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Currently, the underlying causes of endometrial cancer (EMC) have not been completely defined, and treatment options for patients with advanced stages are limited. There are several common genetic alterations in human endometrial cancer. Among those genes, the mutations of phosphatase and tensin homolog (PTEN) and p53 are most frequently observed. Interestingly, the alteration of p53 is observed mainly at the advanced stage of tumors although PTEN mutations are observed in a wide range of endometrial cancers. This indicates that p53 mutation plays a role in the progression, while PTEN mutation is crucial to initiate endometrial cancer.
Animal models in which EMC develops spontaneously are of great advantage for studying mechanisms of cancer initiation and progression. Recently, we generated two EMC mouse models. One hundred percent of these mice develop endometrial cancer within a short period, with invasion occurring by two to three months, which mimics human EMC.
Currently, using these novel EMC mouse models, we are trying to delineate other downstream and upstream signaling pathways critical to the initiation and progression of human EMC.
Daikoku T, Hirota Y, Tranguch S, Joshi AR, DeMayo FJ, Lydon JP, Ellenson LH, Dey SK. Conditional loss of uterine Pten unfailingly and rapidly induces endometrial cancer in mice. Cancer Res. 68(14):5619-5627. 2008.
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