Targeted molecular therapy can stop the growth of oral cancer reported researchers in the August issue of Archives of Otolaryngology—Head and Neck Therapy.
Overexpression of epidermal growth factor, or EGF-R, is associated with an increased chance of a malignancy’s developing and correlates with poor clinical outcome in head and neck cancer. Researchers hypothesized that inhibiting the EGF-R pathway could be a good target for molecular therapy.
They examined the in vitro and in vivo effects of PKI166, an orally administered EGF-R tyrosine kinase enzyme inhibitor, on two human squamous cell carcinomas of the oral cavity, or SCCOC, cell lines. The tyrosine kinase enzyme can increase cell growth.
In the in vitro test, researchers pretreated the cells with PKI116 (1 to 10 micrograms per milliliter) for one hour and then stimulated them with EGF (40 nanograms per milliliter). They found that the EGF-R–specific tyrosine kinase enzyme was inhibited completely by PKI166 at all doses tested. They also found that using PKI166 to block the EGF-R signaling pathway suppressed the growth of human SCCOC.
In the in vivo test, researchers inoculated nude mice subcutaneously with one of the tumor cell types. They observed the mice for seven days, at which time subcutaneous tumors could be palpated. They then delivered daily oral doses of PKI166 for 28 days and observed the mice for tumor growth. They found that the EGF-R protocol significantly reduced tumor growth in mice.
Researchers are planning to conduct preclinical studies to determine the safety of using PKI166 in humans to arrest the growth of oral cancer.
