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and progesterone receptors and progesterone receptors by high risk hormonal exposures (unopposed estrogens) (6) and a histologically discernible premalignant lesion, EIN (7). Prototypical type I tumors are prone to inactiva-tion of the PTEN tumor suppressor gene (8) and a wide variety of ancillary molecular defects. In contrast, type II tumors occur in women who are slightly older (by 5-10 years) and are highly fatal (1). Molecular lesions within the nonendometrioid group are dominated by inactivation of the p53 gene, a change present in almost 90% of cases (4). The patterns of genetic instability differ in significant ways. Type I tumors have a very specific type of genetic instability, mismatch repair defects, caused by epigenetic inactivation of mismatch repair factors, such as MSH1 (9). Genetic instability in type II tumors is manifested globally at the chromosomal rather than microsatellite level, frequently demonstrating high order aneuploidy although having an intact mismatch repair mechanism (10,11).

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