T H E AMERICAN JOURNAL OF CLINICAL PATHOLOGY
Vol. 40, No. 1, pp. 58-66
July, 1963
Copyright © 1963 by The Williams & Wilkins Co.
Printed in U.S.A.
PATTERNS OF METASTATIC CANCER IN THE SPLEEN
JESSE H. MARYMONT, J R . , M.D., AND STANLEY GROSS, M.D.
Division of Laboratories, North Shore Community Hospital, Manhassel, New York
The spleen is the largest single mass of
lymphoid tissue in the body; however, unlike
the other aggregates of this tissue which are
inserted into the lymph stream, the spleen
is interposed in the blood stream. The
anatomic peculiarities of the spleen are
reflected in the low incidence and unusual
patterns of metastatic malignancy in that
organ. It is the authors' purpose in this
paper (1) to review the patterns of secondary
cancer in the spleen, and (2) to correlate
these with its structure.
The spleen has a fibrous framework
composed of a capsule and trabeculae. The
capsule is thickened at the hilus of the
organ where it is. attached to folds of peritoneum and where vessels enter and leave
the viscus. The trabeculae are continuations
of the capsule and penetrate deeply into the
organ. The reticulum network together
with the cells present comprise the splenic
parenchyma. This is composed of white
pulp, venous sinusoids, and pulp cords, the
latter 2 together comprising the red pulp.
The branches of the splenic artery enter the
hilus and pass along the trabeculae, branching frequently and becoming smaller in
caliber. When they reach a diameter of
approximately 0.2 mm. they leave the
trabeculae and become the central arterioles
of the white pulp. The central arterioles
give off numerous capillaries which nourish
the white pulp and then pass into the red
pulp. The arterioles continue to branch and
when they reach a diameter of 40 to 50 M
they, too, leave the white pulp and enter
the red pulp. On entering the red pulp each
divides into 2 to 6 straight branches, called
penicillar arteries. These continue to divide
and ultimately end up as arterial capillaries.
Their exact mode of termination is unknown.
The veins of the spleen begin as venous
sinusoids which have wide irregular lumina
that vary in diameter with the amount of
blood in the organ. The sinusoids empty
into the veins of the pulp; these in turn
coalesce to form the veins of the trabeculae.
The trabecular veins unite to form the
splenic veins which leave the organ at the
hilus and drain into the portal vein.
The communication between arterial and
venous systems is not clear. It is known,
however, that India ink or avian erythrocytes injected into the splenic artery
readily gain access to the pulp cords, and
only later are found in the venous sinusoids.17
The extent of the lymphatics of the human
spleen is a controversial subject. There are
those2 who insist that lymph vessels never
occur in the interior of the spleen, whereas
others 3,18 describe lymphatics in the capsule
and superficially in the thickest trabeculae.
These are thought to be in the region of the
hilus, and not in association with either the
red or white pulp. Still others 13,15,16 believe
that the lymphatics are associated with the
arteries and nerves and penetrate deeply
into the parenchyma. Many writers, 6 ' 9 - 14
however, do not mention deep parenchymal
lymphatics, although comment is made of
lymphatics in the white pulp of other
mammals. Goldberg5 has recently reviewed
the subject and presented evidence that
lymph vessels do indeed extend deeply into
the parenchyma. These are present in the
adventitia of the arteries and arterioles
and are subintimal in location in the veins.
They are found as far as the central arterioles
of the white pulp. Goldberg4 described 2
cases of metastatic carcinoma in the spleen,
both of which were not visible on gross
examination. On microscopic study, however, lymphatics in the adventitia of the
afferent blood vessels were distended by
clusters of tumor cells. In some regions
these were about central arterioles and were
apparently wholly within the white pulp.
In other locations the tumor was beneath
Received, July 18, 1962; revision received, Decembers; accepted for publication April 9, 1963.
Dr. Marymont is Assistant Pathologist and Dr.
Gross is Director of Laboratories.
