A SARCOMA OF THE FOWL TRANSMISSIBLE
BY AN
AGENT SEPARABLE FROM THE TUMOR CELLS.*
BY PEYTON ROUS, M.D.
(From the Laboratories of the Rockefeller Institute for Medical
Research,
New York.)
PLATES XLVII-LII.
A transmissible sarcoma of the chicken has been under observa-
tion in this laboratory for the past fourteen months,1
and it has
assumed of late a special interest because of its extreme malignancy
and a tendency to wide-spread metastasis.2
In a careful study of
the growth, tests have been made to determine whether it can be
transmitted by a filtrate free of the tumor cells. Attempts to so
transmit rat, mouse, and dog tumors have never succeeded; and
it was supposed that the sarcoma of the fowl would not differ from
them in this regard, since it is a typical neoplasm. On the contrary,
small quantities of a cell-free filtrate have sufficed to transmit
the
growth to susceptible fowls.
EXPERIMENTS.
For the first experiments on this point, ordinary filter paper was
used, and the ground tumor was suspended in Ringer's solution.
It was supposed that the slight paper barrier, which allows the
pas-
sage of a few red blood cells and lymphocytes, would suffice to
hold
back the tumor and render the filtrate innocuous. Such has been
the experience of other workers, with rat, mouse, and dog tumors.
But in the present instance characteristic growths followed the
inoculation of small amounts of the watery filtrate, or of the fluid
supernatant after centrifugalization of a tumor emulsion.
These results led to more critical experiments, which will be here
detailed. Tumors of especially rapid growth, and young, well-
grown fowls of the variety in which the tumor originally occurred,
namely, the barred Plymouth Rock, were used throughout.
Experiment II.--Tumor from
chicken 90 (tumor generation, 6th A) was
ground, suspended, and shaken as before. After one
centrifugalization the
fluid was passed through a Berkefeld filter (No. 2,
coarse). Before filtration,
it was pinkish yellow, cloudy; afterwards, faintly
yellow, limpid. Nine fowls
were inoculated with 0.2 c.c. of the filtrate in each
breast, and twenty-two more
received filtrate in one breast, a bit of tumor in
the other. Of the nine, one
slowly developed a sarcoma in each breast, and microscopic
growths, were later
found in its lungs. Of the twenty-two receiving both
filtrate and tumor, five
developed sarcoma where the filtrate had been injected,
and these five showed
especially large growths from the tumor bit.
The Berkefeld filter employed was afterwards found
to be slightly pervious
to Bacillus prodigiosis. The tumor developing
in the fowl injected only with
filtrate has been successfully transplanted to another
individual.
Experiment III.---The filtrate
was similarly prepared except that a small
Berkefeld filter (No. 5, medium) was used., impermeable,
under the conditions,
to Bacillus prodigiosis. As before, the filtration
was done at room temperature.
Fowl 124 (7th generation., A) furnished the material.
Twenty chickens were
inoculated in each breast with the filtrate, but none
have developed tumors.
Experiment IV.--In this experiment
the material was never allowed to cooI.
About fifteen grams of tumor from chicken 140 (7th
generation, B) was ground
in a warm mortar with warm sand; mixed with 200 c.c.
of heated Ringer's solu-
tion; shaken for thirty minutes within a thermostat
at 39 ° C.; centrifugalized;
and the fluid passed through a filter similar to that
used in experiment III.
Both before and after the experiment, this filter
was tested and found to hold
back Bacillus prodigiosis. The filtration of
the fluid was done at 38.5 ° C., and its
injection followed immediately. In four of ten fowls
inoculated into the muscle
of each breast with 0.2 to 0.5 c.c. of the filtrate,
there developed a sarcoma at
one of the points of inoculation; and though the growths
required several
weeks to appear, their subsequent enlargement was
of average rapidity. Pieces
removed at operation showed the characteristic structure,
and transplantation
into other chickens proved successful. Three of the
hosts have died, and in two
profuse metastases were found. One of the growths
furnished the material for
experiment V.
Experiment V.--The tumor used
resulted from the injection into fowl 180
(8th generation, B) of 0.5 c.c. of the filtrate of
experiment
IV. Just as in this
experiment, the material was ground, suspended, and
shaken in the warm, but
300 c.c of Ringer's solution were used to eleven grams
of tumor, and the shaking
was continued only twenty minutes. After centrifuging,
the filtration was done
at 40 ° C., through a new Berkefeld filter (No.
5, medium), impermeable, under
the same conditions, to Bacillus prodigiosis.
Ten young hens were inoculated
in each breast with 0.5 to 1.0 c.c. of the filtrate;
and eleven days later a tumor
nodule was just palpable in two of them. One of these
growths was at once
removed by operation. It took the form of a small
raised disc, firm, grayish, and
translucent, on the outer surface of the pectoral
sheath, presumably at the point
penetrated by the injection needle. Its greatest diameter
was one and one-half
millimeters. In the other fowl the nodule lay deep
in the muscle, and seemed
little, if at all, larger than that described. In
control fowls inoculated with bits
of the neoplastic tissue from No. 180, growths measuring
from 1.3 to 2.7 cm. in
diameter had developed at this time. Twenty-eight
days after inoculation, eight
of the ten fowls given the filtrate showed tumor nodules,
some of them still
very small.3
Thus the tumor resulting from injection of a filtrate itself fur-
nished material capable of producing tumors after injection.
The importance of the above results depends on the characters of
the growth employed. These will now be discussed in detail.
STRUCTURE AND MODE OF GROWTH.
The original tumor was found in the subcutaneous tissue of the
breast of an adult, pure-bred hen. The other individuals of the
small stock were healthy; and though susceptible normal chickens
and chickens with the tumor have been kept together for long
periods, no instance of spontaneous transmission of the growth has
occurred. The characters of the original mass have been detailed
elsewhere.4 A more general description
of the tumor as it has
appeared on transplantation will here be given.
Histologically the growth has always consisted of one type of
cells, namely, spindle cells, usually in bundles, with a slight
vascu-
larizing framework (figure 1 ). Cell division
is usually by amitosis,
but mitosis is frequent. Small giant cells, due to the division
of
the nucleus without corresponding fission of the cytoplasm, are
occasionally seen, especially about regions where the growth is
degenerating. There is considerable variation in the size of the
cells and in the staining qualities of their nuclei, but the growth
has
not changed in general histological character during its propagation
Following implantation of a bit of the neoplastic tissue into the
breast muscle of a susceptible fowl, a circumscribed nodule shortly
becomes evident. It is very firm and definite on palpation, but
on
section proves unencapsulated, though distinct in appearance from
the normal tissue. In general, the neoplastic tissue is gristly
and
grayish white, with a fine striation on the cut surface. Less often,
it is soft, grayish pink, semitranslucent, and friable, or even
gelatin-
ous. In the last instance, it may contain much true mucin. As the
mass grows large, its scanty, thin-walled blood vessels prove insuffi-
cient, and at its center a wide-spread coagulative necrosis, or
cystic
change takes place, the latter not infrequently as the result of
hemor-
rhage. The cysts are filled with serous or ropy fluid, often colored
with blood pigment ; and polypoid extensions into them of the t'umor
are not rare. Continuing to grow, the mass extends to the muscle-
sheath and perhaps through this to connective tissue and skin. In-
filtrating the latter, it may spread rapidly en cuirasse;
but ulceration
is seldom seen. Soon the whole of the inoculated breast is occu-
pied by a bulging, rounded, firm growth (figure 5)
; and the host
rapidly emaciates, becomes cold, somnolent, and dies. In many
cases the viscera, especially the lungs, heart, and liver, are the
site
of discrete metastases, gristly and firm, like the primary growth.
