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• W2588665844 abstract "<i>FHIT</i>, located at FRA3B, is one of the most commonly deleted genes in human cancers, and loss of FHIT protein is one of the earliest events in cancer initiation. However, location of <i>FHIT</i> at a chromosomal fragile site, a locus prone to breakage and gap formation under even mild replication stress, has encouraged claims that FHIT loss is a passenger event in cancers. We summarize accumulated evidence that FHIT protein functions as a genome “caretaker” required to protect the stability of genomes of normal cells of most tissues from agents causing intrinsic and extrinsic DNA damage. FHIT loss leads to intracellular replication stress and subsequent genome instability, which provides an opportunistic mutational landscape in preneoplasias for selection of a variety of other cancer-driving mutations. We also review evidence showing that FHIT loss leads to enhanced activation of other common fragile sites, including the FRA16D/<i>WWOX</i> locus, and creates optimal single-stranded DNA substrates for the hypermutator enzyme, APOBEC3B." @default.
• W2588665844 created "2017-02-24" @default.
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• W2588665844 date "2016-01-01" @default.
• W2588665844 modified "2023-10-01" @default.
• W2588665844 title "Fragile Genes That Are Frequently Altered in Cancer: Players Not Passengers" @default.
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• W2588665844 doi "https://doi.org/10.1159/000455753" @default.
• W2588665844 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28199992" @default.
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