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No Evidence for Point Mutations in Codons 12, 13, and 61 of the ras Gene in a High-Incidence Area for Esophageal and Gastric Cancers¹

MRC Centre for Molecular and Cellular Biology, Department of Medical Physiology and Biochemistry, University of Stellenbosch Medical School, P.O. Box 63, Tygerberg, 7505 Republic of South Africa

The molecular mechanisms underlying the induction of esophageal and gastric cancer are not yet understood. It is possible that different etiological factors from geographically distinct areas play a role in the onset of these cancers. Twenty-seven primary esophageal and 11 gastric cancers originating from the high-incidence areas of South Africa were analyzed for the presence of ras protooncogene mutations. We found no evidence for mutations in codons 12, 13, or 61 or the H-ras, K-ras, and N-ras genes in these primary cancers.

Our results indicate that etiological factors such as fungal contamination of basic foodstuffs in a high-incidence area for these cancers do not play a role in the activation of ras genes and that mutations in these genes are not directly involved in the development of primary esophageal and gastric cancers in the South African population.

¹ This paper is part of a Ph.D. thesis.

² To whom requests for reprints should be addressed.

³ Partially funded by a grant to P.D.v.H. from the National Cancer Association of South Africa.

Received 8/29/89. Revised 4/16/90.

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