16-19
(fig. 11). The extra member of this group found
in the stock tumor line was not present. In all
other respects, most modal cells were karyotypically
indistinguishable from the parent tumor, but there
were further deviations in some cells (figs. 12 and
13). In these cells, in addition to absence of the
extra member of group #16-19, only 3 members of
group #14 were present, instead of 4. In place of
the missing chromosome there was an additional
small chromosome, somewhere between group #20
and 21 in morphology.
The strong karyotypic resemblance between this
tumor and the stock tumor supports the impression
that the #65TM18 tumor cells are direct descendants of some of the stock tumor tissue fed to the
experimental animal. The single chromosome
difference in group #16-19 may result from
selective factors in the feeding situation which
favored the growth of this particular variant,
probably present with a small frequency in the
stock tumor.
typically indistinguishable from the parent tumor
(fig. 15).
CHROMOSOME STUDY OF CONTAGIOUS HAMSTER TUMOR
VOL. 33, NO.4, OCTOBER 1964
in the same optimum modal karyotype. While this
possibility seems more likely than that of directed
karyotypic change, it appears improbable for such
rigid selection to exist that a single minute chromosome, among other specific changes, is always present in the most successful karyotype. It also
seems unlikely that the favored karyotype can so
surpass all others in vigor as to give a nearly uniform
karyotypic picture in the cells of most tumors.
Our findings appear most easily compatible with
the hypothesis that the mechanism of contagion of
the TM hamster tumor is direct implantation of the
original tumor cells.
To our knowledge, the only other tumor shown to
be contagious without artificial intervention and in
which no virus has been demonstrated is the venereal tumor of the dog (73). The histology of this
tumor is disputed, some authors describing it as
lymphocytic (74), others denying this (75), and
still others calling it a reticulum cell sarcoma (76).
Cytogenetic evidence suggests that it may be passed
by direct cell implantation from one animal to
another during copulation (17), although again the
alternatives just considered could not be ruled out.
Other tumors in experimental animals that have
been transmitted by feeding through oral instillation of tumor homogenates are the Yoshida rat
sarcoma, the Walker rat carcinoma, the Jensen rat
sarcoma, the mouse Sarcoma 37, the DMBA
spindle cell sarcoma, and the Ehrlich carcinoma
(78). The report of these transmissions did not
indicate whether the tumors were contagious by
cage contact between normal and tumorous animals.
Another lymphoid tumor, the bovine lymphosarcoma, may be naturally contagious (79), but this
has not been proved. Also, no evidence is yet
available as to the mechanism that might mediate
such contagion.
The evidence presented here supports direct cell
implantation as a mechanism of tumor spread
among hamsters, at least under cage conditions.
The additional possibility that the naturally occurring venereal tumor of the dog is also spread in
this way, together with the fact of successful transmission, by feeding, of a number of mouse and rat
tumors, suggests that direct cell implantation may
be a significant mechanism in the transmission of
other neoplasms, possibly even in humans. The
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of specificity shown in this study, since its occurrence varied in different cultures. When SV40
transforms Syrian hamster cells in vitro, it produces
marked chromosome breakage and rearrangement,
with constantly changing karyotypes (3) 7), the
opposite of the present findings. When SV40 is
used to produce tumors in vivo in hamsters, some
evidence suggests that here, too, chromosomal
breakage and variable changes occur (7). Other
oncogenic viruses, such as polyoma (8) and adenovirus type 12 (9), appear to have less prominent
and rather inconstant cytogenetic effects.
In chronic granulocytic leukemia of man, a
small, specific chromosome deletion is present (70).
However, transmissibility of this neoplasm has not
been demonstrated except in specially treated subjects (77). Such a specific, single chromosome
defect might possibly result from direct viral action,
although no evidence has yet been presented to
suggest that this is true in human chronic granulocytic leukemia.
