Scientists have implicated the beta-catenin oncogene in the process by which HPV infection can trigger cervical cancer. Using a newly-developed mouse model, the Georgetown Lombardi Comprehensive Center researchers, led by associate professor of oncology Aykut Üren, M.D., found that switching the oncogene on in the cervix of HPV-infected animals promoted the development aggressive cervical cancer. The results are being presented at the AACR 102nd annual meeting.
The mouse model was generated by crossing a transgenic strain that expresses HPV genes in its cervix with another that forces the Wnt pathway, which involves beta-catenin, to be constantly activated in the cervix. While the HPV strain does develop cervical cancer, the tumors in the double transgenic animals were larger and more aggressive, the researchers note.
“These early findings suggest clinical implications that are both preventative and therapeutic," Dr. Üren claims. “We can potentially develop a screening method to check for HPV and beta-catenin activation in pap smears. That will identify individuals at a higher risk of developing cancer compared to ones who are only HPV positive.”
The Georgetown team also suggests that developmental anticancer drugs targeting the Wnt pathway could have utility against cervical cancer. “Activation of this pathway is very common in colon cancer and is found in a dozen other cancers, so these same novel drugs might be useful in treating advanced-stage cervical cancer patients,” Dr. Üren concludes.