Case 1 -
Uterine Tumour Resembling Ovarian Sex Cord Tumour (UTROSCT)
Belfast, Northern Ireland
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F60, postmenopausal bleeding, endometrial curettage
Histology shows tissue fragments composed of papillary
arrangements of bland epithelial-like tissue. There is only mild nuclear pleomorphism and only
occasional mitotic figures are present.
endometrium, papillary lesion, uterine tumour
resembling ovarian sex cord tumour.
- papillary fragments of epithelium are not uncommonly encountered in endometrial biopsy specimens.
- when faced with epithelial elements with a papillary architecture in an endometrial biopsy, the
differential diagnosis may range from artefactual papillary epithelium to non-neoplastic lesions to
benign and malignant neoplasms.
- UTROSCT rarely presents in an endometrial biopsy specimen and may have a pronounced papillary
Papillary Lesions of Endometrium
Tissue with a papillary or micropapillary architecture is not uncommonly seen in endometrial biopsy
specimens. A wide range of endometrial lesions may have a papillary architecture, ranging from
artefactual papillary formations to benign epithelial lesions to various carcinomas. Some non-epithelial
lesions may also have a papillary architecture. Table 1 lists endometrial and uterine lesions which
potentially may be present in an endometrial biopsy and exhibit a papillary architecture. These are
discussed in the next sections.
Artefactual Papillary Endometrium
In endometrial biopsies, especially but not exclusively outpatient endometrial pipelle biopsies,
atrophic endometrium may exhibit a pseudopapillary architecture . This change is common and, if
widespread, may result in consideration of a papillary variant of adenocarcinoma. Awareness of the
existence of this phenomenon together with careful high power examination which reveals atrophic
epithelium without mitotic activity assists in establishing the diagnosis.
Papillary Syncytial Metaplasia
The term papillary syncytial metaplasia is a misnomer since this does not actually represent a
metaplasia but rather a degenerative or reparative phenomenon associated with surface breakdown, either
menstrual or non-menstrual in type. However, the term papillary syncytial metaplasia is in widespread
use. Synonymous terms include eosinophilic syncytial change and surface syncytial change. It has been
suggested that papillary syncytial metaplasia is a degenerative or regressive phenomenon based on a low
proliferation and mitotic index . Papillary syncytial metaplasia is common and is characterised by
small syncytia or micropapillary proliferations of endometrial epithelial cells which may contain small
glandular lumina and which are devoid of stromal support, lacking fibrovascular stromal cores. The cells
usually have eosinophilic cytoplasm and there is often a neutrophilic infiltrate. There may be mild
nuclear atypia and in a minority of cases, mitoses are present. In florid cases, papillary syncytial
metaplasia may be confused with an endometrioid or serous adenocarcinoma or with serous endometrial
intraepithelial carcinoma (serous EIC). Another important consideration is that foci similar to
papillary syncytial metaplasia may occur on the surface of some endometrioid adenocarcinomas (discussed
later). The distinction between papillary syncytial metaplasia and papillary adenocarcinomas of
endometrioid or serous type is facilitated by recognition that papillary syncytial metaplasia is limited
to the endometrial surface and is associated with other morphological features of breakdown such as
apoptotic debris, neutrophils and adjacent glandular and stromal breakdown.
Arias- Stella Reaction
Arias-Stella reaction (Arias-Stella effect or change) is almost always associated with pregnancy,
either intrauterine or ectopic, or with trophoblastic disease. It rarely occurs secondary to hormone
therapy, especially progestogens; occasionally there is no obvious cause . Histologically, the
Arias-Stella reaction is characterised by cellular stratification, secretory activity, vacuolated
cytoplasm and enlargement of the epithelial cell nuclei and cytoplasm. The nuclei may be enlarged up to
three times normal and can exhibit considerable atypia and a hobnail appearance with bulging into the
glandular lumina. There may be micropapillary formations. Mitotic figures may be present, although
these are rarely prominent and there is a low MIB1 proliferation index. Atypical mitoses have rarely
been described . The Arias-Stella reaction may be extensive, involving many glands, or focal with
involvement of only a few glands or even part of a gland. The most important differential diagnosis is
clear cell carcinoma but the diagnosis of Arias-Stella reaction is usually straightforward if the patient
is known to be pregnant and if other morphological features of pregnancy are present, such as
decidualisation of the stroma. Arias-Stella reaction involves pre-existing endometrial glands without
evidence of stromal infiltration and there is no mass lesion. Although there is nuclear enlargement and
atypia, a low nuclear to cytoplasmic ratio is maintained.
