What is the diagnosis?
There is a moderately-well-differentiated endometrial adenocarcinoma that is invading into the inner third of the myometrium. The tumor shows a polypoid growth pattern into the endometrial cavity. Compare the histologic features of the adenocarcinoma with those of the proliferative endometrium (Case 1, image 1.1).
The neoplastic endometrial epithelial cells are forming glandular structures, and in some areas there is a cribiform pattern, i.e. bridges of
neoplastic cells growing across gland lumens. Cellular bridging ("cribiforming") is a feature commonly seen in adenocarcinioma. The
neoplastic-cell nuclei are atypical in that they exhibit chromatin clearing,
nuclear membrane irregularity, and, often, prominent nucleoli.
Many of the malignant epithelial cells have lost their normal polarity with respect to the glandular basement membrane. Necrotic cell debris is present in the lumens of many glands. The endometrial stroma surrounding the neoplastic glands has the fibrotic (desmoplastic) appearance commonly seem when malignant epithelium invades stroma. Endometrial stromal invasion is to be distinguished from myometrial invasion. Focally, the neoplastic glands show areas of squamous
differentiation; this does not affect the prognosis.
What determines the prognosis?
As with malignant neoplasms in general, the prognosis is determined by the stage and the grade. The stage is the extent of spread. In general, endometrial adenocarcinomas that are confined to the myometrial wall (Stage I) have a much better prognosis (90% 5 year survival). Lesions of lower stage may not enlarge the uterus, so physical examination will not rule out a carcinoma, and a Pap smear does not have a high sensitivity for detection of uterine lesions--a biopsy must be done. The grade is based upon the degree of histologic differentiation, in this case on a scale of 1 to 3.
What are risk factors for this disease?
Female sex, you say? Good, now several more are: obesity, infertility, hypertension. An unopposed estrogen effect leading to adenomatous hyperplasia and possible subsequent carcinoma can occur either with exogenous estrogen administration or from estrogen-producing ovarian neoplasms.