Oral cancer represents approximately 2.4% of the total cancers that will occur in the United States this year with an estimated 35,720 cases and 7,600 deaths. Even more common internationally, oral cancer is the 6th most prevalent cancer in the world. The majority (90%) of these cancers are oral squamous cell carcinomas (OSCCs), which have been etiologically linked to the individual’s exposure to known carcinogens, mainly in tobacco and alcohol.
The overall prognosis for patients is poor, with a 5-year survival rate ranging from 54 to 65%. Present therapies for OSCC patients typically involve surgical resection (stages I and II), in combination with radiation (stages III and IV), and with chemotherapy for high risk patients with nodal involvement or metastases. In addition to the physical disfiguration associated with surgical procedures, there are significant complications following radiation therapy (tissue necrosis, fibrosis, atrophy, and xerostomia).
Tumor recurrence is also a problem for oral cancer patients, as nearly 20% will exhibit locoregional recurrence within 18 months post-surgery, and an additional 22–42% of patients will present with a second primary tumor 5–8 years after their initial tumor diagnosis. Unfortunately, despite important advances in OSCC treatment over the past 30 years, overall survival rates have remained relatively unchanged.
Since current therapeutic protocols remain modestly effective and physically damaging, it is appropriate that alternative or complementary strategies, such as chemoprevention, be developed and tested in applicable preclinical model systems. These preclinical studies can be translated into early stage clinical investigations and potentially into standard of care practices. The oral cavity is ideally suited for preclinical and clinical chemoprevention studies for several reasons.
First, the anatomical location allows for rapid and largely nonintrusive accessibility to the tissue at risk. Second, chemopreventive agents can be accurately and directly administered to affected areas. Third, tissues can be readily biopsied, lesions accurately measured, and photo documentation acquired. Fourth, high risk populations primarily associated with coupled tobacco use and alcohol consumption are easily identified and readily available. Fifth, it has been proposed that the oral cavity may serve as a reliable surrogate for determining genetic and epigenetic changes that occur in other respiratory tissues due to cigarette smoking.
One of the attractive characteristics of chemoprevention strategies is the extended window of opportunity during which intervention can begin and the desired outcomes obtained. Since the multistep process of cancer development involves the accumulation of critical genetic insults over a 10–20 year period of time and includes numerous molecular pathways, there are many points at which chemopreventive agents can intervene in disease progression.
This may have special relevance to past smokers who remain at higher risk for oral cancer and former OSCC patients who are free of disease after local therapy yet remain at high risk for both recurrent and second primary tumors. In these individuals, an important paradigm in cancer chemoprevention must be to inhibit the progression of premalignant lesions, such as oral dysplasias, into malignant OSCC.
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