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Replicative Stress and the FHIT Gene: Roles in Tumor Suppression, Genome Stability and Prevention of Carcinogenesis

Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA
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These authors contributed equally to this work.
Cancers 2014, 6(2), 1208-1219; https://doi.org/10.3390/cancers6021208
Received: 16 April 2014 / Revised: 21 May 2014 / Accepted: 26 May 2014 / Published: 4 June 2014
(This article belongs to the Special Issue Role of Oxidatively-Induced DNA Damage in Carcinogenesis)
The fragile FHIT gene, encompassing the chromosomal fragile site FRA3B, is an early target of DNA damage in precancerous cells. While vulnerable to DNA damage itself, FHIT protein expression is essential to protect from DNA damage-induced cancer initiation and progression by modulating genome stability, oxidative stress and levels of accumulating DNA damage. Thus, FHIT, whose expression is lost or reduced in many human cancers, is a tumor suppressor and genome caretaker whose loss initiates genome instability in preneoplastic lesions. Ongoing studies are seeking more detailed understanding of the role of FHIT in the cellular response to oxidative damage. This review discusses the relationship between FHIT, reactive oxygen species production, and DNA damage in the context of cancer initiation and progression. View Full-Text
Keywords: oxidative stress; reactive oxygen species; common fragile sites; genome instability oxidative stress; reactive oxygen species; common fragile sites; genome instability
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Karras, J.R.; Paisie, C.A.; Huebner, K. Replicative Stress and the FHIT Gene: Roles in Tumor Suppression, Genome Stability and Prevention of Carcinogenesis. Cancers 2014, 6, 1208-1219.

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