Radiation-induced murine leukemia has been
reported to be associated with a specific single
extra chromosome (72). Further, there is evidence that the disease may be transmitted by a
virus inducing the same karyotypic change in
newly infected animals, which presumably thereby
produces the leukemia. If additional investigation
supports these findings, the possibility of virusinduced specific karyotypic change must be more
seriously considered for the hamster tumor we
have studied. However, the number, specificity,
and reproducibility of the karyotypic changes found
in the TM hamster lymphoma would require a
marvelous precision of action on the part of the
hypothetical virus, much greater than that necessary for a single chromosome alteration. An additional attribute of such a virus would be its ability
to affect female cells differently from male ones,
causing loss of 1 of the X chromosomes in the
former. Nevertheless, the possibility of an oncogenic virus with the required degree of specificity,
however unlikely, cannot be entirely excluded,
since we have little knowledge of the mechanisms
involved in virus-induced chromosomal changes.
Also, an oncogenic virus may repeatedly induce
malignancy with a wide variety of nonspecific
karyotypic alterations, and subsequent selection by
competition during growth may repeatedly result
695
696
COOPER, MACKAY, AND BANFIELD
found in the TM hamster tumor, but the recurrent
finding of a particular type of chromosomal
aberration bears further investigation. Such a
finding is consistent with almost any postulated
mode of oncogenesis, so that the possibility of
direct cellular transmission, perhaps in a segment
of the affected population, may be worthy of
consideration.
ADDENDUM
After completion of this study, a tumor was
observed in an uninoculated female hamster that
had been caged with male carriers. The tumor
was noted in the cervical lymph nodes 70 days
after initial exposure. Chromosome studies of
material taken directly from this tumor showed a
modal chromosome number of 51 and a karyotype
identical to that of the stock tumor. In particular,
the minute marker chromosome was present and,
despite growth in a female, the tumor cells showed
only a single X chromosome.
REFERENCES
(1) BRINDLEY, D. C., and BANFIELD, W. G.: A contagious
tumor of the hamster. J Nat Cancer Inst 26: 949957, 1961.
(2) WELSHONS, W. J., GIBSON, B. H., and SCANDLYN, B.
J.: Slide processing for the examination of male
mammalian meiotic chromosomes. Stain Techn 37:
1-5, 1962.
(3) COOPER, H. L., and BLACK, P. H.: Cytogenetic studies
of hamster kidney cells transformed by the simian
vacuolating virus (SV40). J Nat Cancer Inst 30:
1015-1043,1963.
(4) LEHMAN, J. M., MACPHERSON, I., and MOORHEAD, P.
S.: Karyotype of the Syrian hamster. J Nat Cancer
Inst 31: 639-650, 1963.
(5) SHEIN, H. M., and ENDERS, J. F.: Transformation induced by simian virus 40 in human renal cell cultures. I. Morphology and growth characteristics.
Proc Nat Acad Sci USA 48: 1164-1172,1962.
(6) MOORHEAD, P. S., and SAKSELA, E.: Non-random
chromosomal aberrations in SV40-transformed
human cells. J Cell Comp Physiol 62: 57-83, 1963.
(7) COOPER, H. L., and BLACK, P. S.: Cytogenetic studies
of three clones derived from a permanent line of
hamster cells transformed by SV40. J Cell Comp
Physiol. In press, 1964.
(8) MACPHERSON, I. A.: Characteristics of a hamster cell
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Inst 30: 795-815, 1963.
(9) COOPER, H. L.: Unpublished observations, 1963.
JOURNAL OF THE NATIONAL CANCER INSTITUTE
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occurrence of "epidemics" of leukemia among
groups of children (20) may be the result of such
transmission, possibly by hand-to-mouth or mouthto-mouth passage of viable malignant cells. The
chief objection to such a mode of transmission in
humans, as opposed to inbred laboratory animals,
is histoincompatibility, which would result in
immunological rejection of foreign tumor cells.
However, histoincompatibility is a genetic phenomenon, governed by a finite number of genetic
loci. With karyotypic alterations, reported to be
common in leukemias and solid tumors (21), an
occasional cell type may arise in which chromosomal deletion has led to loss of all or most of the
genetic loci concerned with histoincompatibility.
Malignant cells of this type might then be communicable by direct transmission.