Those on the surface of the liver may be umbilicated (figure
6).
TUMORS RESULTING FROM A FILTRATE.
The tumors which result from the injection of a cell-free filtrate
take much longer to appear. The inoculation into the breast muscle
of a bit of tumor tissue one millimeter in diameter may give rise
in
the course of a week to a growing nodule 1.5 centimeters broad;
whereas, following the injection of a filtrate, not the slightest
trace
of tumor is palpable for from ten days to three weeks. Then one
or
two minute, shotty bodies can be felt, and soon the characteristic
mass develops. At first it is ovoid or spherical in shape, just
as
though it had arisen from an introduced bit of neoplastic tissue.
In one case a flat, irregularly branching mass, flame-shaped, so
to
speak, developed in the sheath of the pectoral muscle at the point
injured by the injecting needle. Many of the injected fowls in
which no growth appeared in the breast muscle have been carefully
examined at autopsy for tumors elsewhere, but none have been
found. Some with a growth in the breast have developed after a
time others in the viscera, probably the usual metastases, to judge
from size and distribution. Careful note has been kept as to
whether the tumors resulting from a filtrate injection grow more
slowly than usual. This has been found to be the case. Following
their tardy appearance, a considerable proportion of them grow
slowly as compared with control tumors resulting from implantation.
INFLUENCE OF THE HOST.
The stock in which the original tumor occurred consisted of
fowls of one pure-bred variety, the barred Plymouth Rock. The
first transplantation was made to chickens from the same setting
of eggs as the individual with the tumor, and the next successful
one to less closely related members of the same stock. Bits of
the growth were placed in the breast muscle by means of a
trocar, a procedure adopted as the routine. Repeated unsuc-
cessful attempts were made to transfer the growth to chickens
resembling the tumor stock, and of similar variety, but obtained
from another source, and probably not pure-bred (chart
1 ).
EFFECTS OF TRANSPLANTATION.
The original tumor had been under observation for two months
before it was brought to the laboratory, and had grown slowly
during that period. With repeated transmission the rate of growth,
as well as the percentage of successful transplantations, has in-
creased; and the period which elapses between implantation and the
appearance of the new sarcoma as a palpable mass has been reduced
from about four weeks to four or five days. The tumor obtained
from the first inoculation required seventy-one days to reach a
size
of 5.0 by 3.3 centimeters, and to affect seriously the health of
the
host. But in later generations, produced by a similar method of
inoculation, the appearance and development of the tumor have
become progressively more rapid. Growths ten or twelve centi-
meters in length by six in width are now found three weeks after
inoculation of a bit of neoplastic tissue, two millimeters in diameter;
and often death of the host ensues within twenty-six to thirty days,
all told.
Repeated transplantation has also greatly increased the frequency,
extent, and rapidity of metastasis formation. The death of the
original fowl was hastened by a successful intraperitoneal implan-
tation with its own growth, and the autopsy did not disclose any
nodule suggesting a metastasis. The tumor fowl of the first gen-
eration was killed after seventy-two days, and had, in its heart,
one
small secondary growth. Metastasis did not take place in the second
MODE OF METASTASIS FORMATION.
The question as to how metastasis of the chicken sarcoma takes
place has great importance. For it might be supposed that the
agent which suffices, independent of the cells, to transmit the
tumor
to new individuals would itself cause secondary masses in the host.
Perhaps sometimes it does act alone to produce such masses, though
we have met no instance in which this can be affirmed. On the con-
trary, the findings all indicate, as with the sarcomata of man,
that the
metastases result from a distribution of tumor cells, usually by
way
of the blood. As has been said, the relations of the sarcoma to
the blood stream are very intimate; quite large vessels walled with
only a layer of endothelium exist within the growth, and in their
neighborhood cell proliferation is at its height. Instances in which
the neoplastic tissue has penetrated a vessel wall are frequent
(figure
9), and sometimes a strand of the growth, quite
bare of endo-
thelium, extends for a considerable distance in the blood stream
(figure 8). The secondary growths in the viscera
are first evident
as small, approximately spherical groups of cells with a blood-vessel
in the midst, occluded by tumor tissue (figure 7).
The cells are of
one type, in active mitotic and amitotic division, unsurrounded
by
inflammatory reaction. This is true of metastases consisting of
only three or four cells. To recognize a single neoplastic cell
lodged
in a capillary has thus far proved impossible because the morphol-
ogy of the single cell does not sufficiently identify it; yet what
would
appear to be such emboli are frequent in the pulmonary tissue. The
question of the transplantability of the tumor cells has been settled
in the affirmative by an examination of grafts of the neoplastic
tissue removed shortly after implantation.
Metastasis by way of the lymph-stream occasionally occurs: the
glands along the great vessels above the heart have been found
enlarged and entirely replaced by sarcomatous tissue. Contact
metastasis is very frequent. For example, a mass in the breast may
penetrate the sternal membrane and give rise to nodules on the liver
surface opposite. In the viscera the tumor preserves its histological
character, but its arrangement is influenced to a certain degree
by
prefixisting structures. In the lung the pattern of the alveoli
may
be perpetuated in tumor cells, as is true also of the striped muscle
(figure 3). The skin may be infiltrated and tightly
stretched.
Frequently the growth recurs in wounds made to remove subcuta-
neous grafts, and here its presence need not greatly impede healing.
The early stages in the development of a sarcoma caused by a cell-
free filtrate are difficult to obtain. When such a growth becomes
palpable, it is already one to two millimeters in diameter, and
histo-
logically no more enlightening than a metastasis or a graft of the
neoplastic tissue would be.
THE TUMOR CELLS ARE TRANSPLANTABLE.
A study of many grafts removed at short intervals from the
connective tissue has shown conclusively that the inoculation of
a
bit of the sarcoma into a susceptible fowl results in an actual
trans-
plantation of the neoplastic cells and growth from them. For the
first two or three days after implantation, the graft is unattached
to the host tissues, but then it unites with them, is vascularized,
and begins to enlarge and to invade the surrounding parts (figure
11 ). Usually a few small mononuclear cells (lymphocytes)
col-
lect at its edge, but no other cellular reaction follows that is
due
to the initial trauma. Indeed, about metastases a cellular reac-
tion is often completely absent. Unless the graft is very small
its
central part dies before vascularization can take place. There re-
mains, however, a living periphery distinct from the normal tissues
of the host, and soon this is vascularized and strands of the spindle-
shaped cells can be seen growing out from it. The findings do not
in the least suggest that the tumor is transmissible apart from
its
cells. Certainly it is transplanted easily and is, at present, best
propagated by this means.
The death of grafts of the tumor in fowls with a natural or
acquired resistance takes place in one of two ways. The implanted
tissue may fail entirely to be vascularized, and its death results
after some days, during which a zone of living cells persists at
its
periphery (figure 12). Or it may be vascularized
and grow for a
brief period, dying at last in the midst of an accumulation of lym-
phocytes. The first process is seen especially in regions poor in
connective tissue and blood-vessels, and may occur there even in
susceptible hosts. The second process is the one found at the edge
of retrogressing tumors. A more detailed account of the fate of
early grafts has been reserved for another paper. The findings
here briefly described are those made familiar to tumor workers
by a study of rat, mouse, and dog tumors.
