Magnetic Resonance Imaging of Benign and

Malignant Uterine Neoplasms

Gustavo Leursen, MD,* Carly Susan Gardner, MD,† Tara Sagebiel, MD,‡
Madhavi Patnana, MD,‡ Silvana de CastroFaria, MD, PhD,‡
Catherine E. Devine, MD,‡ and Priya R. Bhosale, MD‡

Benign and malignant uterine masses can be seen in the women. Some of these are
asymptomatic and incidentally discovered, whereas others can be symptomatic. With the soft
tissue contrast resolution magnetic resonance imaging can render a definitive diagnosis,
which can further help streamline patient management. In this article we show magnetic
resonance imaging examples of benign and malignant masses of the uterus and their treatment
strategies.
Semin Ultrasound CT MRI 36:348-360 Published by Elsevier Inc.

Introduction Fibroids arise from uterine smooth muscle myometrium,

composed of disordered smooth muscle cells and abundant

A myriad of tumors occur in the uterus. In this article we

will discuss the benign and malignant uterine tumors,
with a focus on magnetic resonance imaging (MRI) features,
pathology, and treatment.
Benign
Fibroids
Uterine fibroids (leiomyomas or myomas) are the most
common pelvic tumors in women, seen predominantly in
African-Americans.1-3 Fibroids appear, grow, and regress during
life, especially during reproductive age, pregnancy, and post-
partum period, and are seen in 35% of menstruating women.2,3
Associated risk factors include early menarche age, nulliparity,
old age at first pregnancy, obesity, diabetes, hypertension, and
family history. Although generally asymptomatic, fibroids may
cause abnormal bleeding, pelvic pain, pressure, and infertility,
which often reduce or disappear after menopause.2
*Department of Abdominal Radiology, Hospital Moinhos de Vento, Porto
Alegre, Rio Grande do Sul, Brazil.
†Diagnostic Imaging, UT MD Anderson Cancer Center, Houston, TX.
‡Diagnostic Radiology, UT MD Anderson Cancer Center, Houston, TX.
Supported in part by NIH/NCI, USA Cancer Center Support Grant under
Award no.: P30CA016672.
Address reprint requests to Priya R. Bhosale, MD, UT MD Anderson Cancer
Center, 1400 Pressler St, Unit 1473, Houston, TX 77030. E-mail: Priya.
bhosale@mdanderson.org
extracellular matrix. Grossly, fibroids vary in size and num-
ber.1,2 They are classified as (1) submucosal (adjacent to or in
the uterine cavity), (2) intramural (entirely within the myome-
trium), and (3) subserosal (distort the outer contour or surface
of the uterus). Moreover, subserosal and submucosal fibroids
can be pedunculated (attached to the uterus by a stalk),
extending from the external uterine surface or within the
uterine cavity (intracavitary); pedunculated fibroids can rarely
torse, leading to infarction (Fig. 1).3-5
The myometrium, exposed to repeated hormonal influences
during reproductive years, is vulnerable to mutations. In fact,
the single-gene somatic defect (MED12 mutation) is seen in
most fibroids. Chromosomal rearrangements are often com-
plex and diverse, explaining the variable growth, dormancy,
and regression, and also the heterogeneous response to
medical therapy. Fibroids commonly undergo degeneration,
particularly if they outgrow their blood supply. Types of
degeneration include hyaline, myxoid, cystic, red (carneous or
hemorrhagic), and sarcomatous.1,2
MRI is the most accurate imaging technique for fibroid
detection and localization. Nondegenerated fibroids classically
appear as well-defined, rounded homogeneous masses, with
decreased T2-weighted signal intensity and intermediate T1-
weighted signal intensity compared with normal myometrium.
Cellular fibroids (with more cellular compound and less
extracellular matrix) have high T2 signal intensity and greater
enhancement.1-4 Some fibroids have a rim of T2 hyperintensity
related to dilated lymphatics, veins, or edema that may

348 http://dx.doi.org/10.1053/j.sult.2015.05.003
0887-2171/Published by Elsevier Inc.
MRI of uterine neoplasms 349

Figure 2 A 45-year-old woman with large subserosal fibroid. Sagittal

T2-weighted MR image shows the hypointense fibroid (asterisk) with
T2 hyperintense rim (arrow), attributed to dilated vessels, and
lymphatics and edema or both.

intensity, but in postcontrast images it may have minimal

enhancement around the mucinous lakes or clefts (Fig. 4). Red
degeneration is related to massive hemorrhagic infarction,
resulting in coagulative necrosis, and it is most often found
during pregnancy or is related to oral contraceptives. On MRI,
red degeneration has variable signal intensity, with diffuse T1
hyperintensity and variable T2 signal intensity or even a
peripheral halo of T1 hyperintensity and T2 hypointensity.
Calcifications are found in 4% of fibroids and appear as
hypointense, nonenhancing areas on all MRI sequences.5,6

Figure 1 A 31-year-old woman presenting with acute pelvic pain

secondary to an infarcted fibroid. Sagittal T2-weighted (A) MR image
shows intermediate to hyperintense fibroid (black asterisk) protruding
into the rectouterine space, connected posteriorly to the lower uterus
by a stalk (arrow). Large hypointense fibroid superiorly (white
asterisk) should be noted. (B) Contrast-enhanced MR image shows
absent enhancement of the posterior pedunculated fibroid (black
asterisk) compatible with infarction in the context of acute torsion,
found on laparoscopy.

