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• W184031076 abstract "Cancer is the second leading cause of death in the United States, exceeded only by heart disease. In the United States, one of every four deaths is from cancer (1). It has been established that cancer is a genetic disease. Carcinogenesis can be promoted by a single dominant mutation leading to expression of an oncogene. Alternatively, according to the two-step mutation model proposed by Knudson in 1971 (2), cancer may arise when a recessive mutation in a tumor suppressor gene is expressed (3,4). In familial cancers, this occurs when an inherited mutation is followed by a loss of heterozygosity event removing the wildtype (Wt) allele of the gene. In sporadic cancers, a somatic mutation occurs in one allele followed by loss of heterozygosity of the second allele of a tumor suppressor gene. In a more complex model of tumorigenesis, cancer risk is enhanced by a deficiency in DNA repair. Loss of DNA repair function leads to accumulation of a high frequency of mutations, including tumor-promoting mutations. Such mutations can occur as point mutations or as result of large-scale chromosomal rearrangements, such as chromosomal deletions, duplications, and translocations. Cancer formation can be initiated by these events, if the deleted chromosomal region encodes a tumor suppressor gene or if an amplified region encodes an oncogene. In fact, the genomic instability resulting in loss and gain of whole chromosomes or large portions thereof has been observed in the majority of tumors (5). Such rearrangements can lead to gene disruptions that inactivate a tumor suppressor gene or alter the function of a proto-oncogene. DNA is subject to continuous damage by noxious exogenous chemical and physical agents or oxygen radicals produced by the normal cellular metabolism. About 10,000 oxidative lesions are formed in our genome in each cell every day (6). In addition, some chemical bonds in DNA undergo spontaneous hydrolysis. The cell responds to DNA damage by inducing cell-cycle arrest and DNA repair or, when damage is too severe to be repaired, undergoes cellular death by apoptosis. There are four pathways for DNA repair, such as base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR) and double-stand-break (DSB) repair (7,8). DSBs are repaired by either nonhomologous end-joining (NHEJ) or homologous recombination (HR) (7,9–11). Several inherited syndromes associated with a markedly elevated incidence of cancer involve genes that are essential in DNA repair (Table 1). These include xeroderma pigmentosum (XP)," @default.
• W184031076 created "2016-06-24" @default.
• W184031076 creator A5007306838 @default.
• W184031076 creator A5042838200 @default.
• W184031076 date "2004-01-01" @default.
• W184031076 modified "2023-10-01" @default.
• W184031076 title "DNA Repair Defects in Cancer" @default.
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