Cultures from the growth upon many media have repeatedly been
taken; but with the exception of a large post-mortem bacillus once
obtained, they have remained sterile as regards bacteria. Portions
of the filtrate and fresh smears from the tumor surface have been
examined with the dark-field microscope, but neither this nor the
various histological procedures applied to the neoplastic tissue
has
disclosed anything which can be recognized as a parasitic organism.
DISCUSSION.
It is evident from the foregoing description that our tumor of
the fowl possesses to a marked degree those characters of mor-
phology and behavior which distinguish the true malignant neo-
plasms, especially the sarcomata. It is formed of a single type
of
cells, only slightly differentiated, resembling young connective
tissue cells, and possessed of an enormous proliferative energy
which is exercised to the detriment of the surrounding tissues and
eventually of the entire host. Growth takes place through infiltra-
tion and replacement of normal structures, as well as through
expansive enlargement. Metastasis by way of the blood stream is
common, rarer by the lymphatics; and, to judge from histological
evidence, the transportation, lodgment, and growth of tumor cells
is wholly responsible for the secondary nodules. Indeed, a general
histological study of the sarcoma would not lead one to suspect
that it can be transmitted by another means than a transplantation
of cells. When a small bit of the neoplastic tissue is placed in
a
new and susceptible host, most of its cells survive, are vascularized,
and by their proliferation give rise apparently to all of the growth.
In a resistant host, the graft soon dies and no tumor follows. One
would suppose that the sarcoma developed only "aus sich heraus,"
to use Ribbert's phrase. But histological pictures are not decisive
upon this point. Since the growth is transmissible by a cell-free
filtrate, it seems not unlikely that in its neighborhood the connective
tissue cells of the host undergo a neoplastic change.
A feature of the transmissible tumors, which has largely drawn
the attention of cancer workers and has modified current theories
of cancer origin, is their striking dependence for a successful
transplantation on the character and condition of the individual
host. It is a dependence similar to that shown by transplanted
normal tissue, and apparently the same laws largely influence both.
This trait of tumors is illustrated exceptionally well by the chicken
sarcoma. During a considerable period, it could be propagated only
in fowls of precisely the sort in which the original growth occurred
(chart 1 ); and even now it succeeds best in these.
It has never
been successfully transmitted to birds of other species, or to mam-
mals. Young fowls are the most favorable hosts; and healthy,
well-nourished ones proves more susceptible than the thin and ill.
Indeed, intercurrent illness of the host may cause the sarcoma
transiently to disappear (chart 2).
The above traits have figured largely in current discussions on
cancer etiology, and most of them have been regarded as evidence
against a specific cause for the disease, extrinsic of the cells.
Such
evidence is void, now that a growth has been found possessing the
traits mentioned, yet transmissible independently of its cells.
This
fact, and not the problem of how to classify the growth, merits
attention. Nevertheless, a passing reference should perhaps be
made to the ill-defined group of pathological products called granu-
lomata, with which this neoplasm of the fowl may by some be
classed, owing to its transmission by an agent separable from the
tissue cells. None of the granulomata has the tumor characters,
and none is known to be transplantable. The present growth fails
to resemble any granuloma thus far described; whereas it fulfills
all the conditions for identification as a tumor.
The first tendency will be to regard the self-perpetuating agent
active in this sarcoma of the fowl as a minute parasitic organism.
Analogy with several infectious diseases of man and the lower
animals, caused by ultramicroscopic organisms, gives support to
this view of the findings, and at present work is being directed
to
its experimental verification. But an agency of another sort is
not
out of the question. It is conceivable that a chemical stimulant,
elaborated by the neoplastic cells, might cause the tumor in another
host and bring about in consequence a further production of the
same stimulant. For the moment we have not adopted either
hypothesis.
The ultimate significance of these unusual findings can hardly
be well discussed until more data are obtained through experiment,
especially through carefully devised experiment with the tumors
of
other species of animals. For it is quite possible that the failure
to
separate from these growths an agent causing them may be trace-
able to some interference with the conditions under which this
supposititious agent can exist alone, or reproduce the growth in
new hosts. Work along the line indicated is under way in this
laboratory.
EXPLANATION OF PLATES.
Unless otherwise indicated, the sections are stained with Delafield's
hema-
toxylin and eosin. In each case the tumor generation and series
are given,
followed by the number of fowl from which the specimen came ; thus,
7th A, No.
117.
PLATE XLVII.
FIG. 1. An area in the original growth. Necrosis
is present at one side.
FIG. 2. 8th B, No. 177. Part of a tumor in the
left breast, resulting from
the injection of the filtrate of experiment IV.
The muscle fibres are largely
invaded and replaced by tumor cells. Methylene-blue and eosin.
PLATE XLVIII.
FIG. 3. 8th B, No. 177. A drawing which further
illustrates the invasion
and replacement of muscle fibres by tumor cells. The preparation
is from, the
same growth as Fig. 2.
FIG. 4. 8th B, No. 173. Myxomatous growth caused
by the filtrate of experi-
ment IV.
PLATE XLIX.
Fin. 5. 5th A, No. 82. Growth in the left breast
of a chicken, resulting from
the implantation of a small bit of tumor tissue fifty-two days previously.
The skin
and connective tissue covering have been removed. The length of
the mass is
fourteen centimeters. In the right breast is a nodule that resulted
from injection
of the fluid supernatant after centrifugalization of a tumor emulsion.
FIG. 6. 7th A, No. 117. Metastases from a growth
in the left breast. The
chest, and abdominal wall, and about half of the breast tumor have
been cut
away to expose the viscera. The lungs, much enlarged, are crowded
with dis-
crete tumor nodules. The metastases on the surface of the liver
are umbilicated
and surrounded by a zone of dilated blood-vessels. The duration
of the disease
was thirty-seven days.
PLATE L.
FIG. 7. 6th A, No. l02. A small metastasis in the
lung, with an occluded
blood-vessel at its center. The tumor cells have only short, blunt
processes, a
Variation that is not infrequent. The picture is complicated by
the presence
of many nucleated red cells.
FIG. 8. 4th B, No. 63. Growth of a tumor of the
heart wall into the ven-
tricular blood. A tongue of myxomatous tumor here extends between
two tra-
beculae of heart muscle. The dark mass at its end consists of nucleated
ery-
throcytes. The transverse rent in the heart muscle above the tumor
is an artefact.
PLATE LI
FIG. 9. 4th B, No. 63. Kidney. Extension of the
tumor through the wall
of a vein.
Fig. l0. 7th A, No. 116. Margin of a metastasis
in the muscle of the giz-
zard. At one corner some uninvaded tissue is seen. Note the complete
absence
of any cellular reaction about the tumor.
PLATE LII.
FIG. 11. A graft of the sarcoma removed with the
surrounding tissue four
days after implantation in a susceptible host. Already it has united
at two
points with the host tissue and vascularization is in progress,
though too late
to prevent necrosis at the center of the graft.
FIG. 12. A similar graft removed from a resistant
host nine days after im-
plantation. Despite the long period, the graft is joined to the
host only by two
thin strands of connective tissue shown at either end. It is unvascularized
and
necrotic save for a thin peripheral zone of the characteristic cells,
which is con-
siderably infiltrated by lymphocytes.
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Acta Unio Int Contra Cancrum. 1960;16:129-30. No abstract available.
PMID: 14438380 [PubMed - OLDMEDLINE for Pre1966]
24: Rous P.
Surmise and fact on the nature of cancer.
Nature. 1959 May 16;183(4672):1357-61. No abstract available.
PMID: 13657123 [PubMed - OLDMEDLINE for Pre1966]
25: Rous P, Allen RA.
Fatal keratomas due to deep homografts of the benign papillomas
of tarred mouse
skin; normal proclivities and neoplastic disabilities as determinants
of tumor
course.
J Exp Med. 1958 Jan 1;107(1):63-86. No abstract available.
PMID: 13481256 [PubMed - OLDMEDLINE for Pre1966]
26: Rous P.
Comment.
Cancer Res. 1957 May;17(4):349-51. No abstract available.
PMID: 13427020 [PubMed - OLDMEDLINE for Pre1966]
27: Rous P.
Presentation of the Kober medal to Richard Shope.
Trans Assoc Am Physicians. 1957;70:29-37. No abstract available.
PMID: 13496111 [PubMed - OLDMEDLINE for Pre1966]
28: Dumbell K, Rous P.
Are carcinogens responsible for the superimposed neoplastic
changes occurring
in mouse tumor cells? The effect of methylcholanthrene and
urethane on
pulmonary adenomas and of methylcholanthrene on mammary carcinomas.
J Exp Med. 1955 Nov 1;102(5):517-44. No abstract available.
PMID: 13271668 [PubMed - OLDMEDLINE for Pre1966]
29: Rous P.
Cancer research as viewed along the years.
Acta Physiol Lat Am. 1953;3(2-3):184-7. No abstract available.
PMID: 13138263 [PubMed - OLDMEDLINE for Pre1966]
30: Rous P, Kidd JG, Smith WE.
Experiments on the cause of the rabbit carcinomas derived
from virus-induced
papillomas. II. Loss by the Vx2 carcinoma of the power to immunize
hosts against
the papilloma virus.
J Exp Med. 1952 Aug;96(2):159-74. No abstract available.
PMID: 14955572 [PubMed - OLDMEDLINE for Pre1966]
31: Smith WE, Kidd JG, Rous P.
Experiments on the cause of the rabbit carcinomas derived
from virus-induced
papillomas. I. Propagation of several of the cancers in sucklings,
with
etiological tests.
J Exp Med. 1952 Mar;95(3):299-318. No abstract available.
PMID: 14927795 [PubMed - OLDMEDLINE for Pre1966]
32: Rogers S, Rous P.
Joint action of a chemical carcinogen and a neoplastic virus
to induce cancer
in rabbits; results of exposing epidermal cells to a carcinogenic
hydrocarbon at
time of infection with the Shope papilloma virus.
J Exp Med. 1951 May;93(5):459-88. No abstract available.
PMID: 14832395 [PubMed - OLDMEDLINE for Pre1966]
Papers by Peyton Rous, in: J. Exp. Med. 1908-1979 (115 papers).
http://www.jem.org/cgi/search
James S. Henderson and Peyton Rous
FURTHER EXPERIMENTS ON THE CAUSE OF SEQUENTIAL
NEOPLASTIC
CHANGES: THE EFFECTS OF 20-METHYLCHOLANTHRENE
ON
TRANSPLANTED EPIDERMAL MOUSE PAPILLOMAS AND THE
DERIVATIVE
CARCINOMAS
J. Exp. Med., Aug 1964; 120: 197 - 222.
James S. Henderson and Peyton Rous
THE PLATING OF TUMOR COMPONENTS ON THE SUBCUTANEOUS
EXPANSES OF YOUNG MICE: FINDINGS WITH BENIGN
AND MALIGNANT
EPIDERMAL GROWTHS AND WITH MAMMARY CARCINOMAS
J. Exp. Med., Jun 1962; 115: 1211 - 1230.
Peyton Rous and Raymond A. Allen
FATAL KERATOMAS DUE TO DEEP HOMOGRAFTS OF THE
BENIGN
PAPILLOMAS OF TARRED MOUSE SKIN: NORMAL PROCLIVITIES
AND
NEOPLASTIC DISABILITIES AS DETERMINANTS OF TUMOR
COURSE
J. Exp. Med., Jan 1958; 107: 63 - 86.
Keith Dumbell and Peyton Rous
ARE CARCINOGENS RESPONSIBLE FOR THE SUPERIMPOSED
NEOPLASTIC
CHANGES OCCURRING IN MOUSE TUMOR CELLS?: THE
EFFECT OF
METHYLCHOLANTHRENE AND URETHANE ON PULMONARY
ADENOMAS
AND OF METHYLCHOLANTHRENE ON MAMMARY CARCINOMAS
J. Exp. Med., Nov 1955; 102: 517 - 544.
Peyton Rous, John G. Kidd, and William E. Smith
EXPERIMENTS ON THE CAUSE OF THE RABBIT CARCINOMAS
DERIVED
FROM VIRUS-INDUCED PAPILLOMAS: II. LOSS BY THE
VX2 CARCINOMA
OF THE POWER TO IMMUNIZE HOSTS AGAINST THE PAPILLOMA
VIRUS
J. Exp. Med., Aug 1952; 96: 159 - 174.
William E. Smith, John G. Kidd, and Peyton Rous
EXPERIMENTS ON THE CAUSE OF THE RABBIT CARCINOMAS
DERIVED
FROM VIRUS-INDUCED PAPILLOMAS: I. PROPAGATION
OF SEVERAL OF
THE CANCERS IN SUCKLINGS, WITH ETIOLOGICAL TESTS
J. Exp. Med., Feb 1952; 95: 299 - 318.
Stanfield Rogers and Peyton Rous
JOINT ACTION OF A CHEMICAL CARCINOGEN AND A NEOPLASTIC
VIRUS
TO INDUCE CANCER IN RABBITS: RESULTS OF EXPOSING
EPIDERMAL
CELLS TO A CARCINOGENIC HYDROCARBON AT TIME OF
INFECTION
WITH THE SHOPE PAPILLOMA VIRUS
J. Exp. Med., May 1951; 93: 459 - 487.
William F. Friedewald and Peyton Rous
THE PATHOGENESIS OF DEFERRED CANCER: A STUDY
OF THE
AFTER-EFFECTS OF METHYLCHOLANTHRENE UPON RABBIT
SKIN
J. Exp. Med., May 1950; 91: 459 - 484.
William E. Smith and Peyton Rous
THE NEOPLASTIC POTENTIALITIES OF MOUSE EMBRYO
TISSUES: IV.
LUNG ADENOMAS IN BABY MICE AS RESULT OF PRENATAL
EXPOSURE TO
URETHANE
J. Exp. Med., Nov 1948; 88: 529 - 554.
Peyton Rous
THE ACTIVATION OF SKIN GRAFTS
J. Exp. Med., Apr 1946; 83: 383 - 400.
William E. Smith and Peyton Rous
THE NEOPLASTIC POTENTIALITIES OF MOUSE EMBRYO
TISSUES: II.
