Endometrial cancer


Endometrial cancer

Endometrial cancer starts when cells in the endometrium (the inner lining of the uterus) start to grow out of control. Cells in nearly any part of the body can become cancer, and can spread to other parts of the body. It occurs most often in women 50–70 years of age. Obesity, nulliparity, diabetes, and polycystic ovaries with prolonged anovula­tion, unopposed estrogen therapy, and the extended use of tamoxifen for the treatment of breast cancer are also risk factors. Women with a family history of colon cancer (hereditary nonpolyposis colorectal cancer, Lynch syn­drome) are at significantly increased risk, with a lifetime incidence as high as 30%.

Types of endometrial cancer

Endometrial cancer (also called endometrial carcinoma) starts in the cells of the inner lining of the uterus (the endometrium). This is the most common type of cancer in the uterus


Endometrial carcinomas can be divided into different types based on how the cells look under the microscope. (These are called histologic types.) They include:

  • Adenocarcinoma (most endometrial cancers are a type of adenocarcinoma called endometrioid cancer)
  • Uterine carcinosarcoma or CS
  • Squamous cell carcinoma
  • Small cell carcinoma
  • Transitional carcinoma
  • Serous carcinoma

Clear-cell carcinomamucinous adenocarcinomaundifferentiated carcinomadedifferentiated carcinoma, and serous adenocarcinoma are less common types of endometrial adenocarcinomas. They tend to grow and spread faster than most types of endometrial cancer. They often have spread outside the uterus by the time they’re diagnosed.

Signs and symptoms

Abnormal bleeding is the presenting sign in 90% of cases. Any postmenopausal bleeding requires investiga­tion. Pain generally occurs late in the disease, with metas­tases or infection.


Papanicolaou smears of the cervix occasionally show atypical endometrial cells but are an insensitive diagnostic tool. Endocervical and endometrial sampling is the only reliable means of diagnosis. Simultaneous hysteroscopy can be a valuable addition in order to localize polyps or other lesions within the uterine cavity. Vaginal ultrasonog­raphy may be used to determine the thickness of the endo­metrium as an indication of hypertrophy and possible neoplastic change. The finding of a thin endometrial lining on ultrasound is clinically reassuring in cases where very little tissue is obtainable through endometrial biopsy.

Pathologic assessment is important in differentiating hyperplasias, which often can be treated with cyclic oral progestins.

Prompt endometrial sampling for patients who report abnormal menstrual bleeding or postmenopausal uterine bleeding will reveal many incipient as well as clinical cases of endometrial cancer. Younger women with chronic anovulation are at risk for endometrial hyperplasia and subsequent endometrial cancer; they can significantly reduce the risk of hyperplasia with the use of oral contra­ceptives or cyclic progestin therapy.

Staging and prognosis are based on surgical and pathologic evaluation only. Examination under anesthesia, endome­trial and endocervical sampling, chest radiography, intra­venous urography, cystoscopy, sigmoidoscopy, transvaginal sonography, and MRI will help determine the extent of the disease and its appropriate treatment.


Treatment consists of total hysterectomy and bilateral salpingo-oophorectomy. Peritoneal washings for cytologic examination are routinely taken and lymph node sampling may be done. If invasion deep into the myometrium has occurred or if sampled lymph nodes are positive for tumor, postoperative irradiation is indicated. Patients with stage III endometrial cancer are generally treated with surgery fol­lowed by chemotherapy and/or radiation therapy.


A review by the Society of Gynecologic Oncology Clinical Practice Committee concluded “the use of adjuvant chemotherapy to treat stage I or II endometrial carcinoma is not sup­ported by the available evidence.” Palliation of advanced or metastatic endometrial adenocarcinoma may be accom­plished with large doses of progestins, eg, medroxyproges­terone, 400 mg weekly intramuscularly, or megestrol acetate, 80–160 mg daily orally.


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