Adenosarcoma Uterino

Uterine Adenosarcoma
Andre Pinto, MD; Brooke Howitt, MD
Müllerian adenosarcoma is an uncommon biphasic
tumor composed of malignant stromal and benign epithelial components. Morphologically, adenosarcoma is characterized by a broad leaflike architecture, reminiscent of
phyllodes tumors of the breast. Periglandular cuffing of the
stromal cells around the compressed or cystically dilated
glands is characteristic. The mesenchymal component is
typically a low-grade spindle cell sarcoma, whereas the
epithelial counterpart is commonly endometrioid with
frequent squamous or mucinous metaplasia and may, in
some circumstances, show mild to moderate atypia. In all
cases, it is important to assess for the presence of
sarcomatous overgrowth and myometrial invasion, which
are the prognostic factors. In this brief review, we present
the clinical, histopathologic, and immunohistochemical
features of adenosarcoma, as well as updates on the
molecular biology of this neoplasm.
(Arch Pathol Lab Med. 2016;140:286–290; doi: 10.5858/
arpa.2014-0523-RS)
I
n 1974, Clement and Scully1 reported a series of tumors of
the female genital tract that were described as ‘‘... mixed
tumors of the uterus, in which the stromal component has
been malignant, but the epithelial elements, benign,’’ and
proposed naming these tumors adenosarcoma. A subsequent
study,2 in 1979, added a few cases to the original series, and
the term Müllerian adenosarcoma has since become universally recognized.
Müllerian adenosarcoma is an uncommon biphasic
malignant mesenchymal tumor composed of a benign
glandular component and a malignant, but generally lowgrade, stromal component. With a growing number of cases
reported (now considerably more than 200) in the literature,
the spectrum of morphologies and clinical behavior is fairly
well understood. The molecular pathogenesis of these
tumors, however, remains to be elucidated.
Although uncommon, adenosarcoma affects women of a
broad age range. The incidence is highest in perimenopausal
or postmenopausal women, but cases have been reported in
children as young as 10 years.3 Patients may present
Accepted for publication January 15, 2015.
From the Division of Women’s and Perinatal Pathology, Brigham
and Women’s Hospital, Boston, Massachusetts (Drs Pinto and
Howitt); and Harvard Medical School, Boston (Dr Howitt).
The authors have no relevant financial interest in the products or
companies described in this article.
Reprints: Brooke Howitt, MD, Division of Women’s and Perinatal
Pathology, Brigham and Women’s Hospital, 75 Francis St, Amory 3,
Boston, MA 02115 (e-mail: Bhowitt@partners.org).
286 Arch Pathol Lab Med—Vol 140, March 2016
clinically with abnormal vaginal bleeding and/or pelvic pain
or, in a large percentage of cases, with no symptoms.
Although the uterine corpus is by far the most common
primary site, adenosarcoma may also arise in the cervix,
ovary, fallopian tube, or vagina.4 Adenosarcoma occurring
outside the female genital tract likely represents tumors
arising from preexisting endometriosis.5–7 Some studies
suggest that the use of tamoxifen may have a role in the
pathogenesis of adenosarcoma.8–11
The prognosis of adenosarcoma greatly depends on stage
and the presence of sarcomatous overgrowth.12 A small
series of cases13 found that the 2-year progression-free and
overall survival rates for tumors with sarcomatous overgrowth were 20% compared with 100% for adenosarcoma
lacking sarcomatous overgrowth. Another study14 demonstrated that 36% of adenosarcoma with myometrial invasion
recurred, and the risk of recurrence in the absence of
myoinvasion was only 7%. Overall survival is around 60%
for tumors with myoinvasion and less than 50% for tumors
with associated metastasis.15 Tumors that arise in the ovary
or extrauterine sites tend to have a higher recurrence rate
secondary to lack of a physical barrier to spread within the
pelvis and abdomen. A new FIGO (International Federation
of Gynecology and Obstetrics) staging system for adenosarcoma, identical to that for endometrial stromal sarcoma
(ESS), has been devised recently16 (Table 1).
MACROSCOPIC FEATURES
The uterine cavity is typically filled with an exophytic and
polypoid mass, which may project through the cervix. The
average size is 5 cm, although tumors up to 50 cm have been
reported.17 The cut surface shows variably cystic and solid
areas, and papillary or polypoid projections into cystic
spaces can often be appreciated macroscopically (Figure 1).
