The Human Papilloma Virus (HPV) is recognized as the major cause of cervical cancer. In 2006, an estimated 10,000 women in the United States were diagnosed with this type of cancer and nearly 4,000 will die from it. Cervical cancer strikes nearly half a million women each year worldwide, claiming a quarter of a million lives. A preventive vaccine is available and effective for those individuals not yet exposed to HPV. However, there is a large population of women who have had prior viral exposure where this vaccine is not effective.
The aim of this study is to demonstrate the effectiveness of 3,3'-Diindolylmethane (DIM) for increasing the potency of preventive and therapeutic vaccines after HPV infection using a mouse model. We will test the theory that the preventive vaccine or the therapeutic vaccine or both will prove to be effective vaccines in women who have had prior HPV exposure if these drugs are given after treatment with DIM for a sufficient period of time to suppress circulating virus and increase immune response.
This proposed research addressed a large population of women already infected with the human papilloma virus. These women are at increased risk for cervical cancer. Our goal is to adapt preventive and therapeutic vaccines so that they can be used in this at risk population.
Sepkovic, Daniel W; Pagan, Doris V; Stein, Johann et al. (2013) Evaluation of 3,3'-diindolylmethane with gardasil quadrivalent HPV vaccine in K14-HPV16-transgenic mice cervical histology. In Vivo 27:299-304 |
Sepkovic, Daniel W; Raucci, Laura; Stein, Johann et al. (2012) 3,3'-Diindolylmethane increases serum interferon-ýý levels in the K14-HPV16 transgenic mouse model for cervical cancer. In Vivo 26:207-11 |
Sepkovic, Daniel W; Stein, Johann; Carlisle, Antoine D et al. (2011) Results from a dose-response study using 3,3'-diindolylmethane in the K14-HPV16 transgenic mouse model: cervical histology. Cancer Prev Res (Phila) 4:890-6 |
Sepkovic, Daniel W; Stein, Johann; Carlisle, Antoine D et al. (2009) Diindolylmethane inhibits cervical dysplasia, alters estrogen metabolism, and enhances immune response in the K14-HPV16 transgenic mouse model. Cancer Epidemiol Biomarkers Prev 18:2957-64 |