Oral cancer chemoprevention—the end of epoc, the beginning of an epoch of molecular selection
Mené sur 150 patients présentant des lésions précancéreuses à haut risque de la cavité buccale (durée médiane de suivi : 35 mois), cet essai randomisé évalue l'efficacité, du point de vue de la survie sans cancer à 3 ans, de l'erlotinib
The promise of chemoprevention of head and neck squamous cell carcinoma (HNSCC) was first raised in 1953 in an article by Slaughter et al1 describing epithelial field cancerization, or premalignant changes within grossly normal mucosa adjacent to invasive oral cancers. Slaughter et al hypothesized that an “as-yet-unknown” carcinogen condemned the entire oral mucosa toward malignant progression. Environmental carcinogens, including tobacco and alcohol, are now recognized causes of epithelial field cancerization. Patients curatively treated for a first human papillomavirus-negative HNSCC demonstrate the highest rate of second primary tumor (SPT) formation among patients with cancer. This major source of morbidity and mortality has motivated 3 decades of research in HNSCC chemoprevention. However, no effective and well-tolerated agent has been identified. In this issue of JAMA Oncology, William and colleagues2 present results from the EPOC (Erlotinib Prevention of Oral Cancer) study, a randomized chemoprevention trial evaluating whether the small molecule epidermal growth factor receptor (EGFR) inhibitor erlotinib prevents HNSCC in patients with high-risk oral premalignant lesions (OPLs). Despite compelling rationale, the EPOC study demonstrated that 12 months of erlotinib failed to improve oral cancer-free survival (CFS) vs placebo.
JAMA Oncology , éditorial en libre accès, 2014