Adenocarcinoma (endometrioid, type 1)

Late p53 inactivation

Serous ElC/adenocarcinoma (non-endometrioid, type 2)

Heterogenous or mixed tumor

Fig. 1. Multiple roads to endometrial carcinoma. The phenotype of endometrial carcinoma is determined during carcinogenesis. Type I carcinomas inactivate PTEN very early on, before any discernible histological change (latent precancer). Nongenetic hormonal selection factors modulate cancer risk through their action on preclinical latent clones, which may undergo involution or expansion with additional mutation. Additional mutations are sometimes accelerated by a microsatellite instability phenotype, define stepwise progression events to endometrial intraepithelial neoplasia and then adenocarcinoma. Serous (type II) tumors are first seen as a short-lived preinvasive stage designated serous EIC. Endometrial glandular dysplasia is a newly described lesion with p53 genotype and histology intermediate between normal and serous EIC. Progression and involution rates of endometrial glandular dysplasia lesions after sometime must be defined to determine how often they are actual precursors of type II cancers. Rarely, individual examples of type I tumors may acquire an early or late p53 inactivation event, causing a hybrid or heterogenous tumor, respectively.

of additional mutations needed for progression from a latent or subclinical phase of disease, through EIN, to carcinoma. Cancer prevention and early diagnostic strategies suggested by this model have relevance to clinical management.

Most endometrial adenocarcinomas fall into one of two clinicopathological groups (Fig. 1). Initially, defined by histopathological appearance (1) and natural history as "endometrioid" (type I) and "nonendometrioid"(type II) (2,3), this classification has subsequently been shown to be paralleled by systematic differences in molecular features (4,5). The majority, i.e., more than 95% of sporadic endometrial adenocarcinomas might be readily and easily assigned to one of these groups. Exceptions pose diagnostic dilemmas for the histopathologist, but reflect the reality of a subgroup of individual tumors that are not purely assignable to a cohesive subtype. A common example is the homogenous endometrioid tumor with an unexpected P53 mutation throughout (Fig. 1, "hybrid" type), or the predominantly endometrioid tumor with a geographically delimited nonendometrioid subclone (Fig. 1, heterogenous or mixed type). For purposes of discussion, this chapter focusses primarily on the two major types of endometrial cancer.

Differences in endometrioid and nonendometrioid tumor classes are summarized in Table 1. Type I tumors usually have a nonaggressive behavior, and are often preceded

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