Of particular interest in this connection is the
lymphoma of children in central Africa, described
by Burkitt (22). This tumor is unusually prevalent in an area having certain conditions of climate
and altitude, which suggests that it may be spread
by an arthropod vector transmitting an oncogenic
virus (23).
The African lymphoma has been described
histologically as a poorly differentiated lymphocytic lymphoma with interspersed histiocytes
(24, 25). This description is similar to that of the
contagious TM hamster reticulum cell sarcoma
discussed in this report (1). Moreover, a prominent
feature of the African lymphoma is its appearance
in one or more quadrants of the jaw (26), a location
similar to that of one of the animals fed tumor in
our study. At least one investigator has suggested
the parotid salivary gland as a frequent primary
site for the Burkitt's lymphoma (27), which again
parallels our findings in one of our fed animals, and
in the animal that contracted the tumor following
cage contact.
Direct chromosome studies of several Burkitt's
lymphomas have been reported by Jacobs et al.
(28). Of 1 0 cases, in whom cytogenetic information
could be obtained, these workers found 5 with no
detectable chromosomal abnormality. Of the
remaining 5, 4 had variable abnormalities which
had in common the appearance of an unusually
long acrocentric chromosome and often a missing
#2 chromosome. Clearly there is no specificity of
karyotype in Burkitt's lymphoma resembling that
CHROMOSOME STUDY OF CONTAGIOUS HAMSTER TUMOR
VOL. 33, NO.4, oarOBER 1964
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(19)
(20)
(27)
(22)
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THEILEN, G., ApPLEMAN, R., and WIXOM, H.: Epizootiology of lymphosarcoma in California cattle.
Ann NY Acad Sci 108: (3) 1203-1213, 1963.
HEATH, C. W., JR., and HASTERUK, R. L.: Leukemia
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BURKITT, D.: A sarcoma involving the jaws in African
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- - - : A lymphoma syndrome in African children.
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O'CONOR, G. T.: Malignant lymphoma in African
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WRIGHT, D. H.: Cytology and histochemistry of the
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BURKITT, D., and O'CONOR, G. T.: Malignant lymphoma in African children. I. A clinical syndrome.
Cancer 14: 258-269, 1961.
LEHNER, T.: Involvement of the jaws in African lymphoma. Lancet ii: 39, 1963.
JACOBS, P. A., TOUGH, I. M., and WRIGHT, D. H.:
Cytogenetic studies in Burkitt's lymphoma. Lancet
ii: 1144-1146, 1963.
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(10) NOWELL, P. C., and HUNGERFORD, D. A.: Chromosome
studies in human leukemia. II. Chronic granulocytic leukemia. J Nat Cancer Inst 27: 1013-1035,
1961.
(11) LEVIN, R. H., WUANG, J., TJIo, J. H., CARBONE, P. P.,
FREI, E., and FREIREICH, E. J: Persistent mitosis of
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(12) WALD, N., UPTON, A., JENKINS, V., and BoRGES, W.:
Radiation-induced mouse leukemia: consistent occurrence of an extra and a marker chromosome.
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(13) KARLSON, A. G., and MANN, F. C.: The transmissible
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(14) DE MONBREUN, W. A., and GOODPASTURE, E. W.:
An experimental investigation concerning the nature
of contagious lymphosarcoma of dogs. Amer J
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(15) STUBBS, E. L., and FURTH, J.: Experimental studies
on venereal sarcoma of the dog. Amer J Path 10:
275-286, 1934.
(76) KAALUND-Jj<lRGENSEN, 0., and THOMSEN, A. S.: Das
iibertragbare venerische Sarkom bei Hunden.
Z
Krebsforsch 45: 385-398, 1937.
(77) TAKAYAMA, S., and MAKINO, S.: Cytological studies of
tumors. XXXV. A study of chromosomes in vene-
697
JOURNAL OF THE NATIONAL CANCER INSTITUTE, VOL.
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PLATE
140
39/2
x
y
2
6
3-4
7-8
13
9
14
16 - - - 1 9
FIGURE
10
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11-12
5
15
20
21
l.-Karyotype of normal male Syrian hamster, 44 chromosomes.
