The overall goal of my research group is to better understand the molecular pathogenesis of the common gynecological tumors (carcinomas of the ovary, endometrium and uterine cervix). Our studies are focused primarily on cervical cancer, the second leading cause of cancer-related deaths in women worldwide. Cervical cancer is one of relatively few human cancer types that is strongly and clearly associated with an infectious agent (human papillomavirus). Much of our work has been aimed at better elucidating the molecular mechanisms by which certain types of human papillornaviruses contribute to the development and/or progression of cervical carcinomas. We have previously demonstrated that HPV-infected cells have altered cell cycle regulation, including abrogation of the growth arrest that normally follows DNA damage. These findings suggest a model of cervical tumorigenesis (see Figure 1) in which HPV-infected cells are predisposed to the accumulation of somatic mutations in tumor suppressor genes and/or oncogenes that are required for malignant transformation and tumor progression.

Deletions of specific regions of chromosome 3p are commonly observed in cervical cancers and some precancers. We are currently evaluating the role of a candidate 3p tumor suppressor gene (FHIT) in cervical cancer pathogenesis by evaluating the status of FHIT in primary cervical cancers and precancerous lesions. Both in vitro and in vivo assays are being used to assess the ability of FHIT to suppress the tumorigenic growth properties of cervical cancer cells. In related studies, differential expression screens are being utilized to identify and characterize cellular genes that are differentially expressed in cervical cancers vs. precancers and in cervical cancers vs. normal cervical tissues. Through these and other studies we hope to contribute to the development of better strategies with which to diagnose, treat, and/or prevent cervical cancer.

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