enhance on postcontrast images (Fig. 2).1,2 It should be noted

that this T2 signal is not considered degeneration.2
The presence of degeneration may alter the appearance of
the fibroid in MRI.5,6 Hyaline degeneration is the most
common, occurring in more than 60% of the fibroids. On
MRI, hyalinization within the fibroid is characterized by diffuse
dicreased T2 signal. Cystic degeneration, found in 4% of
fibroids, is seen on MRI as well-defined areas of internal fluid
(high T2 signal intensity, Fig. 3). Myxoid degeneration Figure 3 A 41-year-old woman with submucosal fibroid with cystic
represents cystic foci of gelatinous material, either abundant degeneration. Sagittal T2-weighted MR image shows heterogeneous
or interspersed between smooth muscle cells. On MRI, myxoid predominant T2 hyperintense signal in keeping with cystic degenera-
degeneration also shows low T1 signal and high T2 signal tion (asterisk).
350
Figure 4 A 36-year-old woman with fibroid with myxoid degenera-
tion. Axial T2-weighted MR image shows predominantly T2 hypoin-
tense mass (asterisk) with cystic spaces (arrows). Contrast-enhanced
axial fat-suppressed T1-weighted MR image (B) shows intense stromal
enhancement of the mass (asterisk) and nonenhancement of the cystic
spaces representative of myxoid degeneration (arrows).
Lipoleiomyomas, rare and seen only in 0.8% patients, are
thought to reflect a variant of fibroids containing macroscopic
fat. On MRI, these tumors follow fat signal on all sequences,
characterized by T1 and T2 hyperintensity, signal loss on fat-
saturated sequences, and India ink artifact on out-of-phase
imaging (Fig. 5).6 Currently, there are no reliable imaging
criteria for accurate diagnosis of degeneration into or de novo
leiomyosarcoma.
Rare and unusual fibroid growth patterns, such as atypical
extrauterine locations and aggressive invasive growth, have
been described: intravenous leiomyomatosis (growth into
veins); metastasizing leiomyoma (spread to distant organs,
especially lung); diffuse leiomyomatosis (diffuse growth
throughout the uterine parenchyma, usually innumerable
small nodules symmetrically enlarging the uterus); peritoneal
disseminated leiomyomatosis (dissemination throughout the
peritoneal cavity); retroperitoneal leiomyomatosis (growth in
G. Leursen et al.
Figure 5 A 38-year-old woman with lipoleiomyoma. Axial T1- and T2-
weighted MR images show hyperintense signal (asterisk) indicative
of fat.
the retroperitoneum, usually broad ligament); and parasitic
leiomyomatosis (when a pedunculated leiomyoma loses its
connection by torsion and attaches to other structure with
parasitic vessels).2,5
Therapeutic approaches for uterine fibroids include expect-
ant management, medical treatment, surgery (myomectomy or
hysterectomy), uterine artery ligation or uterine artery embo-
lization (UAE), and high-intensity focused ultrasound abla-
tion.6-8 Management depends on many factors, including
fibroid size; number and location, as well as the presence of
symptoms; patient age; and childbearing desire.7,8 Hysterec-
tomy is the definitive treatment of fibroids, though minimally
invasive procedures such as embolization and ablation are
becoming useful, uterine-sparing alternatives.6-8
MRI is important in pretreatment and posttreatment fibroid
evaluation.3 For example, cervical fibroids may not respond to
UAE because of alternate blood supply; nonenhancing fibroids
are also less likely to respond. Treatment of pedunculated
fibroids should be avoided particularly if the stalk is less than
2 cm, as they can detach after treatment. Following therapy,
a decrease in uterine and fibroid volume and coagulative
MRI of uterine neoplasms 351

necrosis of fibroids indicate response (Fig. 6). On MRI, treated

fibroids become smaller, with well-defined T1 signal of
increased intensity, and more homogeneous T2 signal without
enhancement in the intensity. Continued growth after treat-
ment raises a concern of malignancy.3