Focal hemorrhage and necrosis may also be present. When
sarcomatous overgrowth is present, the mass may acquire a
more fleshy appearance commonly seen in other types of
sarcoma.18,19
MICROSCOPIC FEATURES
Histologically, adenosarcoma is composed of benignappearing epithelium and malignant stroma. Many of the
diagnostic features are best appreciated at low-power
magnification and may reflect the gross appearance of this
tumor (Figure 2). The architecture often demonstrates a
broad leaflike appearance, formed by the malignant stroma
compressing the benign epithelium, somewhat resembling a
phyllodes tumor of the breast (Figure 3). ‘‘Rigid cyst’’
formation is another architectural pattern in which large,
dilated, cystic structures, lined by benign epithelium, are
Uterine Adenosarcoma—Pinto & Howitt
Table 1. The FIGO (International Federation of
Gynecology and Obstetrics) Staging System for
Uterine Adenosarcoma
Stage
I
IA
IB
IC
II
IIA
IIB
III
IIIA
IIIB
IIIC
IV
IVA
IVB
Definition
Tumor limited to uterus
Tumor limited to endometrium/endocervix with no
myometrial invasion
50% myometrial invasion
.50% myometrial invasion
Tumor extends beyond the uterus, within the pelvis
Adnexal involvement
Involvement of other pelvic tissues
Tumor invades abdominal tissues (not just
protruding into the abdomen)
One site
.1 site
Metastasis to pelvic and/or para-aortic lymph nodes
Tumor invades bladder and/or rectum
Distant metastasis
surrounded tightly by malignant stroma (Figure 4). Periglandular cuffing of the stromal cells condensing under the
epithelium is characteristic and can also be appreciated from
low-power microscopic examination. The epithelial or
glandular component is usually endometrioid and frequently demonstrates metaplasia (squamous and mucinous are
most common)12 and may show mild to moderate atypia.
The malignant stroma can have a varied appearance but is
classically a low-grade spindle cell sarcoma, frequently with
myxoid foci, with no specific line of differentiation, although
some consider it to resemble ESS. Mitoses are essentially
required for the diagnosis (at least 2 per 10 high-power
fields). The mitoses are usually most pronounced in areas of
periglandular cuffing. Atypical mitotic figures are generally
absent except in the presence of sarcomatous overgrowth.17
Sex cord-like differentiation can be seen, which has no effect
on prognosis.4
Figure 1. Gross image of Müllerian adenosarcoma of the uterus. The mass has a yellow-tan, exophytic appearance, which fills the entire endometrial
cavity and extends to the cervix. In this case, sarcomatous overgrowth was present.
Figure 2. Section of endomyometrium showing a large, polypoid mass replacing the endometrium. Note the phyllodes architecture and cleftlike
spaces at scanning magnification (hematoxylin-eosin; original magnification 310).
Figure 3. The resemblance with phyllodes tumor of the breast is evident in a section of adenosarcoma at low power. The leaflike appearance with
compressed epithelium is characteristic of these tumors (hematoxylin-eosin; original magnification 3200).
Figure 4. Rigid cyst formation is an architectural pattern also frequently seen in adenosarcoma. Large cystic spaces lined by benign epithelium are
surrounded by low-grade malignant stroma (hematoxylin-eosin; original magnification 3200).
Arch Pathol Lab Med—Vol 140, March 2016
Uterine Adenosarcoma—Pinto & Howitt 287
The presence or absence of sarcomatous overgrowth is an
important prognostic factor and should be assessed in all
tumors.20 Sarcomatous overgrowth is defined as the
presence of pure sarcoma (without any epithelial component) comprising at least 25% of the tumor. Morphologic
features of sarcomatous overgrowth are typically high grade
(Figure 5) and include severe cytologic atypia, brisk mitotic
activity, and necrosis; however, high-grade stroma is not a
requisite for the diagnosis of sarcomatous overgrowth.
When high-grade stroma is present but comprises less than
25% of the tumor, it should be mentioned but no definitive
data exist on the prognostic significance. Of course,
additional tumor should be sampled and examined histologically if possible. Not uncommonly, adenosarcoma with
sarcomatous overgrowth may demonstrate low- to intermediate-grade atypia with a myxoid appearance (Figure 6).
Sarcomatous overgrowth is associated with deeper myometrial involvement and lymphovascular invasion.4
Heterologous elements, most notably rhabdomyoblastic
differentiation, have no prognostic significance alone,
although they occur most commonly in the presence of
sarcomatous overgrowth.
IMMUNOHISTOCHEMISTRY
Diffuse or multifocal expression of CD10 in the stromal
compartment is seen in most adenosarcomas and often
highlights the periglandular cuffing (Figure 7). Immunoreactivity for estrogen and progesterone receptors is also seen
in most cases, both in the glandular and stromal components. However, expression of these markers is significantly
decreased in adenosarcoma with sarcomatous overgrowth.14,21 Mesenchymal markers, such as smooth muscle
actin (SMA), desmin, and CD34 can have variable positivity
in the stromal component. More than one-half of tumors
exhibit expression of SMA and/or desmin, whereas the
percentage of CD34þ tumors is smaller.14,21 Cytokeratins
may rarely be focally positive in the sarcomatous component.21,22 For an expanded summary of the immunohistochemical profile of adenosarcoma, refer to Table 2.
DIFFERENTIAL DIAGNOSIS
The differential diagnosis of adenosarcoma is broad and
consists predominantly of tumors that also have a biphasic
(epithelial and mesenchymal) appearance. The particular
entities considered in the differential diagnosis vary with the
type of adenosarcoma. At the very low end of the spectrum,
the differential diagnosis includes primarily benign entities,
such as the so-called adenofibroma, adenomyoma (benign),
endometrial polyps with unusual features, and atypical
polypoid adenomyoma. In the presence of high-grade
sarcoma and/or sarcomatous overgrowth, the main diagnosis to rule out is carcinosarcoma, although undifferentiated
uterine sarcoma, ESS, and leiomyosarcoma should also be
considered in the differential diagnosis.
Differential Diagnosis of Adenosarcoma Without
Sarcomatous Overgrowth
Endometrial polyps, adenofibroma, and adenomyoma are
tumors in which both the epithelial and stromal components are morphologically benign. So-called adenofibroma
has the architectural features of adenosarcoma, but the
stroma is typically hypocellular and fibrotic. Mitoses should
be absent or rare. Indeed, adenofibroma may represent the
far ‘‘low-grade’’ end of the spectrum of adenosarcoma, and
288 Arch Pathol Lab Med—Vol 140, March 2016
Figure 5. An example of sarcomatous overgrowth, in which the
mesenchymal component comprises at least 25% of tumor with no
associated epithelium. This example demonstrates high-grade stroma
with cytologic atypia and frequent mitoses (hematoxylin-eosin, original
magnification 3400).
Figure 6. Sarcomatous overgrowth with low-grade stroma. Mild
cytologic atypia is present. Myxoid stroma, as shown here, can be
seen in cases of sarcomatous overgrowth (hematoxylin-eosin, original
magnification 3200).
Figure 7. Immunohistochemistry for CD10 highlighting the periglandular ‘‘cuffing’’ of malignant stromal cells (original magnification 3200).
Uterine Adenosarcoma—Pinto & Howitt
Table 2.
a
Immunohistochemical Staining Patterns in
Uterine Adenosarcomaa
Stain
Epithelium
Stroma (No
Sarcomatous
Overgrowth)
Stroma (With
Sarcomatous
Overgrowth)
AE1/AE3
Estrogen
receptor
Progesterone
receptor
Androgen
receptor
CD10
p53
þ
þ
þ/
þ
þ
þ
þ
þ/
þ
þ/
þ/
Key: þ, positive; , negative; þ/, either positive or negative.
thus, a diagnosis of adenofibroma should be rendered with
extreme caution, if at all.14,19 Occasionally, benign uterine
polyps may display features suggestive of adenosarcoma;
however, those features are subdiagnostic, typically subtle,
and only partially involve the polyp.23 Endometrial polyps
with myomatous stroma can resemble adenosarcoma, but
the stromal component is made of smooth muscle cells that
form fascicles. Fascicular growth of the stromal component
in adenosarcoma is unusual. Atypical polypoid adenomyoma is characterized by endometrial glands frequently
displaying mild cytologic and architectural atypia and often
diffuse or focal squamous morular metaplasia. The myofibromatous stroma is cellular but lacks the leaflike architecture of adenosarcoma.
Differential Diagnosis of Adenosarcoma With Sarcomatous
Overgrowth
Perhaps the most challenging differential diagnosis is
carcinosarcoma. As the name implies, both elements of
these neoplasms are malignant, but adenosarcoma can
demonstrate cytologic atypia in the epithelial component;
thus, the distinction from a small carcinoma can be difficult.
To further complicate this differential diagnosis, epithelial
malignancies may arise in the setting of adenosarcoma, and
carcinosarcomas can focally demonstrate areas mimicking
adenosarcoma.4 In most carcinosarcomas, the sarcomatous
component is not predominant; nevertheless, extensive
sampling may be required to distinguish adenosarcoma
with sarcomatous overgrowth from carcinosarcomas composed predominantly of sarcoma.
When the tumor cells are markedly high grade and do not
recapitulate normal endometrial stroma, undifferentiated
uterine sarcoma should be considered. If entrapped glands
are present, it can mimic adenosarcoma. These tumors are
composed of pleomorphic, undifferentiated, malignant cells
with high mitotic index. In the absence of classic features of
adenosarcoma, undifferentiated uterine sarcoma should be
diagnosed, with the understanding that a subset of these
heterogenous tumors may represent extensive sarcomatous
overgrowth of an adenosarcoma.