58
July 1963
METASTATIC CANCER I N T H E
the intima of veins. In neither of the cases
was tumor described in venous sinusoids or
as microscopic nodules in the red pulp.
The literature that deals with secondary
cancer in the spleen is not inconsiderable,
and several aspects have been extensively
studied. Some of these will be briefly mentioned. It has long been appreciated that
the incidence of metastatic tumor in the
spleen is low. In routine autopsy material,
0.3 to 9 per cent of patients with cancer
are found to have splenic involvement."
Yokahata22 made serial sections of spleens
from patients who died of carcinoma, and
found metastases in 34 per cent. Harman
and Daeorso8 found splenic metastases in
50 per cent of a group of 30 patients who
died of carcinoma, and who had metastases
in at least 1 organ in both the thoracic and
abdominal cavities. Warren and Davis20
found no case in wliich the spleen was the
sole site of secondary tumor. In every case
in which the spleen was involved there were
metastases in 3 or more organs. These
observations establish the fact that the
splenic metastases occur only in patients
with widely disseminated tumor and,
therefore, that it usually occurs late in the
course of the disease. The frequency with
which tumors of the various organs involve
the spleen varies greatly in different reports.
In 4 of the most recent articles 1,10,11,20
carcinomas of the lung and breast comprised
30 to 67 per cent of all splenic metastases.
Other common tumors were melanomas of
the skin, as well as carcinomas of the
pancreas, large intestine, and stomach.
Much has been written in an attempt to
explain the paucity of splenic metastases.
The theories fall into 2 main groups,
physiologic and anatomic. The first postulates the existence of substances in the
spleen that destroy the tumor cells that
reach the organ. The evidence for this is
confusing and contradictory. It has been
excellently reviewed by Woglom21 and will
not be considered further. The second
deals with the anatomic peculiarities of
the spleen. Sappington19 stated that the
sharp angle made by the splenic artery at
its origin from the celiac axis made it difficult for tumor emboli to enter the vessel.
SPLEEN
59
The frequency of thrombotic emboli to the
spleen, however, makes this difficult to
accept. Others12 mentioned the contractions
of the spleen that intermittently force
blood from the sinusoids into the splenic
veins. This motion was thought to make
tumor implantation uncommon by keeping
the malignant cells in constant motion. The
hypothesis ignores the fact that there are
other organs that do not have the capacity
for pulsatile movement and that are very
rarely the site of metastatic cancel-.
Little has been written about the patterns
of metastatic cancer in the spleen. Warren
and Davis,20 in their analysis of 42 cases of
indisputable metastases to the spleen,
found that 22 of these patients had grossly
evident secondary tumor, whereas in the
remaining 20, or in 47.6 per cent, the metastases were identified only on microscopic
examination. They mentioned that in some
of the latter group tumor was only in venous
sinusoids, whereas in others there were
microscopic nodules. Their cases of gross
tumor included examples of both nodular
and diffuse metastases. Others 10,22 have
briefly mentioned different types of splenic
metastases, but no authors have treated
the entire subject in a detailed manner.
From the laboratories of pathology of the
North Shore Community Hospital, the
Long Island Jewish Hospital, the Bellevue
Hospital, and the Meadowbrook Hospital, a
total of 109 autopsies were obtained in
which a diagnosis of metastatic cancer of
the spleen had been made, and in wliich
at least 1 section of spleen was available
for study. At this point it is important to
define the conditions under which tumor
cells present within the spleen are to be
regarded as metastatic growths. We agree
with the concept of Warren and Davis,20
who have defined a metastasis as a noncontiguous secondary nodule of tumor cells.
Direct extension of neoplasm from a neighboring focus, or involvement of the splenic
capsule as a part of peritoneal seeding, are
not true metastases. They stated their
position as follows:
"Krumbhaar is of the opinion that the
mere presence of tumor cells in the blood
stream does not constitute a metastatic
60
Vol. 40
MAHYMONT AND GROSS
growth. Since we do not know any method
whereby we can determine whether or not
a particular cluster of tumor cells located
in capillaries, sinusoids or larger vessels,
if undisturbed, would continue to grow and
involve the adjacent parenchyma, we feel
that any cluster of viable tumor cells separated from the primary tumor must be considered as a metastasis. No one would
consider a lymph node as free from tumor if
its sinuses contained tumor tissue."