Polyps
Endometrial polyps, seen in 10%-40% of women, are the most
common pathologic lesions of the uterine corpus.9 They often
present with abnormal premenopausal or postmenopausal
bleeding.10
Endometrial polyps are benign localized overgrowths of the
endometrium; they consist of stroma of dense fibrous tissue or
smooth muscle cells, thick-walled vessels, and endometrial
glands.9-11 The endometrial polyps vary in size and can be
multiple in 20% of the cases. Patients treated with tamoxifen
have an increased incidence (8%-36%) of polyps.11,12 Most
polyps are small and incidental, but can be can be associated
with endometrial hyperplasia and carcinoma.9,10,12
On MRI, polyps are generally well-circumscribed (70%),
isointense on T1 signals, and hypointense on T2 signals (80%)
relative to normal endometrium.11 Polyps typically have rapid
early and persistent enhancement or gradually increasing
enhancement, though the degree of enhancement varies with
respect to the outer myometrium (strong ¼ 17.5%, moderate
¼ 52.5%, and weak ¼ 30%).11 In few cases, a stalk can be
seen, particularly when outlined by intracavitary fluid
(Fig. 7).9,12,13
Polyps can also have a central fibrous core (low T2 signal
intensity), intratumoral cysts (discrete smooth-walled cystic
structure of high T2 signal intensity), and hemorrhage (high T1
signal intensity), described by Hase et al11 in 75%, 55%, and
35%, respectively.9,11 Central fibrous core and intratumoral
cysts favor benign polyps, whereas endometrial invasion,
necrosis, and irregular internal “cystic” areas suggest endome-
trial cancer.9 Polyps, in contrast to endometrial cancer,
typically enhance avidly.11,14 Polyps demonstrate less
restricted diffusion than malignant lesions; Fujii et al15
reported a mean apparent diffusion coefficient value of 1.44
⫾ 0.34 for benign lesions and 0.98 ⫾ 0.19 for malignant
lesions with an accuracy of 92%.15-18
Endometrial polyps are typically removed to alleviate
symptoms and to evaluate for atypical hyperplasia or
carcinoma or both.10-12 The risk of malignancy is related
to polyp size and patient age. In the past, treatment was
hysterectomy, but today, minimally invasive procedures
such as hysteroscopic polypectomy, endometrial ablation,
and postoperative insertion of a levonorgestrel intrauterine
device are used.10

Adenomyosis
Adenomyosis, seen in 21%-47%, is more common in pre-
menopausal multiparous women.19-22 Two-thirds of patients
are symptomatic, experiencing menometrorrhagia, dysmenor-
rhea, and pelvic pain.19,21,22 Associationswith endouterine
surgery, multiparity, and tamoxifen are reported.19,21,22
Figure 6 A 43-year-old woman before and after uterine artery
embolization. Sagittal T2-weighted MR images: (A) preuterine and
(B) postuterine artery embolizations show marked reduction in uterus
and fibroid size. It should be noted that the individual fibroids become
smaller, more well defined, and homogenous in signal intensity after
embolization (asterisk).
352
Adenomyosis is defined as ectopic endometrial mucosa with-
in the myometrium and adjacent smooth muscle hypertrophy.
It often coexists with other hormone-dependent pelvic lesions,
G. Leursen et al.
namely fibroids, deep pelvic endometriosis, polyps, and endo-
metrial hyperplasia.19 Adenomyosis can be focal (with one or
several foci) or diffuse (with numerous foci spread throughout
the myometrium), superficial or deep (penetrating more than
one-third of the myometrium), and is often asymmetric.19,21,23
Adenomyoma represents a nodular aggregate of endometrial
glands with compensatory hypertrophy of surrounding
myometrium.20,23
MRI has a sensitivity of 70%-88%, specificity of 86%-93%,
and accuracy of 85%-90% for diagnosis of adenomyosis.20-26
Findings include (1) globular uterus with regular contours;
(2) asymmetric myometrial thickening (more common of the
posterior wall); (3) focal or diffuse junctional zone (JZ)
thickness Z12 mm; (4) greatest JZ to myometrium thickness
ratio 440%-50%; and (5) myometrium foci of high T2 signal
intensity and sometimes T1 signal intensity.19-21,23-26 JZ
thickening more than 12 mm is highly predictive of adeno-
myosis (Fig. 8); JZ o 8 mm practically excludes the diagnosis.
A thickness between 8 and 12 mm is indeterminate and
additional findings should be evaluated.19-21,23 The high-T2-
signal-intensity foci reflect dilated fluid-filled endometrial
glands (Fig. 8).19,24 This sign is highly specific, but seen in
only approximately half of the cases.21,23
JZ thickness varies in response to several conditions that need
to be considered to avoid misdiagnosis.19-21,24 The JZ thickens
with age up to approximately 50 years and then starts to thin,
being thinner or absent during the menopause. During the men-
strual cycle, JZ thickness is variable; it is the thickest between
8 and 16 days. Pregnancy, contraceptive pills, and gonado-
tropin-releasing hormone agonist cause the JZ to get thin or even
disappear. Myometrial contractions, focal wedge-shaped areas
of low T2 signal intensity, which bulge the uterine cavity, cause
pseudothickening of the JZ and mimic adenomyosis, though
they can be differentiated by their transient nature.19-21,24
Adenomyoma is seen on MRI as a poorly defined mass-like
lesion of low T2 signal intensity containing internal high T2
signal intensity (and occasionally T1 signal) foci (Fig. 8).
Like fibroids, adenomyomas can be intramyometrial, subser-
osal, and submucosal, including intracavitary growth (polypoid
adenomyoma).19-21 Hemorrhagic cystic adenomyosis
(adenomyotic cyst) is related to bleeding of adenomyosis,
characterized on MRI by high T1 signal intensity reflecting
hemorrhage or even fluid-fluid levels.19,21
Treatment of adenomyosis depends on the presence of
symptoms, patient age, and future childbearing desire.19,21
Asymptomatic women do not require treatment.19 Medical
treatment consists of hormonal therapy or nonsteroidal
anti-inflammatory drugs or both.19,21,22 Surgical options
include hysterectomy, myometrial or adenomyoma excision,
Figure 7 A 37-year-old woman with endometrial polyp. (A) Sagittal
T2-weighted MR image shows the polyp (asterisk) with stalk arising
from the endometrium (arrow). Axial T2-weighted (B) and fat-
suppressed contrast-enhanced (C) MR images show the avidly
enhancing polyp with stalk arising from the endometrium (arrow).
Well-circumscribed T2 hypointense fibroid with heterogeneous
enhancement (asterisk) should be noted. The patient also incidentally
has diffuse infiltrating rectal cancer.
MRI of uterine neoplasms 353

