Unfortunately, screening for oropharyngeal HPV infection or premalignant conditions is not very good presently, said Dr. Sturgis. At best, it’s like a ‘pap smear’ of the tonsils whereby we brush off cells that are then sent to the cytologist who does a similar viral oncogenic typing as for cervical pap smears. Such swabs or smears and oral rinses are used to test exfoliated cells in clinical trials, but are not routinely utilized or standardized for the oropharynx. Screening for invasive disease of the oropharynx is by physical examination augmented by CT or MR imaging with invasive biopsy required for a definitive diagnosis.
Explore this issue:September 2006
Histologically, the majority of oropharyngeal cancers are squamous cell carcinomas. Molecular and epidemiologic studies by Dr. Gillison and her colleagues strongly suggest that HPV-positive (usually type 16) oropharyngeal cancers comprise a distinct molecular, clinical, and pathologic disease entity that is causally associated with HPV infection and that has a markedly improved prognosis (J Natl Cancer Inst. 2000; 92(9):675-677).
Studying the Link
To further explore the role of HPV in oropharyngeal cancer, researchers at Yale University School of Medicine conducted a study among 78 patients to determine whether HPV-16 was present or absent, as well as to gather information about levels of a protein known as p16 (J Clin Oncol. 2006;24(5):736-747). High levels of p16 (overexpressing) have been reported in cancers caused by HPV, whereas tumors with low levels of p16 (nonoverexpressing) that are HPV-16-positive may have been caused by factors other than HPV.
The researchers divided subjects into three groups based on the presence of HPV-16 and p16 in tumor tissue and assessed the five-year rates as shown in the chart above.
The researchers conclude that tumors within Class III have the best prognosis.
Although this is a significant discovery, on a more practical basis p16 is highly unlikely to be useful in oral cancer screening in the immediate future as very little is known about the risk factors and natural history of an oral HPV infection or the predictive value of HPV detection for a diagnosis of or risk for oral cancer, Dr. Gillison told ENToday.
At Johns Hopkins Hospital, Dr. William Westra and I make the diagnosis based upon HPV in situ hybridization and the specific demonstration of HPV to the nucleus of the tumor cell, said Dr. Gillison. In our laboratory, HPV in situ data and p16 are strongly correlated and the p16 data does not add to the HPV data in terms of etiologic classification or prognosis.