In 14 of our cases secondary carcinoma
involved the spleen by direct extension from
a neighboring organ, or as a manifestation of
generalized peritoneal carcinomatosis. In 2
instances a decision could not be reached as
to whether nests of cells in venous sinusoids
were metastases or immature cells of the
myeloid series. In both of these the primary
neoplasm was an undifferentiated carcinoma
of the stomach. The remaining 93 cases are
regarded as true splenic metastases and
form the basis of this study.
Any secondary deposit of cancer in the
spleen that is of sufficient size to be visible
grossly must involve all elements of the
parenchyma, as well as a portion of the
supporting fibrous framework. The mode
of origin of such a lesion can not be determined, and for this reason the cases are first
divided on the basis of whether the metastases were microscopic or macroscopic
in size. In 31 instances (33.3 per cent) only
microscopic aggregates of secondary tumor
were present, whereas in the remaining 02
cases they were grossly visible. Within these
2 headings the cases are further subdivided
into 7 groups on the basis of appearance
and location of the metastases, the first 5
being concerned only with the microscopic
metastases. Group I contains 11 cases in
which tumor was solely within venous sinusoids. The tiny collections of malignant
cells slightly distended the vascular channels, but did not replace splenic tissue. The
next 2 headings comprise cases with larger
aggregates of tumor that formed microscopic
nodules, with replacement of small amounts
of parenchyma. In group II are 6 cases in
which tumor was wholly within the red
pulp and resulted in destruction of both
venous sinusoids and pulp cords. The
solitary member of Group III had neoplasm
in the white pulp only. The involvement was
limited to the lymphoid tissue; the central
arteriole was not affected. The sole case in
Group IV had secondary carcinoma limited
to a trabecular vessel. The parenchyma was
free of neoplasm, the involvement being
only of a medium-sized vascular channel in
the supporting fibrous framework. Group
V includes 12 cases in which there were
multiple microscopic metastases that cut
across the subdivisions already enumerated
and did not involve only a single element of
the spleen. Some had microscopic nodules in
both the red and the white pulp, whereas in
others there were nodules as well as tumor
nests in venous sinusoids. Group VI consists
of 54 cases in which grossly evident neoplasm
had a nodular configuration, whereas in
Group VII are 8 examples of diffuse involvement of the entire spleen by tumor. The
locations of the metastases within the
spleen, together with their frequency, are
tabulated in Table 1. The histologic detail
and the probable mode of tumor dissemination of each of these groups will now be
considered.
In Group I the aggregates of malignant
cells in the vascular channels were lying free
within the lumina (Tig. 1). In no instance
was tumor of this type adherent to the
TABLE 1
T H E T Y P E AND LOCATION OK M E T A S T A T I C CANCEU
IN THE S P L E E N — A N ANALYSIS OK 93
Appearance and Location of Metastases
in the Spleen
Microscopic tumor
Group I—in venous sinusoids
only
Group II—in red pulp as microscopic nodules only
Group III—in white pulp as
microscopic nodules only
Group IV—in trabecular vessel
only
Group V—in several different
elements of spleen
Macroscopic tumor
Group VI—nodular type
Group VII—diffuse t y p e
CASES
No. of
Cases
Percentage of
Total
Cases
31
11
33.3
11.S
0
0.5
I
1.1
1
1.1
12
12.S
62
54
8
60.7
5S.1
8.6
FIG. 1 (upper left). Sinusoidal metastases in the spleen from a neuroblastoma of the adrenal gland.
X 105.
FIG. 2 (upper right). Microscopic nodule of metastatic bronchogenic carcinoma in the red pulp of
the spleen. X 260.
