Which putatively pre-malignant oral lesions become oral cancers? Clinical relevance of early targeting of high-risk individuals.
Oral squamous cell carcinomas continue to be a group of diseases with high mortality and increasing incidence rates, particularly among young individuals. This is a paradox finding, since most oral cancers are preceded - even by several years - by readily detectable mucosal changes, most often white or red patches (leukoplakias and erythroplakias, respectively). However, only a small fraction of leukoplakias or erythroplakias are related to cancer development, and the challenge has been to identify the high-risk lesions. From the vast literature on molecular markers in oral pre-cancer, no reliable prognostic marker for risk assessment in putatively pre-malignant lesions has emerged. For this reason, a wait-and-see approach has been adopted for this group of lesions. Recently published data point to gross genomic aberrations (DNA aneuploidy) as a tool for targeting patients at particular risk for future cancerous lesions in the oral cavity. Thus, DNA aneuploidy signalled a very high risk for subsequent development of carcinomas in a wide range of lesions from the oral mucous membrane, ranging from oral leukoplakias to oral erythroplakias and even including lesions that had been explicitly defined as being without a malignant potential by a group of trained pathologists. As an extension of research in oral pre-malignancies, the enzyme cyclooxygenase-2 (COX-2) seems to be enhanced specifically in high-risk oral lesions, as defined by the aberrant DNA content of their lesions. These data strongly indicate that COX-2 inhibitors (coxibs) should be investigated as chemopreventive agents in patients identified to be at high risk of developing oral cancer.
Sudbø
Jon
J
Department of Medical Oncology and Radiotherapy, Norwegian Radium Hospital, University of Oslo, Norway, Montebello, 0310 Oslo, Norway. jon.sudbo@rh.uio.no
Reith
Albrecht
A
D000782:Aneuploidy; D000818:Animals; D017209:Apoptosis / Q000235:genetics; D014408:Biomarkers, Tumor; D002294:Carcinoma, Squamous Cell / Q000175:diagnosis* / Q000201:enzymology / Q000453:epidemiology / Q000235:genetics; D002455:Cell Division; D051546:Cyclooxygenase 2; D016147:Genes, Tumor Suppressor; D006133:Growth Substances; D006801:Humans; D007527:Isoenzymes / Q000096:biosynthesis; D019656:Loss of Heterozygosity; D008565:Membrane Proteins; D018895:Microsatellite Repeats; D009062:Mouth Neoplasms / Q000175:diagnosis* / Q000201:enzymology / Q000453:epidemiology / Q000235:genetics; D011230:Precancerous Conditions / Q000737:chemistry / Q000175:diagnosis* / Q000201:enzymology / Q000235:genetics; D011451:Prostaglandin-Endoperoxide Synthases / Q000096:biosynthesis
D014408:Biomarkers, Tumor; D006133:Growth Substances; D007527:Isoenzymes; D008565:Membrane Proteins; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases