According to the Centers for Disease Control and Prevention,
approximately 20 million Americans are currently infected with human
papillomavirus (HPV). Another 6 million people become newly infected each year.
HPV is so common that at least 50% of sexually active men and women get it at
some point in their lives.
Research observations suggest HPV oncoprotein expression
provides a positive feedback loop for the epidermal growth factor receptor- mitogen-activated
protein kinase (EGFR-MAPK) pathway and maintaining cell proliferation. EGFR plays a crucial role in squamous cell
carcinomas (SCCs) and signals through the Ras-MAPK pathway. EGFR activation of Ras initiates a multistep
cascade that leads to the activation of MAPKs including ERK1/2. Subsequently, ERK1/2 regulates cell
transcription and many other transcription factors involved in cell
proliferation, survival, and transformation in vitro. Increased MAPK activation
has been reported for several human tumors.
Deregulated EGFR-MAPK signaling confers cancer cell survival and
enhances resistance to chemotherapy. Therefore, EGFR pathway inhibitors have
been developed to act as potential molecular targeting drugs for cancer
Researchers from the University of New Mexico’s School of
Medicine have demonstrated that EGFR
functional inhibitors as well as MAPK inhibitors will cause diminished HPV
early gene expression. EGFR pathway
inhibitors act as antivirals that prevent viral gene expression and viral
genome replication. Inhibiting this
feedback by blocking the EGFR pathway with inhibitors can lower viral effects
and leading to viral cure or restoration of tumor suppressor p53 and pRb
expression such that the cells become destined to die. Many of these EGFR pathways inhibitors are FDA
approved for human use, and so could be tested in human tissues and patients.
STC has filed intellectual property on this exciting new technology and is currently exploring commercialization options. If you are interested in information about this or other technologies, please contact Arlene Mirabal at email@example.com or 505-272-7886.