FIG. 3 (lower left). Microscopic nodule of metastatic gastric carcinoma in the white pulp of the
spleen. X 80.
FIG. 4 (lower right). Metastatic gastric carcinoma in the white pulp of the spleen. X 215.
61
62
MARYMONT AND GROSS
vessel wall. The cells usually revealed poor
differentiation and closely resembled the
primary tumor. In no instance was there
necrosis of the small tumor nests, and none
had an associated desmoplastic reaction.
The sinusoidal collections of tumor cells
were distributed uniformly throughout the
parenchyma, and there was no tendency
for them to be more numerous about the
trabeculae, in the subcapsular region, or at
the hilus. In some cases there were very few
tumor aggregates in the sinusoids, whereas
at the other extreme were instances in which
every microscopic field contained nests of
intravascular tumor. Even in cases with
very extensive tumor of this type the trabecular vessels were strikingly free of neoplasm. This type of metastasis is the result
of hematogenous dissemination, through the
splenic artery, of tumor emboli that are
small enough to pass directly to the sinusoids.
The suggestion has been made20 that these
sinusoidal tumor collections represent a
terminal occurrence. We do not agree with
this, for 3 reasons. If this were merely a
shower of malignant cells that were released
into the blood stream and filtered out by the
spleen, then similar aggregates should be
present in other organs, and these were not
observed. In addition, the sinusoidal metastases illustrated in Figure 1 are larger
than the penicillar arteries, and could
not have reached the sinusoids in this form.
Masses of cells (or single cells) sufficiently
small to pass the penicillar arteries would
have needed time to produce aggregates of
the sine shown. Finally, it has been demonstrated 7 that sinusoidal metastases are very
often associated with splenic extramedullar}'
hematopoiesis. Although there are several
explanations for this, it seems most unlikely
that the 2 become coexistent in the agonal
period.
In Group II the tumor aggregates actually
replaced small amounts of splenic parenchyma (Fig. 2). They varied in size from
almost grossly visible down to only very
slightly larger than the nests of intrasinusoidal tumor. These were sometimes the site
of focal necrosis. Only rarely was there an
associated desmoplastic reaction. The nod-
Vol. Jfi
ules did not involve the fibrous framework or
trabecular vessels. The fact that they were
often not associated with sinusoidal metastases makes it unlikely that they are
merely a later stage of these. They are
certainly the result of hematogenous dissemination through the splenic artery. It is
possible that they are the result of slightly
larger tumor emboli than those responsible
for sinusoidal metastases, and that these did
not reach the sinusoids, but became implanted in the pulp cords. This, however, is
only speculation and we did not recognize
tumor collections that were entirely within
the pulp cords.
The rare and very interesting example of
microscopic tumor in the white pulp only
(Group III) will be considered in conjunction
with several other cases in which most, but
not all, of the metastases were confined to
the Malpighian corpuscles. Focal necrosis or
fibrosis was rare in these. In some the tumor
was in close approximation to the adventitia
of the central arteriole. It is possible that
these tumor aggregates represent lymphatic
dissemination (Figs. 3 and 4). This seems
to be the only pattern of microscopic
splenic metastases that may be the result of
lymphatic dissemination. Hematogenous
spread could be responsible for a similar
picture. The infrequency of this pattern
may be a reflection of the relative unimportance of lymphatic spread as a cause of
secondary cancer in the spleen.
The 1 case in Group IV with a microscopic
metastasis only in a single trabecular vessel
was most unusual. The tumor filled the
vessel and seemed to be attached to the
wall. The absence of involvement of all
types of vascular channels in the trabeculae
of spleens that were the site of microscopic
metastases was very striking. Without
doubt tumor cells that reached the spleen
by either lymphatic or hematogenous routes
originally implanted in the tiny vessels of
the red or white pulp, and only rarely
involved larger vessels early. In none of the
entire group of spleens was metastatic
tumor found in a central arteriole.