Hyperplastic Papillary Proliferation of Endometrium
The term hyperplastic papillary proliferation of the endometrium has been used for a lesion, usually
occurring in postmenopausal women, characterised by the presence of papillae with fibrovascular stromal
cores and variable degrees of branching and cellular tufting . The papillae are lined by epithelial
cells with bland nuclei. Epithelial metaplasias, most commonly mucinous, eosinophilic or ciliated in
type, are often also present. Sometimes the papillae are entirely intracystic (projecting into
cystically dilated endometrial glands) while in other instances they involve the endometrial surface.
Papillary proliferation is most commonly seen on the surface of an endometrial polyp and, in some
instances, the features are florid. There may be an association with hormonal preparations. A
misdiagnosis of an adenocarcinoma of endometrioid or serous type is possible, especially if an underlying
polyp is not present or not obvious. Awareness of this phenomenon and the realisation that it often
occurs in a polyp are clues to the diagnosis, although both endometrioid and serous adenocarcinomas may
arise in and be confined to a polyp. An absence of nuclear atypia helps to exclude an adenocarcinoma.
It has been considered that these papillary proliferations are a form of hyperplasia that is closely
associated with epithelial metaplasia. However, given the uneventful outcome in those cases with follow
up, the term hyperplasia may not be appropriate.
Effects of Intrauterine Device
Intrauterine devices (IUDs) are in widespread use, mainly for contraceptive purposes. The
histological features in the endometrium in association with an IUD are largely due to local mechanical
effects. The surface endometrium may take on the configuration of the IUD due to a direct pressure
effect. There may be surface micropapillary formations and focal reactive changes with nuclear
enlargement, mild nuclear atypia, small nucleoli and cytoplasmic vacuolation. When micropapillary
fragments of epithelium exhibiting these features are present in an endometrial biopsy, this may result
in diagnostic difficulty. The glandular epithelium may also exhibit epithelial cytoplasmic change,
including squamous metaplasia, and there may be surface ulceration. Although the features may be subtle,
a focal inflammatory infiltrate is commonly present consisting of polymorphs, lymphocytes, histiocytes
and plasma cells. Foreign body type giant cells and granulomas may be a component of the inflammatory
infiltrate, the severity of which may be related to the type of IUD and the duration of use.
A papillary architecture is very common in various uterine adenocarcinomas, most commonly of
endometrioid and serous type. A papillary architecture is especially common in uterine serous
adenocarcinoma (also known as papillary serous adenocarcinoma). However, some serous adenocarcinomas
have a purely glandular architecture without papillary formations and for this reason the term papillary
serous adenocarcinoma is not recommended. Many otherwise typical endometrioid adenocarcinomas also have
a focal papillary architecture and in some cases the entire tumour or much of this exhibits papillary
formations. In addition to typical endometrioid adenocarcinomas, some variants exhibit a papillary
architecture, including villoglandular endometrioid adenocarcinoma  and endometrioid adenocarcinoma
with small non-villous papillae . In the distinction between an endometrioid and a serous
adenocarcinoma, close attention to the cytological features usually allows a confident distinction.