aged between 50 and 54 years. In patients with normal

menstrual cycle, endometrial hyperplasia is seen in 0.5%-
5%.27 In patients with abnormal bleeding, endometrial hyper-
plasia is found in 2.5% and most of them are
postmenopausal.28 It commonly results from unopposed
estrogen or sequential estrogen-progesterone hormone
replacement therapy. Endometrial hyperplasia can occur in
premenopausal women with polycystic ovary disease and
anovulatory cycles. Obesity and tamoxifen therapy are known
risk factors (Fig. 9).12,29,30
Endometrial hyperplasia is characterized by excessive endo-
metrial gland proliferation, with an increased glands to stroma
ratio.12,29 Endometrial hyperplasia is a precursor to endome-
trial carcinoma.28-30 The most widely used histologic classi-
fication system (World Health Organization) evaluates
architectural features and cytologic atypia to identify precursor
lesions: 1—simple hyperplasia; 2—complex hyperplasia; 3—
simple hyperplasia with atypia; and 4—complex hyperplasia
with atypia.12,27,29,30. Progression rates to carcinoma are 1%,
3%, 8%, and 29% for the 4 precursor classifications, respec-
tively.29 In women undergoing hysterectomy for biopsy-
proven atypical endometrial hyperplasia, approximately 40%
have concomitant carcinoma on surgical pathology.29,30
MRI is generally used only for problem solving, to exclude
other diagnoses, like adenomyosis. The imaging appearance is
nonspecific and may parallel early endometrial carcinoma,
cystic atrophy, and endometrial polyps.12 In postmenopausal
women, an endometrial thickness of 5 mm or more identifies
95% of all carcinomas and an endometrial thickness less than
4 mm has a 1% probability of cancer. In premenopausal
women, there are no reliable criteria for differentiating benign
and malignant endometrial hyperplasia.18,30

Figure 8 A 35-year-old woman with adenomyosis and focal adeno-

myoma. Sagittal and axial T2-weighted (A) MR image shows
thickening of the junctional zone greater than 12 mm (white line)
and more focal mass-like area compatible with an adenomyoma
(asterisk) containing characteristic T2 hyperintense foci (arrow).

myometrial reduction, and endometrial ablation or resec-

tion.19,21,22 UAE may improve or resolve symptoms, especially
the short-term ones, though with increased risk of recur-
rence.19,22 Recently, high-intensity focused ultrasound ablation
has shown promising results for adenomyosis treatment.22 On
MRI, reduction of uterine size, decrease in JZ thickness, and
infarction of focal lesions can be seen following treatment.19

