Encyclopedia of Cancer

Living Edition
| Editors: Manfred Schwab

Fragile Histidine Triad

Living reference work entry
DOI: https://doi.org/10.1007/978-3-642-27841-9_2261-2

Synonym

Definition

In 1996, the first gene spanning a common fragile site (CFS) was reported and named FHIT (fragile histidine triad), owing to the fragility of the gene locus and sequence homology to members of the histidine triad (HIT) family of enzymes. The FHIT gene is located at chromosome band 3p14.2 and overlaps one of the most active CFSs, FRA3B. Alterations, such as deletions, at FRA3B occur early and frequently in over 50 % of cancers of epithelial origin, including but not limited to the lung, breast, throat, esophagus, throat, stomach skin, pancreas, cervix, and kidney. The FRA3B core overlaps FHIT exons 4–6, thus leading to reduction or complete loss of FHIT gene and protein expression in many cancers. Figure 1 illustrates the structure of the FHIT gene and the positions of fragile region landmarks such as the familial renal cancer translocation and the human papillomavirus integration site. The right side of Fig. 1illustrates the types of biallelic deletions...

Keywords

Common Fragile Site FHIT Gene Fhit Protein Fhit Expression Fragile Histidine Triad 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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References

  1. Huebner K, Croce CM (2003) Cancer and the FRA3B/FHIT fragile locus: it’s a Hit. Br J Cancer 88:1501–1506PubMedPubMedCentralCrossRefGoogle Scholar
  2. Iliopoulos D, Guler G, Han S-Y et al (2006) Roles of fragile genes, FHIT and WWOX, in cancer. Cancer Lett 232:27–36PubMedCrossRefGoogle Scholar
  3. Taverniti V, Seraphin B (2015) Elimination of cap structures generated by mRNA decay involves the new scavenger mRNA decapping enzyme Aph1/FHIT together with DcpS. Nucleic Acids Res 43:482–492PubMedPubMedCentralCrossRefGoogle Scholar
  4. Trapasso F, Pichiorri F, Gasparo M Fhit interaction with ferredoxin reductase triggers generation of reactive oxygen species and apoptosis. J Biol chem 283:13736–44Google Scholar
  5. Waters CE, Saldivar JC, Amin ZA, Schrock MS, Huebner K (2014) FHIT loss-induced DNA damage creates optimal APOBEC substrates: insights into APOBEC-mediated mutagenesis. Oncotarget 6(5):3409–3419PubMedCentralCrossRefGoogle Scholar

See Also

  1. (2012) Caretaker genes. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 666. doi:10.1007/978-3-642-16483-5_860Google Scholar
  2. (2012) Common fragile sites. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 960. doi:10.1007/978-3-642-16483-5_1278Google Scholar
  3. (2012) FHIT. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 1394. doi:10.1007/978-3-642-16483-5_2168Google Scholar
  4. (2012) FRA3B. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 1447. doi:10.1007/978-3-642-16483-5_2259Google Scholar
  5. (2012) Genetic instability. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, pp 1527–1528. doi:10.1007/978-3-642-16483-5_2380Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2015

Authors and Affiliations

  1. 1.The Ohio State University College of MedicineColumbusUSA
  2. 2.Department of Molecular VirologyImmunology and Medical Genetics, Ohio State University Comprehensive Cancer CenterColumbusUSA