Serous adenocarcinomas are characterised by markedly atypical nuclei, often with prominent macronucleoli
and smudged chromatin. Secondary budding from the papillary formations is common. The nuclear features
are usually much blander and lower grade in endometrioid adenocarcinomas with a well differentiated
glandular or papillary architecture. Squamoid elements are also commonly present in endometrioid
adenocarcinomas. In the distinction between an endometrioid and a serous adenocarcinoma,
immunohistochemical staining with p53, p16 and ER may assist
Most, although not all, serous
adenocarcinomas exhibit diffuse nuclear immunoreactivity with p53 and diffuse staining with p16. ER is
variable but may be negative, focally positive or sometimes diffusely positive. Most endometrioid
adenocarcinomas are diffusely positive with ER and negative or only focally positive with p53 and p16.
Occasional clear cell carcinomas of the endometrium have a papillary architecture, usually in combination
with the other architectural patterns characteristic of clear cell carcinoma. Primary mucinous
adenocarcinomas of the ovary may also occasionally have a papillary architecture. Rare transitional cell
carcinomas occur as primary neoplasms within the endometrium, usually in association with a component of
endometrioid adenocarcinoma . These are morphologically similar to transitional carcinomas of the
urological tract with a papillary architecture. Immunohistochemically, they exhibit a Mullerian rather
than a transitional immunophenotype ie they are CK7 positive and CK20 negative . Rare primary
squamous carcinomas of the endometrium have a papillary architecture.
It is stressed that the term papillary adenocarcinoma should not be used as a diagnostic label since
this denotes an architectural growth pattern rather than a tumour type. Rather when using the
descriptive terminology of papillary, the tumour type should be stated. For example, the tumour
comprises an endometrioid or serous adenocarcinoma with a papillary architecture. This is important
since surgical and adjuvant therapies may differ between an endometrioid and a serous adenocarcinoma, as
does the prognosis.
Progestogen Treatment of Endometrial Hyperplasia or Endometrioid Adenocarcinoma
The morphological effects of progestogenic compounds on the normal endometrium are well known.
Progestogen therapy, either oral or delived via an IUD such as the Mirena coil, may be employed in the
management of endometrial atypical hyperplasia or well differentiated endometrioid adenocarcinoma in a
woman who wishes to preserve her fertility or who is a poor operative risk due to comorbid features. In
such cases, radiological investigations are necessary to exclude myoinvasive disease. In patients
treated in this manner, a significant response rate can be expected . Patients are maintained on
progestogen for a prolonged period and are monitored by regular endometrial sampling. Pathologists need
to be aware of the effects of progestogen on endometrial hyperplasia and adenocarcinoma as histology is
pivotal in assessing response and determining further management. The effects of progestogens on
endometrial hyperplasia and well differentiated endometrioid adenocarcinoma have recently been described
. Histological changes associated with progestogens included a decreased gland to stroma ratio,
decreased glandular cellularity, decreased mitotic activity, reduction in cytologic atypia and a variety
of epithelial cytoplasmic changes, including mucinous, secretory, squamous and eosinophilic metaplasia.
Architectural changes, specifically cribriform and papillary patterns, were induced by progestogens. In
their study, 67% of women with atypical hyperplasia and 42% with well differentiated endometrioid
adenocarcinoma had a complete resolution while 22% with atypical hyperplasia and 58% with adenocarcinoma
had persistent disease .
Changes on Surface of Endometrial Adenocarcinoma
Not uncommonly on the surface of an endometrial adenocarcinoma of endometrioid or mucinous type, there
is a micropapillary or microglandular architecture. These changes may very closely mimic papillary
syncytial metaplasia or cervical microglandular hyperplasia . Since these surface elements are
likely to be sampled in preference to the underlying typical adenocarcinoma, this phenomenon is
especially noticeable in biopsy material and may result in a misdiagnosis of papillary syncytial
metaplasia or cervical microglandular hyperplasia. Usually there will be areas of obvious adenocarcinoma
and this assists in establishing the diagnosis as does awareness that this phenomenon occurs on the
surface of some endometrial adenocarcinomas. As stated, these foci may bear a very close resemblance to
cervical microglandular hyperplasia and caution should be exercised before making this diagnosis in an
endometrial biopsy in a postmenopausal woman, although cervical microglandular hyperplasia does occur in
this age group, especially with the increasing use of hormonal preparations. Probably the most useful
histologic feature in distinguishing between microglandular areas on the surface of an endometrial
adenocarcinoma and cervical microglandular hyperplasia is subnuclear vacuolation since this is common in
the latter but is uncommon in microglandular areas on the surface of an adenocarcinoma .
