Open Journal of Pathology, 2013, 3, 150-155
Published Online October 2013 (
Copyright © 2013 SciRes. OJPathology
Ovarian Endometrioid Adenocarcinoma with Functioning
Stroma Accompanied with Endometrial Endometrioid
Adenocarcinoma: Immunohistochemical Study and
Literature Review
Takashi Yuri1*, Tomomi Mizokami2, Yuichi Kinoshita1, Katsuhiko Yoshizawa1, Katsuhiko Yasuda3,
Airo Tsubura1
1Department of Pathology II, Kansai Medical University, Divisions of Obsterics and Gynecology, Kansai Medical University, Osaka,
Japan; 2Hirakata Hospital, Osaka, Japan; 3Takii Hospital, Osaka, Japan.
Email: *
Received May 20th, 2013; revised June 20th, 2013; accepted July 20th, 2013
Copyright © 2013 Takashi Yuri et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Background: The ovarian tumors with functioning stroma are defined by the morphological presence of endocrine ac-
tive cells in stroma, and the clinical, biochemical or pathological evidence of endocrine function. Case Report: The
ovarian endometrioid adenocarcinoma with functioning stroma accompanied with endometrial endometrioid adenocar-
cinoma was found in 64-year-old post-menopausal woman complaining abnormal genital bleeding and mammary dis-
tention. Her preoperative serum 17ß-estradiol level was high (53.2 pg/ml) while human chorionic gonadotropin (hCG)
level was within normal limit. Her right ovary with 8.8 × 5.3 cm in size and tan-yellow in color mostly consisted of
solid tumor. Histologically, tumor was composed of estrogen receptor (ER)- and progesterone receptor (PgR)-positive,
and androgen receptor (AR)-negative cancerous endometrial cells with aggregates of vacuolated foamy stromal cells
resembling luteinized cells. These stromal cells contained lipid droplets, and was immunopositive for α-inhibin and
17ß-estradiol. After surgery, serum 17ß-estradiol level decreased and became normal (14.2 pg/ml). These findings in-
dicate the production of steroid hormone (17ß-estradiol) from the foamy stromal cells and may be correlated with the
clinical symptoms. Furthermore, ER- and PgR-positive endometrial endometrioid adenocarcinoma developed synchro-
nously. However, ovary and uterus were totally immunonegative for human chorionic gonadotropin (hCG). Four other
cases from the literature including ours are reviewed. Conclusio n: Cancer cells were positive for ER and PgR in both
ovary and uterus responded to steroid hormone produced by foamy stromal cells, which played a role in proliferation
and progression of ovarian and endometrial endometrioid adenocarcinoma, respectively.
Keywords: Ovarian Cancer; Endometroid Adenocarcinoma; Functioning Stroma; Immunohistochemistry; Estrogen;
1. Introduction
The majority of ovarian cancer patients are diagnosed at
an advanced stage because clinical symptoms such as ab-
dominal swelling or genital bleeding appears in late stage,
and that no symptoms are evident in the early disease
stage [1]. However, certain categories of ovarian tumors
are capable of producing a variety of hormones that occa-
sionally cause hormone-related symptoms on patients,
which may suggest the occurrence of ovarian cancer.
Hormonally functioning ovarian tumors are characterized
as those that secrete a variety of steroid hormones that
may have unique clinical manifestation [2]. These ova-
rian tumors are defined as ovarian tumors with endocrine
function. Such as the majority are of sex cord-stromal
derivation. However, other tumors not usually associated
with hormone secretion have also been implicated. Func-
tioning ovarian tumors include not only sex cord-stromal
tumors but also epithelial tumors with endocrine-func-
tioning stromal cells. Some of ovarian epithelial tumors
have luteinized stroma, and these stromal cells may
possess hormonal activities [3,4]. Almost every type of
ovarian primary and metastatic, benign and malignant
*Corresponding author.
Ovarian Endometrioid Adenocarcinoma with Functioning Stroma Accompanied with Endometrial
Endometrioid Adenocarcinoma; Immunohistochemical Study and Literature Review
tumors has been reported to cause both estrogenic and
androgenic manifestation, but the most commonly en-
countered are primary ovarian mucinous tumor to have
an estrogenic manifestation [5]. Whatever the oncogenic
stimuli is, synchronous development of the same form of
epithelial tumors in the ovary and endometrium is not a
rare event [6-8].
