Risk factors for endometrial cancer include obesity, diabetes, nulliparity, estrogen-producing ovarian tumors, polycystic ovarian syndrome, advanced age, unopposed estrogen therapy, tamoxifen, and a family history of nonpolypoid colorectal cancer.

The prognosis depends on the tumor type and stage. Type 1 endometrial cancer or endometrioid carcinoma accounts for 80% of uterine carcinomas and is associated with increased and unopposed estrogen exposure. It typically arises from a background of endometrial hyperplasia and is frequently low-grade and slow-growing.

Type 2 tumors are not estrogen driven and are generally far more aggressive than type 1. They often occur in the setting of atrophic endometrium and include serous, clear cell, and other cell types. These tumors tend to invade the myometrium earlier and spread rapidly.

More advanced tumors often have a texture of mixed echogenicity and abundant vascularity evident on color Doppler. The tumor vessels are typically multiple, disorganized, and entering from multiple foci. As the tumor continues to grow, the borders become increasingly irregular and ill-defined, invading the myometrium, with loss of definition of the endometrial-myometrial junction. There can be cystic spaces within the characteristically solid tumor and, sometimes, fluid in the endometrial cavity outlining the mass. As the endometrial tumor invades further into the myometrium, the uterus enlarges and becomes blotchy in texture. With extensive myometrial invasion, the residual mantle of myometrium may be very thin. Some tumors seem to be entirely in the myometrium rather than the endometrium (see Figure E2-3).

Endometrial cancer can arise not only in the uterine fundus (most common), but also in the lower uterine segment, at the cervical junction, distorting the shape of the lower segment (see Figure E2-5).