The histology of the gross tumor nodules
(Group VI) was very similar to that of their
microscopic counterparts. The larger nod-
July 1963
METASTATIC CANCER IN THE SPLEEN
ules had a higher incidence of tumor necrosis,
and there was more often an associated
desmoplastic reaction. Trabeculae were
often incorporated into the larger nodules,
and in approximately half there was tumor
in the associated vascular channels. The
absence of this in the microscopic nodules
implies that it is a late occurrence and
develops only after local interference with
splenic circulation. We believe that the
gross and microscopic nodules are merely
different stages of the same process, and
that the pathogenesis is identical.
The 8 spleens with diffuse metastases
comprising Group VII revealed 2 distinctly
different histologic patterns. In 7 there was
diffuse replacement of both red and white
pulp by carcinoma. In the 1 remaining
instance there was extensive involvement
63
of the red pulp, but the Malpighian corpuscles were uniformly free of tumor. In all
of these the tumor was very poorly differentiated, and the pattern was one of small
clusters of anaplastic cells interspersed in
the reticulum framework of the spleen (Fig.
5). Focal tumor necrosis was absent, as was
a significant desmoplastic reaction; the
trabecular vessels were often involved by
the process. The one case with red pulp
involvement alone probably was the result
of hematogenous dissemination of tumor
emboli to venous sinusoids and pulp cords.
It is possible that a very large number of
malignant cells were released from the
primary lesion, and that the resultant
massive embolization contributed to the
diffuse nature of the tumor in the spleen. In
addition, this was the only instance in the
F I G . 5 (left). Complete replacement of splenic parenchyma by metastatic mammary carcinoma
(grossly diffuse involvement of the spleen). X 75.
F I G . 6 (right). Replacement of the white pulp of the spleen with focal extension of mammary carcinoma to the red pulp. X 105.
64
MARYMONT AND GROSS
entire series in which the liver had diffuse
intrasinusoidal metastases, and this suggests
that the carcinoma was one with an unusually great propensity for vascular permeation.
The extensive parenchymal involvement
in the cases with both red and white pulp
tumor makes elucidation of pathogenesis
impossible. In 1 case of breast carcinoma
with only microscopic metastases, however,
there was a unique pattern which, on a
small scale, had great similarity to these 7
cases. Here there was extensive replacement
of the white pulp by carcinoma with focal
extension of the neoplasm into the surrounding red pulp (Fig. 6). It is our impression that this would have gone to complete
parenchymal replacement if the patient
had survived. For the reasons already
stated it is believed that this might have
been the result of massive lymphatic spread,
possibly associated with hematogenous
dissemination.
It would seem, in summary, that the
majority of cases of secondary cancer in the
spleen are the result of hematogenous
dissemination, this being regarded as the
pathogenesis of 1 type of diffuse splenic
carcinomatosis as well as of microscopic red
pulp nodules and sinusoidal metastases.
Lymphatic dissemination, although less
frequent, might be responsible for the
majority of cases of diffuse metastatic
cancer, and for the uncommon examples of
microscopic nodules in the white pulp.
An attempt was made to correlate the
histologic appearance of the primary tumor
with splenic and other metastases. This was
only partially successful because in many
instances surgical extirpation of the original
neoplasm had been performed at a different
institution than the autopsy, and the
material was unavailable for review. The
great majority of cases in which correlation
was possible revealed close similarity between the primary tumor and all metastases.
There were, however, some histologic
differences between the members of several
groups.
The cases with sinusoidal splenic metastases (Group I) were uniformly characterized
by poor differentiation and very minimal
Vol. 40
fibrosis in both primary and metastatic
lesions. Metastases in organs other than
the spleen usually had a nodular configuration, and widespread vascular permeation
was not present. In contrast, approximately
25 per cent of those cases with either gross
or microscopic tumor nodules (Groups II,
III, and VI) revealed well differentiated
architecture. Desmoplasia, although never
extensive, was present in a moderate number. The metastases were predominantly
nodular in pattern. None of the primary
tumors in Group VII were available for
study. The metastases in all cases, however,
were poorly differentiated and manifested
slight to moderate desmoplasia. As previously mentioned, 1 of these cases had diffuse
intrasinusoidal metastases in the liver. The
remaining 7 demonstrated nodular metastases. There was nothing in the distribution
or appearance of these to suggest complete
organ replacement similar to that seen in
the spleen.