As the frequency of endometrioid adenocarcinoma
with functioning stroma is rare, we report herein an
ovarian endometrioid adenocarcinoma with endocrine-
functioning stroma accompanied with endometrial endo-
metrioid adenocarcinoma, which occurred in post-meno-
pausal woman who complained abnormal genital bleed-
ing and mammary distention for past 1 year. Our hypo-
thesis was that human chorionic gonadotropin (hCG)
may most probably stimulate α-inhibin-positive stromal
cells to luteinize and produce steroid hormone (17β-es-
tradiol) [9], then the produced hormone may transform
cells positive for receptors (estrogen receptor, ER). The
histological and immunohistochemical analysis together
with literature review are reported.
2. Case Report
2.1. Clinical Summary
A 64-year-old woman, 3 gravida and 2 para, has been
complained of menses-like monthly abnormal genital
bleeding and mammary distention for past 1 year, and
visited the gynecological out-patient clinic. Her menar-
che was at 14 and menopause was at 49 years of age. She
had no previous gynecologic problems and no medica-
tion with steroid hormones. Her body weight was 64.4 kg
and did not present virilism or hirsutism. The intrapelvic
solid mass sized 7 - 8 cm in diameter suggestive of right
ovarian tumor was pointed out with no ascitic fluid pool-
ing by the pelvic magnetic resonance imaging. Hyper-
trophic endometrium was observed by transvaginal ultra-
sonography, and endometrial cytology revealed the pre-
sence of complex endometrial hyperplasia. The malig-
nant ovarian and endometrial tumor was speculated and
consulted Kansai Medical University Takii hospital for
tumor resection.
Prior to the surgery, the vaginal smear appeared to be
estrogenized and atypical endometrial proliferation was
detected by endometrial brushing cytology. Serum tumor
markers CEA, CA19-9, and CA125 were within normal
range. While serum 17ß-estradiol level was elevated
compared with her age (53.2 pg/ml, normal range in
post-menopausal woman is below 18.0 pg/ml), serum
hCG level was within normal range. Total abdominal
hysterectomy with bilateral salpigooophorectomy, partial
omentectomy and pelvic lymphadenectomy was carried
out. A large tumor of the right ovary was detected. No
atypical cells were found in intraperitoneal washing
cytology. After the surgery, the concentration of serum
17ß-estradiol was decreased to normal post-menopausal
level (14.2 pg/ml), and patient is well and had no recur-
rence or metastatic symptoms for 5 years.
2.2. Gross Findings
The right ovary measuring 8.8 × 5.3 cm in size was com-
pletely replaced by neoplasia. The major part of the tu-
mor was solid and lobulated with partial cystic lesions
(Figure 1), and did not adherent to the surrounding tis-
sues. Cut surface was smooth and was tan-yellow in
color with thin fibrotic septa. Hemorrhagic or necrotic
lesions were not seen in any part of the tumor. The mac-
roscopic findings of uterus and contralateral adnexa were
normal, and metastatic nodules were not detected in re-
sected tissues.
2.3. Histological and Immunohistochemical
Ten paraffin-embedded blocks were made from right
ovary. Ovarian tumor was composed of epithelial proli-
feration with dense stroma (Figure 2(a)). Irregularly
formed glands, papillary and columnar in configuration
with enlarged nucleoli, were composed of tall columnar
cells resembling endometrial gland (Figure 2(b)). Secre-
tory products were apparent within the lumen of epithe-
lial cells, and periodic acid-Schiff staining revealed mu-
cin production in the lumen of irregular glands. Squa-
mous differentiation of columnar epithelium was incons-
picuous. The tumor was diagnosed as well differentiated
ovarian endometrioid adenocarcinoma. Characteristically,
aggregates of plump cells with foamy vacuolated cyto-
plasm were scatteredly seen in the stroma. Scattered
nests of vacuolated cells resembled luteinized theca cells
by the cytological features (Figure 2(c)), which oil red-O
staining showed droplets of intracytoplasmic lipid (Fig-
Figure 1. Resected ovarian tumor before the fixation. Tu-
mor totally replaced the ovary, and was tan-yellow in color.
