The Influence of Resection and Aneuploidy on Mortality in Oral Leukoplakia
Jon Sudbø, M.D., D.D.S., Ph.D., Scott M. Lippman, M.D., J. Jack Lee, D.D.S., Ph.D., Li Mao, M.D., Wanja Kildal, M.Sc., Asle Sudbø, Ph.D., Simone Sagen, M.P.H., Magne Bryne, D.D.S., Ph.D., Adel El-Naggar, M.D., Ph.D., Björn Risberg, M.D., Ph.D., Jan F. Evensen, M.D., Ph.D., and Albrecht Reith, M.D., Ph.D.
Background Although the standard treatment of oral leukoplakiaranges from watchful waiting to complete resection, the valueof these approaches is unknown.
Methods We studied the relations among resection, ploidy status,and death from cancer in 103 patients with diploid dysplasticoral leukoplakia, 20 patients with tetraploid lesions, and 27patients with aneuploid lesions. Data on cancer-specific mortalityand treatment were obtained from the Cancer Registry of Norway,Statistics Norway, and chart reviews.
Results Primary oral carcinoma developed in 47 of the 150 patientswith leukoplakia (31 percent) 5 with diploid, 16 withtetraploid, and 26 with aneuploid leukoplakia duringa mean follow-up of 80 months (range, 4 to 237). The marginstatus of the initial leukoplakia resection had no relationto the development of oral cancer (P=0.95). Twenty-six of the47 patients in whom cancer developed (4 with prior tetraploidand 22 with prior aneuploid lesions) had recurrences (55 percent);the recurrences were more frequently multiple and distant (withinthe oral cavity) among patients with aneuploid lesions thanamong those with tetraploid or diploid lesions. All 47 patientsunderwent a standard regimen of surgery and radiation, followedby chemotherapy in the 26 with recurrent cancer. Only patientswith aneuploid leukoplakia died of oral cancer; the five-yearrate of death from cancer was 72 percent. Aneuploidy-relatedfirst carcinomas were diagnosed at a more advanced stage thanwere carcinomas originating from diploid or tetraploid leukoplakia(P=0.03) and were more likely to be lethal regardless of thestage.
Conclusions Complete resection of aneuploid leukoplakia doesnot reduce the high risk of aggressive carcinoma and death fromoral cancer.
Source Information
From the Departments of Medical Oncology and Radiotherapy (J.S., S.S., J.F.E.), Division of Digital Pathology (W.K.), and the Department of Pathology, Division of Cytology (B.R., A.R.), Norwegian Radium Hospital, University of Oslo, Oslo, Norway; the Departments of Clinical Cancer Prevention (S.M.L.), Biostatistics (J.J.L.), Thoracic/Head and Neck Medical Oncology (S.M.L., L.M.), and Pathology and Head and Neck Surgery (A.E.-N.), University of Texas M.D. Anderson Cancer Center, Houston; the Department of Physics (Norwegian University of Science and Technology, Trondheim, Norway (A.S.); and the Department of Oral Biology, University of Oslo, Oslo, Norway (M.B.).
Address reprint requests to Dr. J. Sudbø at the Department of Medical Oncology and Radiotherapy, Norwegian Radium Hospital, Ullernchausséen 70, Montebello, 0310 Oslo, Norway, or at jon.sudbo{at}rh.uio.no.
Dysplastic Leukoplakia
Damm D. D., Sollecito T. P., Alawi F., Sudbø J., Reith A., Lippman S. M.
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N Engl J Med 2004;
350:2718-2719, Jun 24, 2004.
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