The location of the primary tumors are
listed in Table 2. Carcinomas of the lung
and breast were the most frequent, and
together were responsible for more than
one-half of the cases. It is interesting that
carcinoma of the prostate gland was responsible for 5 of the 31 cases of microscopic
splenic metastases, whereas it caused gross
metastases only once. Carcinoma of the
breast was the primary lesion in 6 of the 8
cases of diffuse metastases. The other 2 were
in women, ages 58 and 76 years, in whom
the primary tumor could not be ascertained.
Both of these were poorly differentiated
carcinomas and were thought to be compatible histologically with a carcinoma of
the breast.
The averages and ranges of weights of
the spleens are summarized in Table 3. The
organs weighed 200 Gm. or less in 25 of the
31 cases with microscopic metastases. None
of these revealed infarcts, and there was
nothing in their gross appearance to suggest
the presence of secondary tumor. Those with
gross nodular metastases had an average
weight of 236 Gm. In 23 of the 39 cases in
which the weights were recorded, however, it
was 200 Gm. or less, and in only 3 instances
did the spleens weigh more than 500 Gm.
July 1.963
METASTATIC CANCER I N T H E
Splenic infarcts were uncommon. The tumor
nodules were sharply circumscribed and similar to those seen so frequently in other
organs that are the sites of metastases. The
spleens with diffuse metastatic carcinoma
were the heaviest, and had an average of
803 Gm. Four of the 8 weighed more than
500 Gm., and the heaviest weighed 3000
Gm. All spleens in this group had a striking
gross appearance. The usual contour was
preserved, but organ size varied tremendously. The capsules were pale gray, very
firm, and greatly thickened. Most were
irregularly granular although several were
described as smooth. A uniform feature of
the cut surface was the complete absence of
normal splenic parenchyma. In 6 cases the
cut surface was smooth, solid, homogeneous,
very firm, and pale gray to brown. In 2
TABLE 2
Tun
LOCATIONS OF THE PRIMAKY T U M O R S AND
T H E I R INCIDENCE IN G R O S S AND MICROSCOPIC
SPLENIC
METASTASES—AN
ANALYSIS
OP
93
CASES
Total
Location of
Primary Tumor No. of
Cases
Lung
Breast
Prostate
gland
Colon
Stomach
Unknown
Esophagus
Liver
Melanoma
Ovary
Tongue
Pharynx
Testis
Adrenal
gland
Mediastinal
teratoma
Meningeal
sarcoma
Kidney
Gallbladder
Neuroblastoma
No.
Cent
No.
Cent Causing Per
MicroCausing Per
Micro- ofscopic
of
Gross
Gross
scopic
MetasMetasMetasMetastases
tases
tases
tases
35
18
G
23
12
1
38
20
2
12
G
5
40
20
16
0
G
5
2
2
2
2
1
1
1
1
4
5
4
2
2
2
1
1
1
1
1
6
8
0
3
3
3
2
2
2
2
2
2
1
1
0
0
0
1
0
0
0
0
G
3
3
0
0
0
0
0
0
0
0
1
1
2
0
0
1
1
2
0
0
1
1
1
0
0
0
0
0
0
1
1
1
3
3
3
65
SPLEEN
TABLE 3
T H E AVERAGE AND R A N G E OF W E I G H T OP S P L E E N S
WITH M E T A S T A T I C CANCER—AN ANALYSIS OP 93
CASES
Type of Metastasis
Average
Weight
of
Spleen
Gm.
Microscopic tumor—groups 1 to
V
Gross tumor
Tumor nodules—Group VI
Diffuse involvement—Group
VII
Range of
Weight of
Spleens
Gm.
