When genomes of tumors are examined, loss of heterozygosity (LOH) is observed as a common mechanism in which the sole functional allele of a tumor suppressor gene is inactivated by somatic mutation [4]–[5]. LOH can be generated by many different mutational events, including point mutations, small deletions or inversions, mitotic recombination or chromosome loss. Recent advances in high-resolution single-nucleotide polymorphism arrays (SNP arrays) have revealed that a surprising number of tumors contain long tracts of homozygosity that are not accompanied by a change in gene copy number. This type of LOH arises from somatic mitotic recombination events and is referred to as partial (or acquired) uniparental disomy (UPD) [6]. Importantly, UPD can alter the genotype for hundreds of genes following a single event, thereby amplifying its potential to contribute to cancer development [7].