Copyright © 2013 SciRes. OJPathology
Ovarian Endometrioid Adenocarcinoma with Functioning Stroma Accompanied with Endometrial
Endometrioid Adenocarcinoma; Immunohistochemical Study and Literature Review
a b
c d
Figure 2. Histology of ovarian tumor. (a) (b) Well-differen-
tiated endometrioid adenocarcinoma (HE); (c) Note clusters
of vacuolated foamy cells that resemble to luteinized theca
cells in the stroma (HE); (d) Stromal foamy cells contain
droplet positive for oil red-O (oil red-O). Bars; (a) and (b) =
100 μm, and (c) and (d) = 25 μm.
ure 2(d)). In addition to ovarian tumor, a single micro-
scopic lesion consisted of well differentiated endometrial
endometrioid adenocarcinoma at the fundus was detected
(IB; slight invasion to myometrium without vessel in-
volvement); noncancerous endometrium revealed not
atrophic but proliferative phase-like endometrium. Al-
though it was difficult not to declare the evidence of
ovarian cancer metastasis to the uterus, because the right
fallopian tube was free of cancer cells, no evidence of
intrapelvic lymph node metastasis, and uterine cancer
was composed of single microscopic lesion, we con-
cluded that ovary and uterus developed separately (right
ovarian endometrioid adenocarcinoma, pT1a and endo-
metrial endometrioid adenocarcinoma, pT1a).
Antibodies used for immunohistochemcal analysis and
staining results of ovarian and endometrial tumors are
summarized in Table 1. Dilution and antigen retrievals
were followed by manufacturer’s instructions. Cytokera-
tins reacted with epithelial cells while vimentin reacts
with stromal messenchymal cells. Vacuolated stromal
cells seen in the ovary was immunoreactive with α-inhi-
bin (Figure 3(a)) and 17β-estradiol (Figure 3(b)) as well
as vimentin. Carcinoma cells in the ovary and endome-
trium were positive for ER (Figure 3(c)) and progesteron
receptor (PgR), while androgen receptor (AR; Figure
3(d)) was negative. Within the tissue sections examined,
β-hCG-positive cells were not detected in either tumor
components, while luteinizing hormone/chorionic gona-
dotropin receptor (LHCGR) was positive in the cyto-
plasm of both uterine and ovarian adenocarcinoma cells
Figure 3. Immunohistochemistry of ovarian tumor. (a)
α-inhibin intensely labels luteinized stromal cells (α-inhibin),
(b) 17ß-estradiol is localized in luternized cells (17ß-estra-
diol), (c) Endometrioid adenocarcinoma cells are ER posi-
tive (ER); (d) No hCG positivity is seen in tumor section (hCG);
(e) Endometrioid adenocarcinoma cells express LHCGR in
the cytoplasm (LHCGR). Bars = 50 μm.
(Figure 3(e)).
3. Discussion
A variety of ovarian tumors, primary and metastatic,
have been reported to be associated with functioning
stroma; this association is more common in malignant
tumor than in benign ones [9]. To reveal an estrogenic
manifestation, ovarian mucinous tumor is most frequent
[5]. The definitions of attributing origin of the hormonal
alterations to the ovarian tumor are 1) the disappearance
of hormonal manifestations after the tumor removal, and
2) histochemical detection of lipids in stromal cell cyto-
plasms [4]. In the present study, following removal of the
ovarian tumor, a marked decrease in the plasma concen-
tration of 17ß-estradiol was observed. Common appear-
ance of ovarian endometrial carcinoma represents solid
nodule or including cystic lesions which may contain
chocolate-colored fluids or mucin [10]. Lipid-rich tan
yellowish-colored cut surface are macroscopical charac-
teristics of theca cell tumor or hyperplasia. Ovarian hy-
perthecosis contains lipid-containing cells morphologi-
cally identical to the ovarian theca cells [11]. α-Inhibin, a
glycoprotein hormone that is produced by ovarian granu-
losa cells and testicular Sertoli cells usually immuno-
reacts with cells comprised of sex cord-stromal cells such
as granulosa cells and theca cells in the ovary [12]; it
intensely labels luteinized theca cells [13]. In our case,
α-inhibin reacted with clusters of stromal vacuolated
cells, ovarian tumor was tan-yellow in color grossly and
contained oil-red-O-positive lipids in the α-inhibin-posi-
tive foamy stromal cells. Ovarian stromal hyperplasia
and hyperthecosis is known to be associated with estro-
genic and androgenic stimulation, and are considered to
be the origin of excessive steroid hormones in the circu-
lation [5,14]. Main source of the excess steroid hormones
in ovarian stromal hyperthecosis can be proven from the
Copyright © 2013 SciRes. OJPathology
Ovarian Endometrioid Adenocarcinoma with Functioning Stroma Accompanied with Endometrial
Endometrioid Adenocarcinoma; Immunohistochemical Study and Literature Review
Copyright © 2013 SciRes. OJPathology
Table 1. Immunohistochemisry of ovarian and endometrial endometrioid adenocarcinoma.