103
60-400
230
S03
70-1100
100-3000
there were innumerable tumor nodules
throughout. These individually were similar
to the more common nodular type of metastasis, but their profusion left no intervening uninvolved tissue. Two of the S had
recent splenic infarcts. This is an incidence
of 25 per cent and, although the number of
cases is small, is in contrast to the spleens
with all other types of metastases in which
infarcts were present in less than 5 per cent.
•SUMMARY
This paper deals with a study of 93 cases
of metastatic cancer in the spleen, as
observed at the time of autopsy. These
included 90 carcinomas, a meningeal sarcoma, a mediastinal teratoma, and a
neuroblastoma.
The metastases were of microscopic size
in 31 instances (33.3 per cent) and grossly
visible in the remaining 62 cases. They were
divided into 7 groups on the basis of appearance and location within the spleen. Group
I contained 11 cases with tumor cells limited
to the venous sinusoids. Groups II and III
were comprised of cases with microscopic
nodules in the red pulp (6 cases) and white
pulp (1 case), respectively. The solitary
case in Group IV had tumor only within a
trabecular vessel, whereas the 12 cases in
Group V had features found in several of
the preceding divisions. Groups VI (54
cases) and VII (8 cases) contained those
with grossly evident tumor. In the former
the neoplasm had a nodular configuration,
whereas in the latter there was diffuse
splenic involvement.
GG
MAHYMONTI' AND GROSS
The probable route of dissemination for
each of the different patterns of secondary
tumor in the spleen was discussed.
SUMMAHIO IN 1NTEBLINGUA
Iste communication reporta un studio de
93 casos de cancere metastatic in le splen,
como illo esseva observate al tempore del
necropsia. Le serie include 90 carcinomas,
un sarcoma meningee, un teratoma mediastinal, e un neuroblastoma.
Le metastases esseva de magnitude microscopic in 31 casos (33.3 pro cento) e macroscopicamente visibile in le remanente 62
casos. Illos esseva dividite in 7 gruppos a
base de lor apparentia e de lor sito in le splen.
Gruppo I contineva 11 casos de restriction
del cellulas tumoric al sinusoides venose.
Gruppos I I e I I I comprendeva casos de
nodulos microscopic in le pulpa rubie (6
casos) e in le pulpa blanc (1 caso). Gruppo
IV consisteva de un sol caso in que le tumor
existeva exclusivemente intra un vaso trabecular, durante que le 12 casos in Gruppo V
habeva characteristicas presente in le casos
de plus que un del prime quatro gruppos.
Gruppo VI (54 casos) e Gruppo VII (8 casos)
esseva distinguite per le visibilitate macroscopic del tumor. In gruppo sex, le configuration del neoplasma esseva nodular; in
gruppo septe le splen esseva diffusemente
afficite.
Es discutite le circuito probabile del dissemination de tumor secundari ad in le splen
pro cata un del diverse configurationes.
Acknowledgments.
I t is a pleasure to acknowledge t h e cooperation of Drs. Marvin Kushner,
James Berkman, and Vincent Palladino, Directors
of Laboratories a t t h e Bellevue Hospital, t h e Long
Island Jewish Hospital, and t h e Meadowbrook
Hospital, respectively, who placed their autopsy
material a t our disposal.
REFERENCES
1. AHKAMS, H . L., S P I R O , R., AND G O L D S T E I N , N . :
Metastases in carcinoma; an analysis of 1000
autopsied eases. Cancer, 3 : 74-85, 1950.
2. BILLROTH, T . : Zur normalen und pathologischen Anatomie der menschlichen Milz.
Arch. path. Anat., 20: 409-425, 1861.
Vol. 40
3. D R I N K E R , C. K . , AND Y O F F E Y , J . M . : L y m -
phatics, Lymph, and Lymphoid Tissue.
Cambridge, Mass.: H a r v a r d
University
Press, 1941, p . 23.
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