the other parent due to errors in meiosis I or meiosis II. This acquired homozygosity could lead to development of cancer if the individual inherited a non-functional allele of a tumor suppressor gene. In tumor cells copy-neutral LOH can be biologically equivalent to the second hit in the Knudson hypothesis. Acquired UPD is quite common in both hematologic and solid tumors, and is reported to constitute 20 to 80% of the LOH seen in human tumors. Determination of virtual karyotypes using SNP-based arrays can provide genome-wide copy number and LOH status, including detection of copy-neutral LOH. Copy-neutral LOH cannot be detected by arrayCGH, FISH, or conventional cytogenetics. SNP-based arrays are preferred for virtual karyotyping of tumors and can be performed on fresh or paraffin-embedded tissues. Retinoblastoma The classical example of such a loss of protecting genes is hereditary retinoblastoma, in which one parent's contribution of the tumor suppressor Rb1 is flawed. Although most cells will have a functional second copy, chance loss of heterozygosity events in individual cells almost invariably lead to the development of this retinal cancer in the young child. Breast Cancer and BRCA1/2 The genes BRCA1 and BRCA2 show loss of heterozygosity in samplings of tumors from patients who have germline mutations. BRCA1/2 are genes that produce proteins which regulate the DNA repair pathway by binding to Rad51. Detection Loss of heterozygosity can be identified in cancers by noting the presence of heterozygosity at a genetic locus in an organism's germline DNA, and the absence of heterozygosity at that locus in the cancer cells. This is often done using polymorphic markers, such as microsatellites or single-nucleotide polymorphisms, for which the two parents contributed different alleles. Genome-wide LOH status of fresh or paraffin embedded tissue samples can be assessed by virtual karyotyping using SNP arrays. In asexual organisms It has been proposed that LOH may limit the longevity of asexual organisms. The minor allele in heterozygous areas of the genome is likely to have mild fitness consequences compared to de-novo mutations because selection has had time to remove deleterious alleles. When allelic gene conversion removes the major allele at these sites organisms are likely to experience a mild decline in fitness. Because LOH is much more common than de-novo mutation, and because the fitness consequences are closer to neutrality, this process should drive Muller's ratchet more quickly than de-novo mutations. While this process has received little experimental investigation,