Immunohistochemistry can assist in the distinction, although there may be significant immunophenotypic
overlap. Probably the most useful marker is vimentin since this is negative in cervical microglandular
hyperplasia but is positive in most uterine endometrioid adenocarcinomas. However, some endometrial
adenocarcinomas are negative, including some mucinous adenocarcinomas. Occasionally much of a uterine
adenocarcinoma will be composed of microglandular formations resembling cervical microglandular
hyperplasia; this is referred to as microglandular adenocarcinoma .
Miscellaneous Uterine Neoplasms with a Papillary or Pseudopapillary Architecture
A few cases of endometrial stromal sarcoma with a pseudopapillary architecture have been reported
. Usually this is a focal phenomenon but occasionally it is widespread, involving much of the
Uterine Tumour Resembling Ovarian Sex Cord Tumour (UTROSCT)
UTROSCTs are rare primary uterine neoplasms which morphologically resemble ovarian sex cord- stromal
tumours. They were originally described by Clement and Scully in 1976 . In this seminal
publication, these neoplasms were classified into two groups: - type I were typical endometrial stromal
neoplasms with focal areas with a sex cord-like pattern and in type II tumours the sex cord-like elements
were exclusive or predominated. Now type I neoplasms are generally referred to as endometrial stromal
tumours with sex cord-like elements while type II tumours are designated UTROSCT, the latter term being
reserved for those uterine neoplasms composed exclusively of sex cord-like elements. In the latest World
Health Organization classification of tumours of the female genital organs, UTROSCT is classified
separately to endometrial stromal neoplasms . However, there is ongoing debate as to the exact
histogenesis ie whether they represent variants of endometrial stromal neoplasm with overgrowth of the
sex cord-like elements or are separate unrelated tumours. This is discussed later.
These neoplasms usually occur in women in the reproductive and postmenopausal age groups
Most are relatively well circumscribed intramural myometrial masses, although submucosal polypoid lesions
occur and may be sampled on endometrial biopsy, as do lesions projecting from the serosal surface of the
uterus. Rare tumours have been described within the cervix . Some neoplasms have a yellow cut
surface, a characteristic, but not specific, feature of UTROSCT, and a point of similarity to ovarian sex
cord-stromal tumours. The morphology of UTROSCT is variable with corded, trabecular, insular, nested,
solid and glandular or tubular growth patterns described, often in combination. Other growth patterns
include papillary (as in the present case), retiform and glomeruloid arrangements. Often, the tumour
cells have an epithelioid appearance and sometimes there is a rhabdoid phenotype with eccentric nuclei
and abundant eosinophilic cytoplasm. There is generally only mild nuclear pleomorphism and little in the
way of mitotic activity. Foam cells may occur, as may smooth muscle cells. It is controversial whether
this represents entrapped smooth muscle or an integral component of the neoplasm.
Several studies have examined the immunophenotype of UTROSCT
In a recent series we
reported, we undertook a detailed immunohistochemical analysis and reviewed the results of previous
studies in which immunohistochemistry was performed . In general, UTROSCTs have a polyphenotypic
immunophenotype, often with coexpression of epithelial, myoid and ovarian sex cord markers as well as
hormone receptors. Three of our 4 neoplasms were diffusely positive with the broad spectrum cytokeratin
AE1/3. Of the previously reported UTROSCTs, 22 of 26 had been positive with anti-cytokeratins,
illustrating that these neoplasms commonly express epithelial markers. An interesting observation in our
study was that all 4 tumours expressed EMA, albeit of weak or moderate intensity. This is perhaps
slightly surprising since UTROSCT is thought by some to represent the uterine counterpart of an ovarian
sex cord-stromal tumour and possibly to be derived from misplaced gonadal tissue. Cytokeratin
immunoreactivity is not uncommon in ovarian sex cord-stromal tumours, but EMA positivity is unusual. EMA
positivity argues against a true sex cord-stromal neoplasm, similar to those which arise in the ovary,
although immunoreactivity with sex cord markers (discussed below) suggests that UTROSCT exhibits sex cord
differentiation to some extent.