CONTRIBUTORY EXPERIMENTS; RESULTS WITH THE SKIN
OF C3H AND
WEBSTER-SWISS EMBRYOS; GENERAL CONSIDERATIONS
J. Exp. Med., Jun 1945; 81: 621 - 646.
Peyton Rous and William E. Smith
THE NEOPLASTIC POTENTIALITIES OF MOUSE EMBRYO
TISSUES: I. THE
FINDINGS WITH SKIN OF C STRAIN EMBRYOS TRANSPLANTED
TO ADULT
ANIMALS
J. Exp. Med., Jun 1945; 81: 597 - 620.
William F. Friedewald and Peyton Rous
THE DETERMINING INFLUENCE OF TAR, BENZPYRENE,
AND
METHYLCHOLANTHRENE ON THE CHARACTER OF THE BENIGN
TUMORS
INDUCED THEREWITH IN RABBIT SKIN
J. Exp. Med., Aug 1944; 80: 127 - 144.
William F. Friedewald and Peyton Rous
THE INITIATING AND PROMOTING ELEMENTS IN TUMOR
PRODUCTION: AN
ANALYSIS OF THE EFFECTS OF TAR, BENZPYRENE, AND
METHYLCHOLANTHRENE ON RABBIT SKIN
J. Exp. Med., Aug 1944; 80: 101 - 126.
Peyton Rous and William F. Friedewald
THE EFFECT OF CHEMICAL CARCINOGENS ON VIRUS-INDUCED
RABBIT
PAPILLOMAS
J. Exp. Med., May 1944; 79: 511 - 538.
Ian MacKenzie and Peyton Rous
THE EXPERIMENTAL DISCLOSURE OF LATENT NEOPLASTIC
CHANGES IN
TARRED SKIN
J. Exp. Med., Mar 1941; 73: 391 - 416.
Peyton Rous and John G. Kidd
CONDITIONAL NEOPLASMS AND SUBTHRESHOLD NEOPLASTIC
STATES: A
STUDY OF THE TAR TUMORS OF RABBITS
J. Exp. Med., Mar 1941; 73: 365 - 390.
John G. Kidd and Peyton Rous
A TRANSPLANTABLE RABBIT CARCINOMA ORIGINATING
IN A
VIRUS-INDUCED PAPILLOMA AND CONTAINING THE VIRUS
IN MASKED OR
ALTERED FORM
J. Exp. Med., Jun 1940; 71: 813 - 838.
Peyton Rous and John G. Kidd
THE ACTIVATING, TRANSFORMING, AND CARCINOGENIC
EFFECTS OF THE
RABBIT PAPILLOMA VIRUS (SHOPE) UPON IMPLANTED
TAR TUMORS
J. Exp. Med., Jun 1940; 71: 787 - 812.
John G. Kidd and Peyton Rous
CANCERS DERIVING FROM THE VIRUS PAPILLOMAS OF
WILD RABBITS
UNDER NATURAL CONDITIONS
J. Exp. Med., Apr 1940; 71: 469 - 494.
Peyton Rous and John G. Kidd
A COMPARISON OF VIRUS-INDUCED RABBIT TUMORS WITH
THE TUMORS
OF UNKNOWN CAUSE ELICITED BY TARRING
J. Exp. Med., Mar 1939; 69: 399 - 424.
John G. Kidd and Peyton Rous
THE CARCINOGENIC EFFECT OF A PAPILLOMA VIRUS
ON THE TARRED
SKIN OF RABBITS: II. MAJOR FACTORS DETERMINING
THE PHENOMENON:
THE MANIFOLD EFFECTS OF TARRING
J. Exp. Med., Oct 1938; 68: 529 - 562.
Joseph W. Beard and Peyton Rous
THE FATE OF VACCINIA VIRUS ON CULTIVATION IN
VITRO WITH
KUPFFER CELLS (RETICULO-ENDOTHELIAL CELLS)
J. Exp. Med., Jun 1938; 67: 883 - 910.
Peyton Rous and John G. Kidd
THE CARCINOGENIC EFFECT OF A PAPILLOMA VIRUS
ON THE TARRED
SKIN OF RABBITS: I. DESCRIPTION OF THE PHENOMENON
J. Exp. Med., Mar 1938; 67: 399 - 428.
Peyton Rous, J. W. Beard, and John G. Kidd
OBSERVATIONS ON THE RELATION OF THE VIRUS CAUSING
RABBIT
PAPILLOMAS TO THE CANCERS DERIVING THEREFROM:
II. THE EVIDENCE
PROVIDED BY THE TUMORS: GENERAL CONSIDERATIONS
J. Exp. Med., Sep 1936; 64: 401 - 424.
Peyton Rous, John G. Kidd, and J. W. Beard
OBSERVATIONS ON THE RELATION OF THE VIRUS CAUSING
RABBIT
PAPILLOMAS TO THE CANCERS DERIVING THEREFROM:
I. THE INFLUENCE
OF THE HOST SPECIES AND OF THE PATHOGENIC ACTIVITY
AND
CONCENTRATION OF THE VIRUS
J. Exp. Med., Sep 1936; 64: 385 - 400.
John G. Kidd, J. W. Beard, and Peyton Rous
SEROLOGICAL REACTIONS WITH A VIRUS CAUSING RABBIT
PAPILLOMAS
WHICH BECOME CANCEROUS: II. TESTS OF THE BLOOD
OF ANIMALS
CARRYING VARIOUS EPITHELIAL TUMORS
J. Exp. Med., Jul 1936; 64: 79 - 96.
John G. Kidd, J. W. Beard, and Peyton Rous
SEROLOGICAL REACTIONS WITH A VIRUS CAUSING RABBIT
PAPILLOMAS
WHICH BECOME CANCEROUS: I. TESTS OF THE BLOOD
OF ANIMALS
CARRYING THE PAPILLOMA
J. Exp. Med., Jul 1936; 64: 63 - 77.
Peyton Rous and J. W. Beard
THE PROGRESSION TO CARCINOMA OF VIRUS-INDUCED
RABBIT
PAPILLOMAS (SHOPE)
J. Exp. Med., Oct 1935; 62: 523 - 548.
Peyton Rous, Philip D. McMaster, and Stephen S.
