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The loss of heterozygosity is a common occurrence in cancer development. Originally, a heterozygous state is required and indicates the absence of a functional tumor suppressor gene copy in the region of interest.
The FAT1 cadherin has been ascribed both as putative tumour suppressor or oncogene in different contexts. Loss of heterozygosity for FAT1 has been reported in primary oral carcinomas [20] and astrocytic tumours. [21] There are also reports of over expression of FAT1 in different cancers including DCIS breast cancer, [22] melanoma, [15] and ...
First, the genetic loci coding for PHLPP1 and 2 are commonly lost in cancer. The region including PHLPP1, 18q21.33, commonly undergoes loss of heterozygosity in colon cancers, while 16q22.3, which includes the PHLPP2 gene, undergoes LOH in breast and ovarian cancers, Wilms tumors, prostate cancer and hepatocellular carcinoma. [1]
For example, SNP arrays can be used to study loss of heterozygosity (LOH). LOH occurs when one allele of a gene is mutated in a deleterious way and the normally-functioning allele is lost. LOH occurs commonly in oncogenesis. For example, tumor suppressor genes help keep cancer from developing.
Thus, loss of any of these processes (arising from loss of ARHI) can lead to cancer. The "ARHI" gene is maternally imprinted (expressed monoallelically) and mapped specifically to 1p31, which is a common site for loss of heterozygosity (LOH). This locus on chromosome 1 is the most frequent deletion in breast and ovarian cancers.
The human DLC1 gene is located on the short arm of chromosome 8 (8p21.3-22), within a region that frequently undergoes loss of heterozygosity by either genomic deletion or epigenetic silencing mechanisms in several types of solid cancers. [8]
It was later found that carcinogenesis (the development of cancer) depended both on the mutation of proto-oncogenes (genes that stimulate cell proliferation) and on the inactivation of tumor suppressor genes, that keep proliferation in check. Knudson's hypothesis refers specifically, however, to the heterozygosity of tumor suppressor genes.
The deregulation of beta-catenin is an important event in the genesis of a number of malignancies. The AXIN2 gene has been mapped to 17q23-q24, a region that shows frequent loss of heterozygosity in breast cancer, neuroblastoma, and other tumors. Mutations in this gene have been associated with colorectal cancer with defective mismatch repair. [6]