2.-Metaphase chromosomes of a modal cell from specimen #60TM13, the stock tumor; 51 chromosomes plus a minute marker chromosome (arrow).
FIGURE
COOPER, MacKAY, AND BANFIELD
737-891-64----14
699
PLATE 141
JOURNAL OF THE NATIONAL CANCER INSTITUTE, VOL. 33
52/10
60TM13
. ~ BRlllionl
X
2
'4
,. r. r.
).t'"
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8
9
I '1,0 U" 11(\ n"
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',~,~-
,14
'- --'---,(z
"
16
:_'-:,-="-,-
""S~"~~~
19
.,
3.-Karyotype of cell shown in figure 2. Compare with figure 1. Note: single X chromosome, extra
member of group #1-4, 2 extra members of group #14, 1 extra member of group #16-19, 3 extra members of
group #20. Other groups appear normal.
FIGURE
4.-Metaphase chromosomes of a modal cell from specimen #60TM12 (see text); 51 chromosomes plus
a minute marker chromosome (arrow).
FIGURE
700
COOPER, MacKAY, AND BANFIELD
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II~J2
10
PLATE 142
JOURNAL OF THE NATIONAL CANCER INSTITUTE, VOL. 33
60TMI2
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«i In )0 1~
6
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8-9
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14
- - 13
II
IX
15
06AG(\lOOQ
16
19
6
5.-Karyotype of cell shown in figure 4. Indistinguishable from stock tumor (fig. 3). Sex-chromosome
constitution appears to be XY, though host was female.
FIGURE
6.-Metaphase chromosomes of a modal cell from specimen #67TM25 (see text); 51 chromosomes plus
a minute marker chromosome (arrow).
FIGURE
COOPER, MaCKAY, AND BANFIELD
701
JOURNAL OF THE NATIONAL CANCER INSTITUTE, VOL. 33
PLATE 143
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FIGURE
7.-Karyotype of cell shown in figure 6.
Indistinguishable from stock tumor (see fig. 3).
8.-Metaphase chromosomes of a modal cell from specimen #68TM14 (see text); 51 chromosomes plus
a minute marker chromosome (arrow).
FIGURE
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COOPER, MacKAY, AND BANFIELD
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PLATE 144
JOURNAL OF THE NATIONAL CANCER INSTITUTE, VOL. 33
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9.-Karyotype of cell shown in figure 8. Indistinguishable from stock tumor (see fig. 3). The
sex-chromosome constitution appears to be XY, though the host was female.
FIGURE
1 O.-Metaphase chromosomes of a modal cell from specimen #65TM18 (see text); 50 chromosomes plus
a minute marker chromosome (arrow).
FIGURE
COOPER, MacKAY, AND BANFIELD
703
JOURNAL OF THE NATIONAL CANCER INSTITUTE, VOL. 33
PLATE 145
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11.-Karyotype of cell shown in figure 10. This karyotype differs from that of stock tumor (fig. 3) by
the presence of 8 rather than 9 members of group #16-19. Otherwise the karyotype is indistinguishable from
that of the stock tumor.
FIGURE
FIGURE
704
12.-Metaphase chromosomes of a nonmodal cell from specimen #65TM18.
COOPER, MacKAY, AND BANFIELD
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11-12
XI
JOURNAL OF THE NATIONAL CANCER INSTITUTE, VOL. 33
PLATE 146
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13.-Karyotype of cell shown in figure 12. Only 3 members of group #14 are present.
chromosome is present in size range of group #20 or 21.
FIGURE
An atypical
14.-Metaphase chromosomes of modal cell from specimen #77TM7 (see text); 51 chromosomes plus
a minute marker chromosome (arrow).
FIGURE
COOPER, MacKAY, AND BANFIELD
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PLATE 147
JOURNAL OF THE NATIONAL CANCER INSTITUTE, VOL. 33
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FIGURE
706
1S.-Karyotype of cell shown in figure 14.
Indistinguishable from stock tumor (fig. 3).
COOPER, MacKAY, AND BANFIELD
Downloaded from http://jnci.oxfordjournals.org/ at Pennsylvania State University on May 11, 2016
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