Differences in Disease Progression Between the Two Types of Endometrial Adenocarcinoma

The timing and pattern of metastatic dissemination of endometrial adenocarcinoma varies in part related to the histological cell type. Based on clinical observations, the sequence in the progression of endometrioid adenocarcinoma seems to be as follows:

1. Years of endogenous or exogenous hyperestrinism associated with hyperplasia of increasing architectural complexity and cytological atypia;

2. Evolution of a clonal population often with a mutation in the PTEN gene, accompanied by histological features of adenocarcinoma (91);

3. A slow increase in the mass of carcinoma, with progressively deeper myometrial invasion and mechanical spread to the surface of the uterine cervix by exfoliation and superficial implantation, or direct spread to the cervical stroma as the mass of tumor increases in three dimensions;

4. Permeation of capillary or lymphatic spaces;

5. a. Metastases to the regional (pelvic and para-aortic) lymph nodes or retrograde spread to the vagina.

b. Penetration of the uterine serosa or reflux of neoplastic cells through the fallopian tubes with spread to the ovaries or upper abdomen.

6. Eventual distant metastases.

In contrast is the typical progression of UPSC, which differs as follows:

1. The development (in a women typically 10 years older than one with endometrioid adenocarcinoma) of EIC with mutant p53 and wild-type PTEN in the absence of hyper-estrinism and instead in a background of atrophy or polyp;

2. a. Probable rapid progression to invasive UPSC.

b. Reflux of neoplastic cells through the fallopian tubes.

3. a. Increase in tumor mass with spread to the cervical surface or stroma. b. Implantation and growth of neoplastic cells on the pelvic peritoneum.

4. a. Invasion into the myometrium usually accompanied by capillary or lymphatic invasion.

5. a. Metastasis to regional (pelvic or para-aortic) lymph nodes.

b. Direct mechanical dissemination to other intraperitoneal sites, such as omentum and the surface of the diaphragm and liver.

6. Distant metastasis.

Either the (a) or (b) pathways, and frequently both, might occur for any given tumor. It is common for UPSC to have extended beyond the uterus to involve the peritoneum at the time of initial diagnosis. Indeed, the tumor may metastasize, presumably by a mechanism that includes exfoliation of neoplastic cells and trans-tubal reflux, whereas histologically still an in situ process (92).

Not all of the second type of endometrial carcinomas behave in the same fashion. Clear cell carcinoma also has an aggressive behavior, with an overall 5-year survival rate of about 40-50% (45,48,49,93-96). However, it differs from both endometrioid adenocarci-noma and UPSC, with frequent early lymphatic invasion and nodal spread, but without the propensity to spread by direct exfoliation and implantation on peritoneal surfaces. Although women with tumors confined to the endometrium have an approx 90% 5-year survival, deep myometrial invasion or vascular invasion carries a poor prognosis.

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