Ovarian tumor Endometrial tumor
Antibody Clone Source Dillution
Cancer cells Stromal cells Cancer cells Stromal cells
Cytokeratin AE1/AE3 Nichirei Predilluted+ +
CK7 OV-TL Nichirei Predilluted+ +
CK20 Ks 20.8 Nichirei Predilluted
Vimentin V9 Nichirei Predilluted + +
α-Inhibin R1 DAKO ×100 +
CEA COL-1 Nichirei Predilluted
17β-Estradiol PolyclonalMerck Millipore ×150 +
ER 6F11 Novocastra ×40 + + +
PgR 10A9 Biodesign ×50 + +
AR AR27 Novocastra ×50
β-hCG CG04.05 Neo Markers ×100
LHCGR PolyclonalSanta Cruz ×200 + +
Abbreviations: CEA, carcinoembryonic antigen; ER, estrogen receptor; PgR, progesterone receptor; AR, androgen receptor; β-hCG; β-Human chorinic gon-
dotropin; LHCGR, Luteinizing hormone chorionic gonadotropin receptor.
marked decrease in the plasma levels of steroid hor-
mones after ovarian wedge resection or oophorectomy
[15]. The source of excess steroid hormones is consi-
dered to be produced by the luteinized cells present in the
ovarian stroma [16-18]. We have localized 17β-estradiol
in foamy cells in the ovarian stroma. Taken together, we
diagnosed this ovarian tumor as endometrioid adenocar-
cinoma with 17β-estradiol secreting stromal cells from
histological, histochemical, and clinical aspects.
hCG may act as a mitogen and most probably sti-
mulates the stromal cells to luteinize and to produce ster-
oid hormones estrogen, progesterone, or androgen [4].
Tumor containing syncytiotrophoblastic cells and patient
during pregnancy is responsible to luteinize the stromal
cells via hCG action. However, stromal luteinization is
seen in patient who is not pregnant, and whose tumor
which do not contain syncytiotrophoblast [9]. Some study
suggest that tumor cells derived from ovarian epithelial
cells produce hCG and cause the luteinization of stroma
[3,17,19]. Another study suggests that epithelial ovarian
cancer cells can produce 17ß-estradiol by itself through
interactions between cancer cells and luteinized stromal
cells [20]. As the present ovarian tumor was totally nega-
tive with hCG, the explanation for the stromal cell stimu-
lator and the mitogen for estrogen secretion needs further
study. Although hCG levels were within normal levels
and could not immunohistochemically localize hCG in
the ovary, luteinized cells are postulated to be responsive
to even normal levels of serum hCG [4]. It was note-
worthy that LHCGR was present in ovarian and uterine
endometrioid adenocarcinoma cells that carcinoma cells
may mediate hCG or hCG-like signals to cause luteini-
zation of the stromal cells to secrete 17ß-estradiol. Then,
estradiol may bind to the endometrioid adenocarcinoma
cells positive for ER to promote the cancer cell proli-
feration. Estrogen secreting stromal cells may play a role
in proliferation and progression of both ovarian and
uterine adenocarcinoma cells.
Whatever the oncogenic stimuli, synchronous develop-
ment of same form of epithelial tumors in the endome-
trium and ovaries is not a rare event [6-8]. Hyperestro-
genic status plays an essential part in the origin of endo-
metrioid adenocarcinoma. The histologically similar car-
cinoma in the endometrium and ovary may indicate ei-
ther metastatic or independently developing neoplasms.