Figure 9 A 51-year-old woman with tamoxifen-induced endometrial

Endometrial Hyperplasia hyperplasia and diffuse polyps. Sagittal T2-weighted MR image shows
Endometrial hyperplasia has an incidence of 133 per 100,000 heterogeneous thickening of the endometrium related to hyperplasia
woman-years, and 389 per 100,000 woman-years in women and polyps in a patient treated with tamoxifen.
354
On MRI, endometrial hyperplasia is typically diffuse, with a
well-defined endometrial-myometrial interface (Fig. 9). The
thickened endometrium is isointense or slightly hypointense
on T2 relative to normal endometrium (Fig. 9).12,18 On
dynamic contrast-enhanced (DCE)-MRI, endometrial hyper-
plasia shows progressive enhancement, enhancing similar to or
greater than adjacent myometrium.12-14 Sometimes, small low-
signal-intensity cystic foci (cystic glandular dilatations) can be
seen on delayed contrast-enhanced images.12,13 Diffusion
weighted imaging (DWI) has been shown to be helpful in
differentiating malignant from benign lesions, including endo-
metrial hyperplasia, with reported sensitivity and specificity of
96% and 95%, respectively.16-18
Endometrial thickening is evaluated by curettage or biopsy.
Management options can be surgical and nonsurgical.12,29,30
Simple and complex hyperplasia without atypia is usually
treated with hormonal therapy (progesterone) and followed by
imaging or endometrial sampling or both.12 Total hysterec-
tomy is the current treatment of atypical endometrial hyper-
plasia or endometrial intraepithelial neoplasia.30
Malignant
Endometrial Cancer
Endometrial carcinoma is the most common gynecologic and
10th most common malignancy, with an incidence of 24.6 per
100,000 women per year.31 It is most common in women aged
45-74 years, with median age at diagnosis of 62 years.31 Most of
the endometrial cancers are diagnosed at an early stage (68%)
with 5-year survival rate of 81.5% overall, 17.5% for metastatic
disease, and 95.1% for localized disease.31 Symptoms include
abnormal uterine bleeding and vaginal discharge.32 The main
risk factor is exposure to unopposed estrogen, exogenous
(hormone replacement) or endogenous (anovulation in
polycystic ovary syndrome, estrogen-producing tumors, and
excessive peripheral conversion in adipose tissue in obesity).
Tamoxifen, nulliparity, infertility, early menarche, and late
menopause are also known risk factors.12,32 Combined or
progesterone-based oral contraceptive pills are protective.
Lynch syndrome (hereditary nonpolyposis colon cancer) and
Cowden syndrome have increased risk of endometrial cancer.32
Endometrial carcinomas are classified into 2 major types
(type I and type II). Type I tumors comprise 80% and include
grade 1 or 2 endometrioid histology. These tumors are
hormone responsive and have favorable prognosis. Type II
tumors comprise 10%-20% and include grade 3 endometrioid
and nonendometrioid carcinomas (serous, clear cell,
mucinous, squamous, transitional cell, mesonephric, and
undifferentiated). These tumors are of higher grade and have
poor prognosis, without clear association to estrogen stim-
ulus.33 Endometrioid carcinoma has a different genetic profile
from that of nonendometrioid neoplasms. The former shows
microsatellite instability and specific mutations of PTEN, K-ras,
and β-catenin genes, whereas in the latter, p53 mutations
predominate.33
MRI in diagnosis and staging of endometrial carcinoma
uses a multiparametric approach, including high-resolution
G. Leursen et al.
T2-weighted, DW, and DCE image acquisitions.34,35 The
tumor shows intermediate T2 signal intensity relative to
normal endometrium, and mildly T2 hyperintesity compared
with myometrium, the latter of which helps determine the
depth of myometrial invasion (Figs. 10 and 11).34-36
On quantitative evaluation, apparent diffusion coefficient value
is lower in endometrial carcinoma (0.86-0.98) than in
normal endometrium (1.28-1.65), indicating restricted
diffusion.15-18,34,35,37-40 Contrast-enhanced images distinguish
tumor from blood products and tumor from normal myome-
trium; tumor enhances to a lesser degree than both endome-
trium and myometrium in equilibrium and delayed contrast-
enhanced images (Fig. 11).14,34-36,41,42
The staging of endometrial cancer is based on International
Federation of Gynecology and Obstetrics (FIGO). The most
important factors of local staging on MRI are depth of
myometrial invasion and cervical stromal involvement.34,35
Depth of myometrial invasion, defined as less than or greater
than 50% thickness of the myometrium, is best assessed on
DCE images, as JZ thinning in postmenopausal patients, and
underlying adenomyosis or fibroids can confound assessment
on T2-weighted images alone.12,34,35 Cervical stromal involve-
ment is characterized by extension into the cervix, best seen in
T2-weighted (sagittal) or DCE images. High-resolution T2-
weighted imaging has a 55%-77% accuracy for staging.34 The
addition of DCE improves accuracy to 83%-98%.12,34-36,40,42
DWI has shown high accuracy for tumor staging (62%-90%)
and may be helpful in noncontrast examinations.34,35,37,43
Endometrial cancer spreads via different routes (direct,
lymphatic, transtubal peritoneal seeding, or hematogenous).
Metastases to paraaortic lymph nodes before pelvic lymph
nodes can occur via gonadal vessels.12 The involvement of
lymph nodes based on size criteria has substantial limitations.
Figure 10 A 30-year-old woman with endometrioid adenocarcinoma.
Sagittal T2-weighted MR image shows solid tumor (asterisk) and
surrounding cystic hyperplasia.
MRI of uterine neoplasms
Figure 11 A 67-year-old woman with endometrial cancer. Sagittal T2-
weighted (A) and contrast-enhanced fat-suppressed T1-weighted
(B) images show disruption of the junction zone (arrow in A) and
greater than 50% tumor invasion into the myometrium (arrow in B).
Incorporation of morphologic features (internal heterogeneity,
spiculated margins, necrosis, and signal intensity comparable
to that of the primary tumor) improves lymph node evalua-
tion.34,35 The incidence of nodal involvement correlates with
depth of myometrial invasion: 3% if less than 50% myometrial
invasion, 46% if greater than 50%.12,34,35
The management of endometrial cancer is based on stage of
the disease. The International Federation of Gynecology and
Obstetrics (FIGO) recommendation is total hysterectomy,
bilateral salpingo-oophorectomy, bilateral pelvic and paraaortic
lymphadenectomy, peritoneal washing, and omental
biopsy.32,35 However, in patients with early stage disease, the