Our neoplasms were typically positive with smooth muscle markers with desmin and α SMA being
positive in 3 and 4 cases respectively. Other studies have also revealed smooth muscle marker positivity
in UTROSCT with altogether 8 of 25 and 13 of 18 cases respectively being positive with desmin and α
We stained our cases with a variety of markers which are commonly expressed in ovarian sex
cord-stromal tumours. Calretinin and inhibin are the two best known and most widely utilised markers of
an ovarian sex cord-stromal tumour
the former being slightly more sensitive and the latter a
more specific marker of this group of neoplasms. Two of the cases were positive with inhibin and all 4
with calretinin. Melan A and CD99 may also be positive in ovarian sex cord-stromal tumours and one and 2
of our neoplasms respectively were immunoreactive. Positivity with these markers has been demonstrated
previously in UTROSCT. Fourteen of 26, 10 of 11, 7 of 15 and 22 of 24 cases examined have been positive
with inhibin, calretinin, melan A and CD99 respectively, suggesting that UTROSCT may exhibit sex cord
differentiation although, as discussed, EMA positivity is unusual in ovarian sex cord-stromal tumours and
argues against a true sex cord-stromal neoplasm. Furthermore, although the overall morphological
appearances are suggestive of a sex cord-stromal neoplasm, the histological picture in most cases is not
characteristic of any particular type of ovarian sex cord-stromal tumour. For example, although the
various patterns, such as solid, nested, trabecular, corded and glandular, would be compatible with an
adult granulosa cell tumour, the nuclear features are not typical of this neoplasm. However, occasional
cases have been considered to be indistinguishable from a Sertoli or Sertoli-Leydig cell tumour. All 4
neoplasms in our study were diffusely and strongly positive with CD56, a widely used neuroendocrine
marker. It has been demonstrated recently that ovarian sex cord-stromal tumours are almost invariably
positive with CD56 ; therefore CD56 positivity in UTROSCT may be a manifestation of sex cord
All of our cases exhibited nuclear immunoreactivity with ER and PR which has been demonstrated in
other studies of UTROSCT with 13 of 15 and 15 of 16 cases respectively being positive. Three of 4 cases
were positive with androgen receptor.
The differential diagnosis of UTROSCT is potentially wide and may include an endometrial stromal and
an epithelioid smooth muscle neoplasm, a metastatic ovarian sex cord-stromal tumour, a carcinosarcoma and
primary and metastatic epithelial neoplasms, especially endometrioid adenocarcinoma with sex cord-like
features and lobular breast carcinoma. A perivascular epithelioid cell tumour (PEComa) might
also be considered. This would be positive with HMB45. Interpreted in isolation, immunoreactivity with
any of the markers discussed may result in an erroneous diagnosis. A polyphenotypic immunophenotype is
characteristic of UTROSCT and may be useful in differential diagnosis.