Using microsatellite analysis, the loss of heterozygosity
provides the difference in origin between the two tumors
[6]. In the present case, histological subtype, degree of
differentiation, immunore activities which we examined
were similar between ovarian and endometrial carcinoma.
The difficulty in the discrimination of the endometrial
metastasis of ovarian carcinoma include the discrepancy
in tumor sizes, the lack of multiple lesions often seen in
metastatic site, and evidence of transtubal spread [7]. In
our case, only one fundic lesion was found, the regional
lymph nodes as well as fallopian ducts were free of
tumor cells, and the discrepancy in size of each tumors
(8.8 × 5.3 cm-sized ovarian tior vs. endometrial lesion m
Ovarian Endometrioid Adenocarcinoma with Functioning Stroma Accompanied with Endometrial
Endometrioid Adenocarcinoma; Immunohistochemical Study and Literature Review
Table 2. Cases of ovarian endometrioid adenocarcinoma with functioning stroma.
Serum estradiol (pg/ml) Follow up
Case Age
(yr) Pre-surgery Post-surgery
Tumor size (cm)FIGO stagingEndometrial
lesiona Treatmentb
(Disease free yrs)
1 31 553 Decreased 12 I a EC, G2 1 3 [6]
2 69 22.8 10 7 × 6 III b PA 1, 2 1.25 [16]
3 81 83 Undetectable (<10) 12 × 10 Ic (a) PA 1 1 [20]
4 70 162.4 11.6 10 × 9 Ic (b) AEH-C 1, 2 2 [21]
5 64 53.2 14.2 8.8 × 5.3 Ia EC, G1 1, 2 5 Present case
aPA, proliferative activity: AEH-C, atypicalendomelrial hyperplasia,complex; EC, endometrial carcinoma. b1 means total abdominal hysterectomy with bilateral
salpigooophorectomy; 2 means platinum-based combined chemotherapy.
at the microscopic level). Therefore we concluded that
the tumors in ovary and endometrium despite the similar
morphological features, was different origin.
Among ovarian epithelial tumors with functioning
stroma, mucinous tumors are most frequent [4]. To the
best of our knowledge, well-documented literatures of
ovarian endometroid adenocarcinoma with functioning
stroma was found in only 4 cases; 5 cases including our
present case are summarized in Table 2 [6,16,20,21].
Age distribution ranged from 31 to 81, which the average
was 63 years of age. Elevations of serum estradiol value
were seen in all cases (22.8 - 553 pg/ml, mean 174.9
pg/ml), and which declined to the average ranges for
patient’s age after the tumor resection. Surgical tumor
resection was the principle treatment of this ovarian neo-
plasm (7 - 12 cm in the largest diameter, mean 10.0 cm),
adjuvant chemotherapy was added if the tumor extend
outside the ovary. Endometrial proliferative lesions in-
cluding malignancy were detected in all cases regardless
of patient’s age. Estrogen secretion from luteinized theca
cells in postmenopausal ovary may promote the growth
of endometrial adenocarcinoma. In previous reports,
theca cell hyperplasia seen in post-menopausal women
has a marked incidence of endometrial adenocarcinoma
[22]. Ovarian endometrial tumors frequently resemble to
sex cord-stromal tumors by morphology [23]. However,
α-inhibin is positive in luteinized stromal cells but ne-
gative in endometrioid adenocarcinoma cells [19]. In con-
trast, ER and PgR are frequently positive in endometrioid
adenocarcinoma cells [24] while negative in luteinized
stromal cells. These markers may be useful in differential
4. Conclusion
We reported a rare case of ovarian endometrioid adeno-
carcinoma with functioning foamy stromal cells accom-
panied with endometrial endometrioid adenocarcinoma.
Immunohistochemistry revealed α-inhibin and the pro-
duction of sex steroid hormone (17ß-estradiol) in foamy
stromal cells, which may be related to the promotion and
proliferation of ER-positive ovarian and endometrial en-
dometrioid adenocarcinomas. Therefore endometrial ex-
amination is essential in patients suffering ovarian endo-
metrioid adenocarcinoma with functioning stroma. Addi-
tional cases are required to elucidate the precise mechan-
isms of this complication and to predict the patient’s
5. Acknowledgements
The authors thank Ms. T. Akamatsu for her technical
assistance of immunohistochemical assistance and Ms. A.
Shudo for preparing the manuscript.
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