Hudack
THE FIXATION AND PROTECTION OF VIRUSES BY THE
CELLS OF
SUSCEPTIBLE ANIMALS
J. Exp. Med., May 1935; 61: 657 - 688.
Peyton Rous and J. W. Beard
A VIRUS-INDUCED MAMMALIAN GROWTH WITH THE CHARACTERS
OF A
TUMOR (THE SHOPE RABBIT PAPILLOMA): III. FURTHER
CHARACTERS OF
THE GROWTH: GENERAL DISCUSSION
J. Exp. Med., Dec 1934; 60: 741 - 766.
J. W. Beard and Peyton Rous
A VIRUS-INDUCED MAMMALIAN GROWTH WITH THE CHARACTERS
OF A
TUMOR (THE SHOPE RABBIT PAPILLOMA): II. EXPERIMENTAL
ALTERATIONS OF THE GROWTH ON THE SKIN: MORPHOLOGICAL
CONSIDERATIONS: THE PHENOMENA OF RETROGRESSION
J. Exp. Med., Dec 1934; 60: 723 - 740.
Peyton Rous and J. W. Beard
A VIRUS-INDUCED MAMMALIAN GROWTH WITH THE CHARACTERS
OF A
TUMOR (THE SHOPE RABBIT PAPILLOMA): I. THE GROWTH
ON
IMPLANTATION WITHIN FAVORABLE HOSTS
J. Exp. Med., Dec 1934; 60: 701 - 722.
J. W. Beard and Peyton Rous
THE CHARACTERS OF KUPFFER CELLS LIVING IN VITRO
J. Exp. Med., May 1934; 59: 593 - 607.
Peyton Rous and J. W. Beard
SELECTION WITH THE MAGNET AND CULTIVATION OF
RETICULO-ENDOTHELIAL CELLS (KUPFFER CELLS)
J. Exp. Med., May 1934; 59: 577 - 591.
Peyton Rous and Elizabeth Botsford
THE INCIDENCE OF CANCER IN TARRED AND SHELTERED
MICE
J. Exp. Med., Feb 1932; 55: 247 - 266.
Philip D. McMaster, Stephen Hudack, and Peyton
Rous
THE RELATION OF HYDROSTATIC PRESSURE TO THE GRADIENT
OF
CAPILLARY PERMEABILITY
J. Exp. Med., Feb 1932; 55: 203 - 221.
Frederick Smith and Peyton Rous
THE GRADIENT OF VASCULAR PERMEABILITY: IV. THE
PERMEABILITY OF
THE CUTANEOUS VENULES AND ITS FUNCTIONAL SIGNIFICANCE
J. Exp. Med., Oct 1931; 54: 499 - 514.
Peyton Rous and Frederick Smith
THE GRADIENT OF VASCULAR PERMEABILITY: III. THE
GRADIENT ALONG
THE CAPILLARIES AND VENULES OF FROG SKIN
J. Exp. Med., Feb 1931; 53: 219 - 242.
Frederick Smith and Peyton Rous
THE GRADIENT OF VASCULAR PERMEABILITY: II. THE
CONDITIONS IN
FROG AND CHICKEN MUSCLE, AND IN THE MAMMALIAN
DIAPHRAGM
J. Exp. Med., Feb 1931; 53: 195 - 217.
Peyton Rous, H. P. Gilding, and Frederick Smith
THE GRADIENT OF VASCULAR PERMEABILITY
J. Exp. Med., May 1930; 51: 807 - 830.
Peyton Rous and H. P. Gilding
IS THE LOCAL VASODILATATION AFTER DIFFERENT TISSUE
INJURIES
REFERABLE TO A SINGLE CAUSE?
J. Exp. Med., Jan 1930; 51: 27 - 39.
Peyton Rous and H. P. Gilding
THE FINAL RESPONSE OF THE SMALL CUTANEOUS VESSELS
J. Exp. Med., Oct 1929; 50: 489 - 512.
H. P. Gilding and Peyton Rous
STUDIES OF TISSUE MAINTENANCE: III. PERSISTING
BLOODLESSNESS
AFTER FUNCTIONAL ISCHEMIA
J. Exp. Med., Oct 1929; 50: 471 - 487.
Peyton Rous and H. P. Gilding
STUDIES OF TISSUE MAINTENANCE: I. THE CHANGES
WITH DIMINISHED
BLOOD BULK
J. Exp. Med., Aug 1929; 50: 189 - 211.
Peyton Rous and Douglas R. Drury
OUTLYING ACIDOSIS DUE TO FUNCTIONAL ISCHEMIA
J. Exp. Med., Mar 1929; 49: 435 - 460.
D. R. Drury, W. W. Beattie, and Peyton Rous
THE RELATIVE REACTION WITHIN LIVING MAMMALIAN
TISSUES: IX. ON
THE TISSUE REACTION AS INFLUENCED BY INHALATIONS
OF CO2 AND BY
OVERBREATHING.
J. Exp. Med., Dec 1926; 45: 41 - 58.
Peyton Rous, D. R. Drury, and W. W. Beattie
THE RELATIVE REACTION WITHIN LIVING MAMMALIAN
TISSUES: VIII. ON
THE COURSE OF THE TISSUE ACIDOSIS SECONDARY TO
BLOOD ACIDOSIS
INDUCED WITH HYDROCHLORIC ACID.
J. Exp. Med., Dec 1926; 45: 23 - 39.
Peyton Rous and W. W. Beattie
THE RELATIVE REACTION WITHIN LIVING MAMMALIAN
TISSUES: VII. THE
INFLUENCE OF CHANGES IN THE REACTION OF THE BLOOD
UPON THE
REACTION OF THE TISSUES.
J. Exp. Med., Nov 1926; 44: 835 - 854.
Peyton Rous
THE RELATIVE REACTION WITHIN LIVING MAMMALIAN
TISSUES: VI.
FACTORS DETERMINING THE REACTION OF SKIN GRAFTS;
A STUDY BY
THE INDICATOR METHOD OF CONDITIONS WITHIN AN
ISCHEMIC TISSUE.
J. Exp. Med., Nov 1926; 44: 815 - 834.
Douglas R. Drury and Peyton Rous
THE RELATIVE REACTION WITHIN LIVING MAMMALIAN
TISSUES: V. (b)
INFLUENCE OF LYMPH-INSOLUBLE TISSUE MATERIALS
ON THE
SIGNIFICANCE OF THE COLORATION WITH SOME PHTHALEIN
INDICATORS.
J. Exp. Med., Apr 1926; 43: 687 - 701.
Douglas R. Drury and Peyton Rous
THE RELATIVE REACTION WITHIN LIVING MAMMALIAN
TISSUES: V. (a)
INFLUENCE OF LYMPH-SOLUBLE TISSUE MATERIALS ON
THE
SIGNIFICANCE OF THE COLORATION WITH SOME PHTHALEIN
INDICATORS.
J. Exp. Med., Apr 1926; 43: 669 - 686.
Peyton Rous
THE RELATIVE REACTION WITHIN LIVING MAMMALIAN
TISSUES: IV.
INDICATED DIFFERENCES IN THE REACTION OF THE
ORGANS ON VITAL
STAINING WITH PHTHALEINS.
J. Exp. Med., May 1925; 41: 739 - 759.
D. R. Drury and Peyton Rous
SUPPRESSION OF BILE AS A RESULT OF IMPAIRMENT
OF LIVER
FUNCTION
J. Exp. Med., Apr 1925; 41: 611 - 622.
Peyton Rous and D. R. Drury
JAUNDICE AS AN EXPRESSION OF THE PHYSIOLOGICAL
WASTAGE OF
CORPUSCLES
J. Exp. Med., Apr 1925; 41: 601 - 609.
Peyton Rous
THE RELATIVE REACTION WITHIN LIVING MAMMALIAN
TISSUES: III.
INDICATED DIFFERENCES IN THE REACTION OF THE
BLOOD AND TISSUES
ON VITAL STAINING WITH PHTHALEINS.
J. Exp. Med., Mar 1925; 41: 451 - 470.
Peyton Rous
THE RELATIVE REACTION WITHIN LIVING MAMMALIAN-TISSUES:
II. ON
THE MOBILIZATION OF ACID MATERIAL WITHIN CELLS,
AND THE
REACTION AS INFLUENCED BY THE CELL STATE.
J. Exp. Med., Feb 1925; 41: 399 - 411.
Peyton Rous
THE RELATIVE REACTION WITHIN LIVING MAMMALIAN
TISSUES: I.
GENERAL FEATURES OF VITAL STAINING WITH LITMUS.
