Mitotic recombination map of 13cen-13q14 derived from an investigation of loss of heterozygosity in XXXX .

@entity1 @entity5 @entity995
Loss of heterozygosity at tumor-suppressor loci is an important oncogenic mechanism first discovered in @entity995 . We explored this phenomenon by examining a set of matched @entity995 and leukocyte DNA samples from 158 @entity1 informative for DNA polymorphisms. Loss of heterozygosity at the @entity995 locus (13q14) was observed in 101 cases, comprising 7 cases with a somatic deletion causing hemizygosity and 94 with homozygosity (isodisomy). Homozygosity was approximately equally frequent in @entity5 from male and female @entity1 , among @entity1 with a germ-line vs. somatic initial mutation, and among @entity1 in whom the initial mutation occurred on the maternal vs. paternal allele. A set of 75 @entity5 exhibiting homozygosity was investigated with markers distributed in the interval 13cen-13q14. Forty-one @entity5 developed homozygosity at all informative marker loci, suggesting that homozygosity occurred through chromosomal nondisjunction. The remaining cases exhibited mitotic recombination. There was no statistically significant bias in apparent nondisjunction vs. mitotic recombination among male vs. female @entity1 or among @entity1 with germ-line vs. somatic initial mutations. We compared the positions of somatic recombination events in the analyzed interval with a previously reported meiotic recombination map. Although mitotic crossovers occurred throughout the assayed interval, they were more likely to occur proximally than a comparable number of meiotic crossovers. Finally, we observed four triple-crossover cases, suggesting negative interference for mitotic recombination, the opposite of what is usually observed for meiotic recombination.