role of lymphadenectomy is controversial and these women
may be appropriately treated with minimally invasive laparo-
scopic hysterectomy and bilateral salpingo-oophorectomy,
355
decreasing morbidity and hospital stay.32,35 In selected patients
with cervical or vaginal involvement, adjuvant radiation therapy
may be used. Chemotherapy is reserved for advanced disease.44
Uterine Sarcomas
Uterine sarcomas are a rare and heterogeneous group of
tumors that account for 5%-8% of all uterine malignancies,
and include leiomyosarcoma, endometrial stromal sarcoma
(ESS), and malignant mixed epithelial and mesenchymal
tumors (MEMTs). ESS and leiomyosarcoma are composed of
purely nonepithelial components, whereas MEMTs are com-
posed of epithelial and mesenchymal components. The clinical
presentation is nonspecific but these tumors classically present
as rapidly growing masses, which may be accompanied by
vaginal bleeding and abdominal or pelvic pain.45-49 Associa-
tions include African-American ethnicity, long-term tamoxifen
therapy, and previous pelvic irradiation.47
Leiomyosarcomas are a common subtype, representing
40%, and arising from the myometrial smooth muscle.46-48
Diagnosis is based on atypia, mitosis, and tumor necrosis.46,48
They are usually solitary intramural masses and may arise
rarely from a fibroid.46-48 Less than 0.5% of uteri removed for
presumed fibroids have incidental leiomyosarcoma. Patholog-
ically, it can be difficult to distinguish leiomyomas with
abundant mitosis from well-differentiated leiomyosarcomas.46
ESSs arise from endometrial stroma, accounting for 10%-
15% of uterine sarcomas and are characterized by resemblance
to endometrial stroma with cells of varying atypia (well differ-
entiated or low grade to undifferentiated or high grade).46-48
Extrauterine ESS may originate in endometriosis.46 Association
with tamoxifen and estrogen use has been reported.47
MEMTs can be benign (adenofibromas and adenomyomas)
or malignant (adenosarcomas, carcinosarcomas, and carcinofi-
bromas). In adenosarcomas, the epithelial component is
benign and mesenchymal component malignant; in carcinofi-
bromas the epithelial component is malignant and mesenchy-
mal component benign; in carcinosarcomas both components
are malignant. The mesenchymal aspect of MEMTs can have
homologous (elements normally found within the uterus) or
heterologous components (elements not usually seen within
the uterus, including benign or malignant cartilage, fat, bone,
and rhabdoid tissues).46,49
Carcinosarcoma, formerly called malignant mixed müllerian
tumor, is the most common uterine sarcoma, representing
nearly 50% of all uterine sarcomas and 2%-3% of all uterine
malignancies.45,46,48-50 This tumor behaves more like endo-
metroid adenocarcinoma than like sarcoma, with common
risk factors and similar patterns of clonality, lymphatic
metastases, and recurrence; however, the prognosis is generally
poor.46,48 It is accepted that carcinosarcoma represents meta-
plastic transformation of carcinoma to sarcoma; some
researches argue that the carcinosarcoma represents an aggres-
sive form of endometrial carcinoma.45,46,49 Associations to
long-term tamoxifen therapy and previous pelvic irradiation
have been reported.12,45,49
The 5-year survival rates vary according to the histologic
type. Leiomyosarcomas for example, range from 18.8%-68%,
356
ESSs from 25%-98%, and MEMTs from 22%-39% (carcino-
sarcomas) to more than 80% (adenosarcomas).47,50,51
Imaging differentiation of leiomyosarcomas from leiomyo-
mas is difficult. The most common MRI appearance is a large
infiltrating myometrial mass with irregular, ill-defined margins;
heterogeneous T1 signal; intermediate- to high-intensity T2
signal; and heterogeneous enhancement owing to areas of
necrosis and hemorrhage (Fig. 12).47,48 These characteristics
do not differentiate it from benign degenerating fibroids.48,52
Rapid growth remains suspicious for leiomyosarcoma though
not reliable.47,48,53 In a large retrospective study (n ¼ 580), less
than 3% of leiomyosarcomas showed rapid growth and
Figure 12 A 63-year-old woman with rapidly growing pelvic mass,
diagnosed with leiomyosarcoma in the context of multiple fibroids.
Sagittal T2-weighted (A) and contrast-enhanced fat-suppressed T1-
weighted (B) images show markedly heterogeneous appearing fibroid
(arrow in A) containing irregularly enhancing internal soft tissue
(arrow in B).
G. Leursen et al.
leiomyosarcoma was discovered in just 1 woman among 371
women with rapidly growing masses (presumed fibroids).53
Restricted diffusion and T2 signal of the mass have shown
potential for differentiating benign from malignant tumors.54
ESS frequently appears as a polypoid endometrial mass on
MRI, with low-intensity T1 and heterogeneous T2 signals.
These tumors involve the myometrium and have a tendency
for lymphatic and vascular invasion, appearing as worm-like
bands of low-intensity T2 signal within areas of myometrial
involvement.47,48 Compared with endometrial carcinoma,
ESS is larger with more delayed contrast enhancement,
irregular nodular margins, and nodular extension into the
myometrium.47,48
Malignant mixed müllerian tumors have similar imaging
characteristics to those of endometrial carcinoma.45,47,48 MRI
findings of carcinosarcoma have been described mainly in case
series; these tumors are generally well defined with the tumor
epicenter in the endometrium (88%), cervix (8%), or myome-
trium (4%), and can present even as prolapsed uterine tumors
(Fig. 13).45,49,50,55,56 The tumor typically has high-intensity or
heterogeneous T2 signal relative to myometrium and can have
intratumoral T1 hyperintensity related to hemorrhage.
Enhancement pattern varies, though delayed heterogeneous
enhancement contrasts with the relative hypoenhancement of
more common endometrial carcinomas.45
The primary treatment of uterine sarcoma is surgery. Pelvic
lymphadenectomy and adjuvant radiotherapy are usually
performed, even in early stage disease, owing to the high
incidence of lymph node involvement and pelvic recurrence.
Chemotherapy may be indicated, especially in MEMTs, owing
to the epithelial component.48,50
Figure 13 A 61-year-old woman with uterine carcinosarcoma. Sagittal
T2-weighted MR image shows the classic prolapse of a polypoid
uterine mass (arrow) into the vagina or vulva, known as the “broccoli
sign.” Abnormal heterogeneous thickening of the endometrial cavity
related to combined tumor and blood products (asterisk) should be
noted.
MRI of uterine neoplasms 357

