Endometrial Carcinoma

General characteristics

Endometrial carcinoma is the fourth most common female cancer and the most common malignancy of the female reproductive tract (Jemal et al. 2007).

Epidemiology

Five-year survival rates vary between 96% for stage I disease and 26% for stage IV disease (Jemal et al. 2007).

Presenting as post-menopausal bleeding, the disease occurs most frequently in white women, with peak incidence between ages 55 and 65.

Risk factors include unopposed estrogen intake, nulliparity, obesity, and diabetes and Stein-Leventhal syndrome.

Prognosis

The prognosis of endometrial carcinoma depends on a number of factors, including stage, depth of myometrial invasion, lymphovascular invasion, nodal status, and histological grade. Determination of the depth of myometrial invasion is important, since it correlates with the incidence of lymph node metastases.

The depth of myometrial invasion is probably the single most important morphologic prognostic factor as it correlates with tumor grade, tumor extension into the cervix and the prevalence of lymph node

Treatment

Standard treatment is total abdominal hysterectomy and bilateral salpingo-oophorectomy.

Diagnosis

Endometrial carcinomas are typically diagnosed at endometrial biopsy or dilatation and curettage with imaging being reserved to evaluate extent of disease.

On unenhanced T1-weighted images, endometrial carcinoma is isointense with the normal endometrium. Although endometrial cancer may demonstrate high signal intensity on T2-weighted sequences, it is more typically heterogeneous, and may even be of low signal intensity. Routine use of dynamic intravenous contrast enhancement is necessary for state-of-the-art MR evaluation of endometrial carcinoma (Frei et al. 2000; Hricak et al. 1991; Manfredi et al. 2004). Following intravenous contrast medium administration, there is early enhancement of endometrial cancer relative to the normal endometrium, allowing identification of small tumors, even those contained by the endometrium. In the later phases of enhancement, i.e., equilibrium phase, tumor appears hypointense relative to the myometrium.

Staging

Stage I

Stage I endometrial cancers include tumors confined to the corpus. Stage IA tumors (limited to endometrium) appear as a normal or widened (focal or diffuse) endometrium. An intact JZ and a band of early subendometrial enhancement exclude deep myometrial invasion. Regardless of sequence, the tumor- myometrium interface is smooth and sharp.

In stage IB disease, tumor extends less than 50% into the myometrium with associated disruption or irregularity of the JZ and subendometrial enhancement. If these landmarks are not present, stage IB tumor is suggested by an irregular tumor-myometrium interface.

Presence of low-signal-intensity tumor (later phases of enhancement) within the outer myometrium or beyond indicates deep myometrial invasion—stage IC disease. Erroneous MRI assessment of the depth of myometrial invasion may occur there is a large polypoid endometrial carcinoma, which distends the uterus so that the thin rim of myometrium is stretched over it rather than deeply infiltrated (Yamashita et al. 1993). Other causes include the presence of leiomyomas, congenital anomalies, and indistinct zonal anatomy.

Stage II

Stage II includes tumor extension beyond the uterine corpus into the cervix. In stage IIA, invasion of the endocervix appears as widening of the internal os and endocervical canal with preservation of the normal low-signal-intensity fibrocervical stroma on T2-weighted images. Disruption of the fibrocervical stroma by high-signal-intensity tumor on T2-weighted images together with disruption of normal enhancement of the cervical mucosa by low-signal-intensity tumor on late dynamic contrast-enhanced MRI indicate cervical stroma invasion—stage IIB disease.

Stage III

In stage III disease, tumor extends outside the uterus but not outside the true pelvis. Parametrial involvement stage IIIA appears as disruption of the serosa with direct extension into the surrounding parametrial fat. In stage IIIB disease, tumor extends into the upper vagina, and there is segmental loss of the low-signal-intensity vaginal wall. In stage IIIC disease lymphadenopathy is present.

Stage IV

Stage IV disease is tumor that extends beyond the true pelvis or invades the bladder or rectum. Loss of low signal intensity of the bladder or rectal wall indicates stage IVA disease. In stage IVB disease, distant metastasis, malignant ascites, or peritoneal deposits are present. Peritoneal deposits are better demonstrated on the delayed contrast-enhanced MR images.

Metastases

MRI is the modality of choice for detection of tumor recurrence within the pelvis. Approximately 17% of patients with endometrial carcinoma develop local or distant recurrence.

The prevalence of recurrence depends on the tumor grade, size, and stage at presentation in addition to the histological type.

Recurrence is most common in the first five years after diagnosis, with 70% of patients with endometrial carcinoma presenting with recurrent disease in the first 3 years.

The vagina is the sole site of recurrence in 30–50% of patients, the remainder developing pelvic or para-aortic lymph node involvement or systemic spread manifesting as hepatic, pulmonary or osseous metastasis or peritoneal carcinomatosis.

On MRI, recurrent disease at the vaginal vault appears as a mass or nodule on T1-weighted imaging and has high signal intensity on T2-weighted imaging