J. Exp. Med., Feb 1925; 41: 379 - 397.
Peyton Rous and Philip D. McMaster
THE LIVER REQUIREMENT OF THE FASTING ORGANISM
J. Exp. Med., Feb 1924; 39: 425 - 446.
Douglas R. Drury, Philip D. McMaster, and Peyton
Rous
OBSERVATIONS ON SOME CAUSES OF GALL STONE FORMATION:
III. THE
RELATION OF THE REACTION OF THE BILE TO EXPERIMENTAL
CHOLELITHIASIS.
J. Exp. Med., Feb 1924; 39: 403 - 423.
Peyton Rous, Douglas R. Drury, and Philip D. McMaster
OBSERVATIONS ON SOME CAUSES OF GALL STONE FORMATION:
II. ON
CERTAIN SPECIAL NUCLEI OF DEPOSITION IN EXPERIMENTAL
CHOLELITHIASIS.
J. Exp. Med., Dec 1923; 39: 97 - 116.
Peyton Rous, Philip D. McMaster, and Douglas R.
Drury
OBSERVATIONS ON SOME CAUSES OF GALL STONE FORMATION:
I.
EXPERIMENTAL CHOLELITHIASIS IN THE ABSENCE OF
STASIS,
INFECTION, AND GALL BLADDER INFLUENCES.
J. Exp. Med., Dec 1923; 39: 77 - 96.
G. O. Broun, Philip D. McMaster, and Peyton Rous
THE RELATION BETWEEN BLOOD DESTRUCTION AND THE
OUTPUT OF
BILE PIGMENT
J. Exp. Med., May 1923; 37: 733 - 757.
G. O. Broun, Philip D. McMaster, and Peyton Rous
STUDIES ON THE TOTAL BILE: IV. THE ENTEROHEPATIC
CIRCULATION OF
BILE PIGMENT.
J. Exp. Med., Apr 1923; 37: 699 - 710.
Philip D. McMaster, G. O. Broun, and Peyton Rous
STUDIES ON THE TOTAL BILE: III. ON THE BILE CHANGES
CAUSED BY A
PRESSURE OBSTACLE TO SECRETION; AND ON HYDROHEPATOSIS.
J. Exp. Med., Apr 1923; 37: 685 - 698.
Peyton Rous, G. O. Broun, and Philip D. McMaster
STUDIES ON THE TOTAL BILE: II. THE RELATION OF
CARBOHYDRATES TO
THE OUTPUT OF BILE PIGMENT.
J. Exp. Med., Feb 1923; 37: 421 - 428.
Philip D. McMaster, G. O. Broun, and Peyton Rous
STUDIES ON THE TOTAL BILE: I. THE EFFECTS OF
OPERATION, EXERCISE,
HOT WEATHER, RELIEF OF OBSTRUCTION, INTERCURRENT
DISEASE, AND
OTHER NORMAL AND PATHOLOGICAL INFLUENCES.
J. Exp. Med., Feb 1923; 37: 395 - 420.
Peyton Rous and Philip D. McMaster
A METHOD FOR THE PERMANENT STERILE DRAINAGE OF
INTRAABDOMINAL DUCTS, AS APPLIED TO THE COMMON
DUCT
J. Exp. Med., Dec 1922; 37: 11 - 19.
Herbert Haessler, Peyton Rous, and G. O. Broun
THE RENAL ELIMINATION OF BILIRUBIN
J. Exp. Med., Mar 1922; 35: 533 - 552.
Philip D. McMaster, Peyton Rous, and Louise C.
Larimore
SIGNIFICANCE OF THE HEMOSIDEROSIS OF PERNICIOUS
ANEMIA
J. Exp. Med., Mar 1922; 35: 521 - 531.
Oswald H. Robertson and Peyton Rous
SOURCES OF THE ANTIBODIES DEVELOPING AFTER REPEATED
TRANSFUSION
J. Exp. Med., Jan 1922; 35: 141 - 152.
Peyton Rous and Philip D. McMaster
PHYSIOLOGICAL CAUSES FOR THE VARIED CHARACTER
OF STASIS BILE
J. Exp. Med., Jun 1921; 34: 75 - 95.
Peyton Rous and Philip D. McMaster
THE CONCENTRATING ACTIVITY OF THE GALL BLADDER
J. Exp. Med., Jun 1921; 34: 47 - 73.
Philip D. McMaster and Peyton Rous
THE BILIARY OBSTRUCTION REQUIRED TO PRODUCE JAUNDICE
J. Exp. Med., May 1921; 33: 731 - 750.
Peyton Rous and Louise D. Larimore
THE BILIARY FACTOR IN LIVER LESIONS
J. Exp. Med., Jul 1920; 32: 249 - 272.
Peyton Rous and Louise D. Larimore
RELATION OF THE PORTAL BLOOD TO LIVER MAINTENANCE:
A
DEMONSTRATION OF LIVER ATROPHY CONDITIONAL ON
COMPENSATION.
J. Exp. Med., Apr 1920; 31: 609 - 632.
Peyton Rous, George W. Wilson, and Jean Oliver
EXPERIMENTS ON THE PRODUCTION OF SPECIFIC ANTISERA
FOR
INFECTIONS OF UNKNOWN CAUSE: III. THE EFFECTS
OF A SERUM
PRECIPITIN ON ANIMALS OF THE SPECIES FURNISHING
THE
PRECIPITINOGEN.
J. Exp. Med., Feb 1920; 31: 253 - 265.
Peyton Rous, Oswald H. Robertson, and Jean Oliver
EXPERIMENTS ON THE PRODUCTION OF SPECIFIC ANTISERA
FOR
INFECTIONS OF UNKNOWN CAUSE: II. THE PRODUCTION
OF A SERUM
EFFECTIVE AGAINST THE AGENT CAUSING A CHICKEN
SARCOMA.
J. Exp. Med., Feb 1919; 29: 305 - 320.
Peyton Rous, Oswald H. Robertson, and Jean Oliver
EXPERIMENTS ON THE PRODUCTION OF SPECIFIC ANTISERA
FOR
INFECTIONS OF UNKNOWN CAUSE: I. TYPE EXPERIMENTS
WITH KNOWN
ANTIGENS—A BACTERIAL HEMOTOXIN (MEGATHERIOLYSIN),
THE
PNEUMOCOCCUS, AND POLIOMYELITIC VIRUS.
J. Exp. Med., Feb 1919; 29: 283 - 304.
Peyton Rous and George W. Wilson
THE INFLUENCE OF ETHER ANESTHESIA, OF HEMORRHAGE,
AND OF
PLETHORA FROM TRANSFUSION ON THE PRESSOR EFFECT
OF MINUTE
QUANTITIES OF EPINEPHRINE
J. Exp. Med., Jan 1919; 29: 173 - 186.
Peyton Rous
URINARY SIDEROSIS: HEMOSIDERIN GRANULES IN THE
URINE AS AN AID
IN THE DIAGNOSIS OF PERNICIOUS ANEMIA, HEMOCHROMATOSIS,
AND
OTHER DISEASES CAUSING SIDEROSIS OF THE KIDNEY.
J. Exp. Med., Oct 1918; 28: 645 - 658.
Peyton Rous and Jean Oliver
EXPERIMENTAL HEMOCHROMATOSIS
J. Exp. Med., Oct 1918; 28: 629 - 644.
Peyton Rous and Oswald H. Robertson
FREE ANTIGEN AND ANTIBODY CIRCULATING TOGETHER
IN LARGE
AMOUNTS (HEMAGGLUTININ AND AGGLUTINOGEN IN THE
BLOOD OF
TRANSFUSED RABBITS)
J. Exp. Med., Apr 1918; 27: 509 - 517.
Peyton Rous
METHOD FOR INTRAVENOUS INJECTION OF GUINEA PIGS
J. Exp. Med., Apr 1918; 27: 459 - 462.
Oswald H. Robertson and Peyton Rous
THE NORMAL FATE OF ERYTHROCYTES: II. BLOOD DESTRUCTION
IN
PLETHORIC ANIMALS AND IN ANIMALS WITH A SIMPLE
ANEMIA.
