Genetic etiology of gastric carcinoma: I. Chronic atrophic gastritis
β Scribed by Dr. George E. Bonney; Robert C. Elston; Pelayo Correa; William Haenszel; Diego E. Zavala; Guillermo Zarama; Tito Collazos; Carlos Cuello; D. C. Rao
- Publisher
- John Wiley and Sons
- Year
- 1986
- Tongue
- English
- Weight
- 622 KB
- Volume
- 3
- Category
- Article
- ISSN
- 0741-0395
No coin nor oath required. For personal study only.
β¦ Synopsis
Scientific evidence has accumulated to show that chronic atrophic gastritis (CAG) is a precursor of gastric carcinoma, especially its intestinal histologic type; thus the etiology of CAG is of interest. Data on 110 families (557 individuals) collected as part of a large cohort from the Nanno region of Colombia, South America, are analyzed to determine the familiality of CAG as a risk factor, and the possible involvement of a major gene in its etiology. We found that age and having an affected mother are important risk factors. In the sample, 45% are affected; 56% of individuals above 30 are affected, whereas only 28% of those 30 and under are affected; 48% of those with affected mothers are affected, but only 7% of those with unaffected mothers are affected. A positive spouse association was confounded with age. Sex and an affected father are not significant risk factors. The genetic (segregation) analysis showed Mendelian transmission of a recessive autosomal gene with penetrance dependent on age and mother's CAG status. Homozygous recessives account for an estimated 61 % of the sampled population and have penetrance reaching 72 % at age 30 if the mother is affected, and 41 % if the mother is not affected. Carriers and non-carriers, who make up an estimated 39% of the sampled population, have an appreciable estimated risk after age 50.
The environment, particularly diet, as the sole determinant of CAG needs reevaluation; some combined action of genes and environment seems more plausible.
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