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Genetic etiology of gastric carcinoma: I. Chronic atrophic gastritis
Author(s) -
Bonney George E.,
Elston Robert C.,
Correa Pelayo,
Haenszel William,
Zavala Diego E.,
Zarama Guillermo,
Collazos Tito,
Cuello Carlos,
Rao D. C.
Publication year - 1986
Publication title -
genetic epidemiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.301
H-Index - 98
eISSN - 1098-2272
pISSN - 0741-0395
DOI - 10.1002/gepi.1370030402
Subject(s) - penetrance , etiology , mendelian inheritance , atrophic gastritis , population , spouse , biology , genetics , risk factor , cohort , medicine , gastritis , gene , helicobacter pylori , environmental health , sociology , anthropology , phenotype
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 Narino 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 re‐evaluation; some combined action of genes and environment seems more plausible.