Given the polyphenotypic immunophenotype, I believe that UTROSCT is most likely derived from an
uncommitted cell with the capacity to differentiate along several lines and express epithelial, myoid and
sex cord markers. Some neoplasms express markers of all these lineages and others of 1 or two. An
origin from displaced gonadal sex cord cells is also a possibility but EMA positivity is against this
theory. As discussed, another major theory of histogenesis is that UTROSCT represents a variant of
endometrial stromal neoplasm. Focal sex cord-like elements may be present in otherwise typical
endometrial stromal neoplasms and it is possible that UTROSCT represents an endometrial stromal tumour in
which these elements are exclusive or predominate. However, it is my opinion that the sex cord-like
elements in endometrial stromal neoplasms differ morphologically in most cases from UTROSCT, the former
being composed of typical endometrial stromal cells which form tubular, trabecular and other
arrangements. Most UTROSCTs are relatively well circumscribed while most endometrial stromal neoplasms
(endometrial stromal sarcomas) exhibit a widely infiltrative growth pattern and this is a further
argument against an endometrial stromal origin. Moreover, judging by previous studies the sex cord-like
elements in endometrial stromal neoplasms exhibit less of a polyphenotypic immunophenotype and it is my
belief that these neoplasms are not related to UTROSCT. Greater than 60% of endometrial stromal
neoplasms have been shown to exhibit rearrangements involving chromosomes 6, 7 and 17, most commonly a
t(7;17)(p15;q21) translocation which results in a JAZF1-JJAZ1 gene
fusion . This translocation has
also been demonstrated in endometrial stromal sarcomas with sex cord-like elements. In a recent study,
using FISH and RT-PCR, we examined a series of 24 UTROSCTs to look for JAZF1-JJAZ1 gene fusion
(manuscript in preparation). The translocation was not identified in any neoplasm, providing evidence
that UTROSCT is not a variant of endometrial stromal neoplasm.
UTROSCTs usually exhibit a benign behaviour, especially when well circumscribed. However, since some
of these neoplasms may exhibit a more infiltrative growth pattern and even vascular invasion, rare
tumours have metastasised and only a few cases have been reported with long term follow-up, UTROSCT
should be regarded as a neoplasm of uncertain but low malignant potential.
Table 1 – Endometrial and Uterine Lesions Which May Exhibit a Papillary
- Papillary syncytial metaplasia
- Arias-Stella reaction
- Hyperplastic papillary proliferation
- Secondary to intrauterine device
- Usual endometrioid
- Villoglandular endometrioid
- Endometrioid with small non-villous papillae
- Surface changes in endometrioid
- Clear cell
- Progestogen effect on hyperplasia or adenocarcinoma
- Endometrial stromal sarcoma
- Uterine tumour resembling ovarian sex cord tumour
- McCluggage WG. My approach to the interpretation of endometrial biopsies and currettings. J Clin Pathol 2006;59;801-812.
- Shah SS, Mazur MT. Endometrial eosinophilic syncytial change related to breakdown: immunohistochemical evidence suggests a regressive process. Int J Gynecol Pathol 2008;27;534-538.
- Huettner PC, Gersell DJ. Arias-Stella reaction in nonpregnant women: a clinicopathologic study of nine cases. Int J Gynecol Pathol 1994;13; 241-247.
- Arias-Stella Jr J, Arias-Velasquez A, Arias-Stella J. Normal and abnormal mitoses in the atypical endometrial change associated with chorionic tissue effect. Am J Surg Pathol 1994;18;694-701.
- Lehman MB, Hart WR. Simple and complex hyperplastic papillary proliferations of the endometrium: a clinicopathologic study of nine cases of apparently localized papillary lesions with fibrovascular stromal cores and epithelial metaplasia. Am J Surg Pathol 2002;25;1347-1354.
- Zaino RJ, Kurman RJ, Brunetto VL, et al. Villoglandular adenocarcinoma of the endometrium: a clinicopathologic study of 61 cases: a gynecologic oncology group study. Am J Surg Pathol 1998;22;1379-1385.
- Murray SK , Young RH, Scully RE. Uterine Endometrioid Carcinoma with Small Nonvillous Papillae: An Analysis of 26 Cases of a Favorable-Prognosis Tumor To Be Distinguished from Serous Carcinoma. Int J Surg Pathol 2008;8;279-289.
- McCluggage WG. A critical appraisal of the value of immunohistochemistry in diagnosis of uterine neoplasms. Adv Anat Pathol 2004;11;162-171.
