"Our results suggest that targeting therapies to the RNA that encodes a specific pair of proteins in HPV may break a chain that, left unhindered, promotes cellular proliferation and, potentially, cervical cancer," said Gary Clawson, M.D., Ph.D., professor of pathology, and biochemistry and molecular biology, Penn State College of Medicine. "Until now, there have been no effective and specific molecular treatments reported for HPV infections or for related papillomavirus infections."
The study, titled "The Inhibition of papilloma progression by antisense oligonucleaotides targeted to HPV11 E6/E7 RNA" was published July 1, 2004, in the online version of the journal Gene Therapy.
HPV is one of the most common causes of sexually-transmitted infection in the world. Types of HPV can cause fast-growing lesions such as genital and planter warts, and a number of HPV types are considered to be "high-risk" for development of cervical dysplasia, a known precursor to cervical cancer. According to the U.S. Department of Health and Human Services, 20 million Americans are already infected with HPV.
To survive and proliferate, HPV-infected cells require continued production of two proteins called E6 and E7, which are created according to the instructions of RNA, or ribonucleic acid, templates. Clawson and his team supposed that by destroying RNAs used for production of E6 and E7 proteins, the virus would no longer be able to trigger cellular proliferation.
"There are some unique characteristics of E6 and E7 which make them good targets, most importantly, their critical role in overcoming cell growth control pathways," said Clawson, who is also director of the Jake Gittlen Cancer Research Center at Penn State Milton S. Hershey Medical Center
Contact: Valerie Gliem