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Carcinogenesis |
Division Human Genetics, Medical School [L. D. P., M. P. M., M. J. K.], and MRC Center for Molecular and Cellular Biology, Department of Medical Biochemistry [P.V.H.], University of Stellenbosch, 7505 Tygerberg, South Africa; Department of Medical Biochemistry, University of Cape Town Medical School, Observatory, 7925 Cape Town, South Africa [E. D., M. I. P.]; Department of Human Genetics, University Hospital Ziekenhuis, Ghent, Belgium [M. V. G., N. V. R., F. S.]; Department Cardiothoracic & Vascular Surgery, Faculty of Medicine, University of Transkei, UNITRA, 5100 Umtata, South Africa [D. K. M.], Department of Cardio-Thoracic Surgery, Groote Schuur Hospital, Observatory, 7925 Cape Town, South Africa [M. D. G.]
Esophageal cancer (EC) is the leading cause of cancer death in the Black male population in South Africa. Although several oncogenes and tumor suppressor genes have previously been found altered in this cancer, many novel genes remain to be identified. To identify the chromosomal location of these unknown genes, we have analyzed DNA of 29 South African EC patients by comparative genomic hybridization. Frequent loss occurred at chromosome 1p (52%), 4p (52%), 18q (48%), 19p (52%), 19q (55%), and 22q (41%). The most common gains were detected at 1q (41%), 2q (52%), 3q (72%), 5p (31%), 7p (48%), 7q (45%), 8q (55%), and Xq (69%). High level amplification was detected at 2q2433, 6p21.1q14, 7p12q21, 7q11.231, 8q2224, 8q13qter, 13q2134, and at 13q3234. The present comparative genomic hybridization study opens the way for additional targeted studies on these particular chromosomal regions to identify the specific genes involved in the higher susceptibility to specific subtypes of esophageal carcinoma in different geographical regions. The loss of 8p (28%) and Xp (17%) in tumors of male individuals may provide clues to the basis of the sex-biased frequency of occurrence of EC favoring men.
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