Gestational trophoblastic disease MRI of molar pregnancy is nonspecific, and difficult to be

Gestational trophoblastic disease (GTD) has abnormal tropho- distinguished from those of retained products of concep-
blastic proliferation and comprises a spectrum of lesions with tion.57,61,62,64,65 Findings include expansion of the endome-
varying malignant potential.57-59 The trophoblast is a richly trial cavity containing heterogeneous low-intensity T1 and
vascular gestational tissue that provides nourishment between high-intensity T2 signal with multiple cystic spaces represent-
maternal endometrium and developing embryo. This tissue ing hydropic villi, with enhancement of tumor and surround-
produces beta-human chorionic gonadotrophin (β-hCG), ing cystic spaces (Fig. 14).57,59-64 Invasive moles infiltrate and
which is most frequently elevated in GTD.57,58 GTD is divided disrupt the JZ and myometrium on T2-weighted and post-
into 5 main types: (1) hydatidiform mole, (2) invasive mole, contrast images (Fig. 14).59,61-63 However, loss of zonal
(3) choriocarcinoma, (4) placental-site trophoblastic disease anatomy may also be observed after missed or incomplete
(PSTD), and (5) epitheloid topoblastic disease. abortions or recent curettage.62-65
The clinical presentation, laboratory findings, and prognosis The management of patients with GTD varies according to
vary among the different types of GTD, with moles most histologic subtype. Molar pregnancies are treated preferably by
commonly manifesting as vaginal bleeding or as missed or suction curettage. β-hCG, an excellent tumor biomarker, is
incomplete abortions.59 Gestational hypertension in the first useful in tumor surveillance and recurrence.57-59 Invasive mole
trimester is virtually diagnostic of hydatidiform mole.59 Over- and choriocarcinoma are treated primarily with chemotherapy
all, 80%-85% of molar pregnancies follow a benign course (Fig. 15). Other recommendations for chemotherapy include
without local recurrences or metastases, 15%-20% locally
invasive, and 3%-5% developing metastases.59 Vaginal seeding
is seen in up to 30% of the cases. Metastases are primarily
hematogeneous, most commonly to the lungs (76%-87%),
liver (10%), and brain (10%), and tend to be hypervascular
with propensity to hemorrhage.57,59,60
Hydatidiform moles, either complete or partial, result from
aberrant fertilization and represent 80% of all GTDs, with an
incidence of 0.6-1.1 per 1000 pregnancies.57-61 Both subtypes
are premalignant, with 15% of complete moles and
0.5%-1.0% of partial moles undergoing malignant transforma-
tion.57-59 The invasive lesions include invasive mole, chorio-
carcinoma, and PSTD; epitheloid topoblastic disease is a rare
variant of PSTD. Hydatidiform moles and choriocarcinoma
arise from villous trophoblast, which produces β-hCG,
whereas PSTD arises from interstitial trophoblast.57-60 The
term gestational trophoblastic neoplasia or persistent tropho-
blastic neoplasia refers to invasive GTD, including invasive
mole, choriocarcinoma, and PSTD.57,59
Complete moles are characterized by absence of an embryo
and severe villous swelling and trophoblast hyperplasia,
resembling a bunch of grapes. Partial moles usually have
an embryo that may survive up to the second trimester
and exhibit less intense villous swelling and patchy hyper-
plasia.57-60 Invasive moles extend into or beyond the
myometrium, considered locally invasive nonmetastasizing
neoplasm.57,61 Choriocarcinoma represents malignant troph-
oblast proliferation, arising from any type of pregnancy (50%
from moles, 25% term or preterm, and 25% aborted or
ectopic) and occurring in 1 of 20,000-50,000 pregnancies.58,59
It is highly malignant with extensive necrosis and hemorrhage
and early vascular invasion resulting in metastases even if the
primary tumor is small.57,60
Diagnosis of GTD is based on clinical history and examina-
tion, quantitative β-hCG titers, and pelvic ultrasonography.57
MRI does not play a role in routine evaluation but may be used
for problem solving and better delineating extent of myome- Figure 14 A 23-year-old woman with gestational trophoblastic disease,
trial and extrauterine invasion in invasive mole and chorio- rising beta-HCG after dilation, and curettage for molar pregnancy.
carcinoma.57,59,62,63 In 25%-40% of patients with complete Sagittal T2-weighted (A) and contrast-enhanced fat-suppressed T1-
moles, theca lutein cysts are seen, resulting in bilateral multi- weighted (B) images show an avidly enhancing uterine mass (arrow)
cystic ovarian enlargement.59,60 with invasion into the myometrium.
358
A nuclei, high nuclear-to-cytoplasmic ratio, and positive markers
B MRI, the tumor usually has low T1 and high T2 signal
Figure 15 A 23-year old with gestational trophoblastic disease, after
treatment with chemotherapy. Sagittal T2-weighted (A) and contrast-