- Chiesa-Vottero AG, Malpica A, Deavers MT, et al. Immunohistochemical overexpression of p16 and p53 in uterine serous carcinoma and ovarian high-grade serous carcinoma. Int J Gynecol Pathol 2007;26;328-333.
- Marino-Enriquez A, Gonzalez-Rocha T, Burgos E, et al. Transitional cell carcinoma of the endometrium and endometrial carcinoma with transitional cell differentiation: a clinicopathologic study of 5 cases and review of the literature. Hum Pathol 2008;39;1606-1613.
- Wheeler DT, Bristow RE, Kurman RJ. Histologic alterations in endometrial hyperplasia and well-differentiated carcinoma treated with progestins. Am J Surg Pathol 2007. 31; 988-998.
- Jacques SM, Qureshi F, Lawrence WD. Surface epithelial changes in endometrial adenocarcinoma: diagnostic pitfalls in curettage specimens. Int J Gynecol Pathol 1995;14;191-197.
- Qui W, Mittal K. Comparison of morphologic and immunohistochemical features of cervical microglandular hyperplasia with low-grade mucinous adenocarcinoma of the endometrium. Int J Gynecol Pathol 2003;22;261-265.
- McCluggage WG, Young RH. Endometrial stromal sarcomas with true papillae and pseudopapillae. Int J Gynecol Pathol 2008;27;555-561.
- Clement PB, Scully RE. Uterine tumors resembling ovarian sex-cord tumors. A clinicopathologic analysis of fourteen cases. Am J Clin Pathol 1976;66;512-25.
- Tavassoli FA, Devilee P, eds. World Health Organization Classification of Tumours. Pathology and Genetics. Tumours of the Breast and Female Genital Organs. IARC Press. Lyon,2003.
- Baker RJ, Hildebrandt RH, Rouse RV, et al. Inhibin and CD99(MIC2) expression in uterine stromal neoplasms with sex-cord-like elements. Hum Pathol 2002;41;277-279.
- Krisnamurthy S, Jungbluth AA, Busam KJ, et al. Uterine tumors resembling ovarian sex-cord tumors have an immunophenotype consistent with true sex-cord differentiation. Am J Surg Pathol 1998;22;1078-1082.
- Hurrell DP, McCluggage WG. Uterine tumour resembling ovarian sex cord tumour is an immunohistochemically polyphenotypic neoplasm which exhibits coexpression of epithelial, myoid and sex cord markers. J Clin Pathol 2007;60;1148-1154.
- Irving JA, Carinelli S,Prat J. Uterine tumors resembling ovarian sex cord tumors are polyphenotypic neoplasms with true sex cord differentiation. Mod Pathol 2006;19;17-24.
- Kabbani W, Deavers MT, Malpica A, et al. Uterine tumor resembling ovarian sex-cord tumor:report of a case mimicking cervical adenocarcinoma. Int J Gynecol Pathol 2003;22;297-302.
- McCluggage WG. Uterine tumours resembling ovarian sex cord tumours: immunohistochemical evidence for true sex cord differentiation. Histopathology 1999;34;375-376.
- McCluggage WG, Maxwell P. Immunohistochemical staining for calretinin is useful in the diagnosis of ovarian sex cord-stromal tumours. Histopathology 2001;38:403-408.
- McCluggage WG, Maxwell P, Sloan JM. Immunohistochemical staining of ovarian granulosa cell tumors with monoclonal antibody against inhibin. Hum Pathol 1997;28:1034-1038.
- McCluggage WG, McKenna M, McBride HA. CD56 is a sensitive and diagnostically useful immunohistochemical marker of ovarian sex cord-stromal tumors. Int J Gynecol Pathol 2007;26;322-327.
- Dal Cin P, Aly MS, De Wever I, et al. Endometrial stromal sarcoma t(7;17) (p15-21;q12-21) is a nonrandom chromosome change. Cancer Genet Cytogenet 1992;63;43-6.