Low-grade ESS may resemble adenosarcoma with sarcomatous overgrowth, particularly if glandular elements and/
or entrapped benign endometrial glands are present. In ESS,
the tumor cells are monomorphic and have fusiform, round
to ovoid nuclei and fine chromatin. The cell borders are
indistinct, and cytoplasm is scant. Delicate vasculature is
characteristic of these tumors, which is composed of thinwalled blood vessels surrounded by whorling of tumor cells.
Arch Pathol Lab Med—Vol 140, March 2016
Because CD10 immunostain is positive in both adenosarcoma and ESS, it is not helpful in distinguishing between
these tumors. Many ESSs have a t(7;17) translocation
resulting in JAZF1-SUZ12 gene fusion, and cytogenetic
studies may be used in difficult cases.
A high-grade ESS has also been described,24 which is
characterized by malignant cells with uniform atypia and
high mitotic index. The immunohistochemical profile varies,
but these tumors are generally nonreactive for CD10,
estrogen receptor, and progesterone receptor, in contrast
to adenosarcoma. High-grade ESSs are positive for cyclin
D1, which indirectly reflects the presence of a YWHAEFAM22 gene fusion product created by the characteristic
translocation t(10;17).24
Given its frequency among mesenchymal tumors of the
gynecologic tract, leiomyosarcoma may also be considered.
Leiomyosarcoma may uncommonly entrap benign endometrial glands but does not demonstrate features characteristic for adenosarcoma. The presence of typical fascicular
architecture and immunohistochemical positivity for smooth
muscle markers, particularly caldesmon, is diagnostic of
leiomyosarcoma.
MOLECULAR DIAGNOSTICS
The precise molecular mechanism of tumorigenesis in
adenosarcoma remains unclear. One reported karyotype of
adenosarcoma with sarcomatous overgrowth revealed a
hyperdiploid karyotype with multiple structural and numerical
abnormalities involving chromosomes 2, 8, 10, 13, 19, and
21.25 Some studies have found low rates of TP53 mutations,26–28 and others have described low-level amplification of
MDM2 and other genes on band 12q14-15.26,27 Recently
described alterations in adenosarcoma include MYBL1
amplification and ATRX mutation, which are each present
in 50% of adenosarcomas with sarcomatous overgrowth.27
MYBL1 is a transcription factor that regulates cell proliferation
and is amplified in subsets of other types of tumors, including
10% of uterine carcinosarcoma (http://www.cbioportal.org;
accessed January 14, 2015). ATRX regulates DNA methylation
and chromatin remodeling; loss-of-function mutations in
ATRX have prognostic significance in other tumor types.29
TREATMENT
Total abdominal or laparoscopic-assisted vaginal hysterectomy is the treatment of choice for uterine adenosarcoma,
with or without bilateral salpingo-oophorectomy. One
study13 did not identify any ovarian metastases in patients
who underwent bilateral salpingo-oophorectomy for uterine
adenosarcoma. However, given the frequent positivity of
estrogen and progesterone receptors in adenosarcoma,
removal of the ovaries could potentially benefit patients,
even in the absence of metastatic disease—but that benefit
needs to be weighed against the age of the patient and cost
of surgical menopause.
There is no standardized chemotherapy, hormonal
therapy, or radiation therapy in adenosarcoma, but standard
sarcoma chemotherapy regimens, such as doxorubicin,
ifosfamide, or gemcitabine/docetaxel, and newer drugs,
such as trabectedin, appear to have some efficacy in
adenosarcoma with sarcomatous overgrowth.13,30,31
CONCLUSION
Müllerian adenosarcoma is a relatively uncommon entity
in gynecologic pathology that has distinctive clinical and
Uterine Adenosarcoma—Pinto & Howitt 289
histologic characteristics. It is important for pathologists to
be aware of the morphologic features of these neoplasms to
distinguish them from other biphasic (epithelial and
mesenchymal) tumors, both benign and malignant. Adenosarcoma is of generally low malignant potential, except
when accompanied by sarcomatous overgrowth and myoinvasion. Patients with adenosarcoma lacking these 2
histopathologic features have an excellent prognosis.
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CAP16 Abstract Program Submission Dates
Announced
Abstract and case study submissions to the College of American Pathologists (CAP) 2016 Abstract
Program will be accepted beginning on Friday, January 8 through 5 p.m. Central time Friday, March
11, 2016.
Accepted submissions will appear on the Archives of Pathology & Laboratory Medicine Web site as
a Web-only supplement to the September 2016 issue. The CAP16 meeting will be held from
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Visit the CAP16 Web site (www.cap.org/cap16) for additional abstract program information as it
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290 Arch Pathol Lab Med—Vol 140, March 2016
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