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Cancer Center Member

Takeshi Kurita, Ph.D.

Academic Title:
Research Associate Professor, Obstetrics and Gynecology; Feinberg School of Medicine

Member of:
Signal Transduction in Cancer,Women's Cancer

Email:
t-kurita@northwestern.edu

Publications:(34)
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Cancer Focused Research:

Molecular etiology of cervical and vaginal adenocarcinoma Dr. Kurita studies the molecular etiology of cervical and vaginal adenosis and its progression to clear cell adenocarcinoma (CCAC). Cervical/vaginal adenoses are congenital anomalies defined as the presence of columnar glandular cells in the normally squamous epithelium of the ectocervix and vagina. Cervical/vaginal adenosis has been studied in the context of cervical/vaginal CCAC associated with in utero exposure to diethylstilbestrol (DES), a synthetic estrogen. Women exposed to DES in utero are at increased risk of developing CCAC, which is believed to arise from preexisting adenosis lesions. Although incidences have declined significantly after DES use for pregnant women was banned in 1971, cervical/vaginal adenoses and CCAC are still reported in women without a history of DES exposure, suggesting that there are other factors that contribute to these conditions. Using a mouse model, his group has previously demonstrated that developmental exposure to DES induces cervical/vaginal adenosis by disrupting expression of transcription factor p63, which is essential for the development of squamous epithelia. To elucidate the pathogenesis of cervical/vaginal adenosis, Dr. Kurita studies the signaling mechanism that induces p63 expression in the developing cervical/vaginal epithelium, and how developmental signaling is disrupted by exposure to DES. Furthermore, his team studies how adenosis lesions transform into CCACs. The cervical and vaginal CCACs are generally negative for human papilloma virus (HPV) infection, and their etiology is not understood. Recently, a high incidence of mutations in the PTEN gene was reported. In light of these findings, Dr. Kurita’s group has been using mouse models to study whether uncontrolled activation of PI3K signaling transforms adenosis into adenocarcinoma.