enhanced fat-suppressed T1-weighted (B) images show decrease in
size and enhancement of the previously seen uterine mass (arrow)
compatible with treatment response.
persistently elevated or rising hCG levels and metastatic
disease.57-59 Surgery and radiotherapy are reserved for high-
risk patients.59
Other Uncommon Uterine Malignancies
(Small Cell Cancer and Lymphoma)
Neuroendocrine Tumor (Small Cell Cancer)
Small cell carcinoma is a group of malignant neoplasms
showing neuroendocrine differentiation, mainly arising in the
lung and digestive tract.66-68 In the uterus, small cell carcino-
mas are rare, accounting for less than 1% of all endometrial
malignancies.66-70 On pathology, these tumors are character-
ized by sheets of small densely packed cells, hyperchromatic
G. Leursen et al.
for neuroendocrine differentiation on immunohistochemis-
try.66,67,69-72 Uterine small cell carcinomas exhibit aggressive
behavior, local invasion, extrauterine spread, early lymph node
involvement, and distant metastasis at diagnosis.66,67,71-73
Clinically, the most common symptoms include abnormal
vaginal bleeding and pelvic pain.67,69,73 Uterine small cell
carcinomas may produce and secrete metabolically active
amines and peptides and cause paraneoplastic syndromes,
including syndrome of inappropriate secretion of antidiuretic
hormone, retinopathy, Cushing syndrome, and membranous
glomerulonephritis.66,68,69,71,73 These tumors have been
described in a wide age range of women (23-84 years), with
a mean age of 60 years.67,69 The prognosis is poor and most
patients present with advanced disease.67,69,72,73
MRI features of uterine small cell carcinoma are limited to
case reports, and generally speaking indistinguishable from
those of other uterine neoplasms.66-73 Typically, the tumor is
seen as an intracavitary mass, frequently associated with diffuse
myometrium invasion and extrauterine spread.66,67,69 On
intensity.66-69,72,73 The tumor may demonstrate irregular
heterogeneous enhancement because of tumor infiltration,
hemorrhage, and necrosis,66,67,73 though a homogeneous
enhancement resembling lymphoma has also been
described.68 Enlarged lymph nodes and distant metastasis
are commonly found at diagnosis.66,67,73
The treatment of uterine small cell neuroendocrine carcino-
mas includes chemotherapy along with local treatment, which
may be surgery, radiotherapy, or both. The surgical approach
typically is total hysterectomy and pelvic lymphadenectomy.
Hormonal therapy and octreotide are also sometimes
used.69-72
Lymphoma
Uterine lymphoma may be primary or secondary. Distinguish-
ing primary from secondary lymphoma is important as they
differ in treatment and prognosis.74 Involvement of the female
reproductive organs in secondary lymphoma has been
reported in 40% of cases in autopsy series, whereas primary
uterine lymphomas are rare, representing less than 1% of
extranodal lymphomas.74,75 Most of the primary uterine
lymphomas are non-Hodgkin lymphomas , the most common
being diffuse large B-cell and follicular lymphoma.74 By
pathology, tumor is characterized by infiltrates of lymphocytes
and plasma cells in the uterine stroma.74 These tumors are
difficult to detect on Papanicolaou test as they may not involve
the epithelium. For this reason, primary lymphoma usually is a
large lesion at diagnosis.74 Lymphoma infiltrates the uterus,
causing diffuse enlargement without disruption of the uterine
architecture; polypoid lesions are less common. Local spread is
most common to the vagina and bladder.74-76 The age range of
presentation is broad (20-80 years) with a mean age of 40
years, and most patients present with vaginal bleeding.74,75
MRI is a useful imaging modality to assess the extent of
uterine lymphoma.74 Lymphoma causes homogeneous
enlargement of the uterus with preservation of the zonal
architecture on T2-weighted images, though loss of zonal
MRI of uterine neoplasms
anatomy and endometrial disruption have also been
described.74,77,78 Typically, the lesion has a low to intermediate
T1 signal and high T2 signal intensity.74-78 Though no imaging
findings have been described on DWI in uterine lymphoma,
lymphomas in general show restricted diffusion because of
hypercellularity and little extracellular space.79 The tumor
typically enhances homogenously, though it can be heteroge-
neous.74,77,78 Differentiating lymphoma from other pelvic
malignancies is crucial to prevent unnecessary surgery. Stand-
ard treatment is with chemotherapy or radiation therapy.74,75
Conclusion
A wide spectrum of benign and malignant pathologies occur in
the uterus. MRI is helpful in delineating the anatomy, extent of
growth in both benign and malignant diseases, staging of
common and uncommon primary uterine malignancies, and
response to targeted and systemic treatment.
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