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Oral Cancer Prevention and the Evolution of Molecular-Targeted Drug Development

Scott M. Lippman, Jon Sudbø, Waun Ki Hong

From the Departments of Clinical Cancer Prevention and Thoracic/Head and Neck Medical Oncology, and Division of Cancer Medicine, The University of Texas M. D. Anderson Cancer Center, Houston, TX; and Department of Medical Oncology and Radiotherapy, The Norwegian Radium Hospital, University of Oslo, Oslo, Norway

Address reprint requests to Scott M. Lippman, MD, Department of Clinical Cancer Prevention, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030; e-mail: slippman{at}mdanderson.org.

The multifaceted rationale for molecular-targeted prevention of oral cancer is strong. Oral cancer is a major global threat to public health, causing great morbidity and mortality rates that have not improved in decades. Oral cancer development is a tobacco-related multistep and multifocal process involving field carcinogenesis and intraepithelial clonal spread. Biomarkers of genomic instability, such as aneuploidy and allelic imbalance, can accurately measure the cancer risk of oral premalignant lesions, or intraepithelial neoplasia (IEN). Retinoid–oral IEN studies (eg, of retinoic acid receptor-beta, p53, genetic instability, loss of heterozygosity, and cyclin D1) have advanced the overall understanding of the biology of intraepithelial carcinogenesis and of preventive agent molecular mechanisms and targets—important advances for monitoring preventive interventions and assessing cancer risk and pharmacogenomics. Clinical management of oral IEN varies from watchful waiting to complete resection, although complete resection does not prevent oral cancer in high-risk patients. New approaches, such as interventions with molecular-targeted agents and agent combinations in molecularly defined high-risk oral IEN patients, are urgently needed to reduce the devastating worldwide consequences of oral cancer.

Supported in part by grants P01 CA106451 and N01-CN-35159 (S.M.L.) and CA16672 (M. D. Anderson Cancer Center Support Grant) from the National Cancer Institute, National Institutes of Health, Department of Health and Human Services; grants from The Norwegian Cancer Society (E 03010/002, E 03010/003, and HF-51019), the Research Foundation of the Norwegian Radium Hospital (702526-13 and SE 0207) and Astrid and Birger Torstedts Legat (J.S.); and by grants P01 CA52051 and U01 CA79437 (W.K.H.).

Dr Lippman holds the Ellen F. Knisely Distinguished Chair, and Dr Hong holds the Samsung Distinguished University Chair in Cancer Medicine at M. D. Anderson Cancer Center. Dr Hong also is an American Cancer Society Professor.

Authors' disclosures of potential conflicts of interest are found at the end of this article.

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