J. Exp. Med., May 1917; 25: 665 - 673.
Peyton Rous and Oswald H. Robertson
THE NORMAL FATE OF ERYTHROCYTES: I. THE FINDINGS
IN HEALTHY
ANIMALS.
J. Exp. Med., May 1917; 25: 651 - 663.
F. S. Jones and Peyton Rous
THE PHAGOCYTIC POWER OF CONNECTIVE TISSUE CELLS
J. Exp. Med., Jan 1917; 25: 189 - 193.
Peyton Rous and F. S. Jones
THE PROTECTION OF PATHOGENIC MICROORGANISMS BY
LIVING TISSUE
CELLS
J. Exp. Med., May 1916; 23: 601 - 612.
Peyton Rous and F. S. Jones
A METHOD FOR OBTAINING SUSPENSIONS OF LIVING
CELLS FROM THE
FIXED TISSUES, AND FOR THE PLATING OUT OF INDIVIDUAL
CELLS
J. Exp. Med., Apr 1916; 23: 549 - 555.
Peyton Rous and J. R. Turner
THE PRESERVATION OF LIVING RED BLOOD CELLS IN
VITRO: II. THE
TRANSFUSION OF KEPT CELLS.
J. Exp. Med., Feb 1916; 23: 239 - 248.
Peyton Rous and J. R. Turner
THE PRESERVATION OF LIVING RED BLOOD CELLS IN
VITRO: I. METHODS
OF PRESERVATION.
J. Exp. Med., Feb 1916; 23: 219 - 237.
Peyton Rous
THE INFLUENCE OF DIET ON TRANSPLANTED AND SPONTANEOUS
MOUSE
TUMORS
J. Exp. Med., Nov 1914; 20: 433 - 451.
Peyton Rous and James B. Murphy
ON IMMUNITY TO TRANSPLANTABLE CHICKEN TUMORS
J. Exp. Med., Oct 1914; 20: 419 - 432.
Peyton Rous and Linda B. Lange
ON THE GREATER SUSCEPTIBILITY OF AN ALIEN VARIETY
OF HOST TO AN
AVIAN TUMOR
J. Exp. Med., Oct 1914; 20: 413 - 418.
F. S. Jones and Peyton Rous
ON THE CAUSE OF THE LOCALIZATION OF SECONDARY
TUMORS AT
POINTS OF INJURY
J. Exp. Med., Oct 1914; 20: 404 - 412.
Peyton Rous
ON CERTAIN SPONTANEOUS CHICKEN TUMORS AS MANIFESTATIONS
OF
A SINGLE DISEASE: I. SPINDLE-CELLED SARCOMATA
RIFTED WITH
BLOOD SINUSES.
J. Exp. Med., Jun 1914; 19: 570 - 576.
Peyton Rous and James B. Murphy
ON THE CAUSATION BY FILTERABLE AGENTS OF THREE
DISTINCT
CHICKEN TUMORS
J. Exp. Med., Jan 1914; 19: 52 - 68.
Peyton Rous and Linda B. Lange
THE CHARACTERS OF A THIRD TRANSPLANTABLE CHICKEN
TUMOR DUE
TO A FILTERABLE CAUSE. A SARCOMA OF INTRACANALICULAR
PATTERN
J. Exp. Med., Dec 1913; 18: 651 - 664.
Peyton Rous
RESISTANCE TO A TUMOR-PRODUCING AGENT AS DISTINCT
FROM
RESISTANCE TO THE IMPLANTED TUMOR CELLS: OBSERVATIONS
WITH A
SARCOMA OF THE FOWL.
J. Exp. Med., Oct 1913; 18: 416 - 427.
Peyton Rous
THE GROWTH OF TISSUE IN ACID MEDIA
J. Exp. Med., Aug 1913; 18: 183 - 186.
Peyton Rous
FALSE TRANSITIONS BETWEEN NORMAL AND CANCEROUS
EPITHELIUM
J. Exp. Med., Apr 1913; 17: 494 - 497.
Peyton Rous and James B. Murphy
VARIATIONS IN A CHICKEN SARCOMA CAUSED BY A FILTERABLE
AGENT
J. Exp. Med., Feb 1913; 17: 219 - 231.
Peyton Rous and James B. Murphy
THE HISTOLOGICAL SIGNS OF RESISTANCE TO A TRANSMISSIBLE
SARCOMA OF THE FOWL
J. Exp. Med., Mar 1912; 15: 270 - 286.
James B. Murphy and Peyton Rous
THE BEHAVIOR OF CHICKEN SARCOMA IMPLANTED IN
THE DEVELOPING
EMBRYO
J. Exp. Med., Feb 1912; 15: 119 - 132.
Peyton Rous
A SARCOMA OF THE FOWL TRANSMISSIBLE BY AN AGENT
SEPARABLE
FROM THE TUMOR CELLS
J. Exp. Med., Apr 1911; 13: 397 - 411.
Peyton Rous
THE EFFECT OF PREGNANCY ON IMPLANTED EMBRYONIC
TISSUE
J. Exp. Med., Feb 1911; 13: 248 - 256.
Peyton Rous
THE RELATIONS OF EMBRYONIC TISSUE AND TUMOR IN
MIXED GRAFTS
J. Exp. Med., Feb 1911; 13: 239 - 247.
Peyton Rous
A TRANSMISSIBLE AVIAN NEOPLASM. (SARCOMA OF THE
COMMON
FOWL.)
J. Exp. Med., Sep 1910; 12: 696 - 705.
Peyton Rous
AN EXPERIMENTAL COMPARISON OF TRANSPLANTED TUMOR
AND A
TRANSPLANTED NORMAL TISSUE CAPABLE OF GROWTH
J. Exp. Med., May 1910; 12: 344 - 366.
Peyton Rous
PARABIOSIS AS A TEST FOR CIRCULATING ANTI-BODIES
IN CANCER:
FIRST PAPER.
J. Exp. Med., Nov 1909; 11: 810 - 814.
Peyton Rous
THE RESISTANCE TO A SPECIFIC HEMOLYSIN OF HUMAN
ERYTHROCYTES
IN HEALTH AND DISEASE
J. Exp. Med., Nov 1909; 11: 763 - 785.
F. Peyton Rous
SOME DIFFERENTIAL COUNTS OF THE CELLS IN THE
LYMPH OF THE DOG:
THEIR BEARING ON PROBLEMS IN HÆMATOLOGY
J. Exp. Med., Jul 1908; 10: 537 - 547.
F. Peyton Rous
THE EFFECT OF PILOCARPINE ON THE OUTPUT OF LYMPHOCYTES
THROUGH THE THORACIC DUCT
J. Exp. Med., May 1908; 10: 329 - 342.
F. Peyton Rous
AN INQUIRY INTO SOME MECHANICAL FACTORS IN THE
PRODUCTION OF
LYMPHOCYTOSIS
J. Exp. Med., Mar 1908; 10: 238 - 270.
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