The role of the FHIT/FRA3B locus in cancer

Kay Huebner, Preston N. Garrison, Larry D. Barnes, Carlo M. Croce

Research output: Contribution to journalReview articlepeer-review

179 Scopus citations


Common fragile sites form gaps at characteristic chromosome bands in metaphases from normal cells after aphidicolin induction. The distribution of common fragile sites parallels the positions of neoplasia-associated chromosomal rearrangements, prompting the proposal that fragility disposes to chromosomal rearrangements. Implicit in this hypothesis is that genes at fragile sites are altered by chromosome rearrangement and thus contribute to neoplastic growth. Chromosome band 3p14.2, encompassing the most inducible common fragile region, FRA3B, has been cloned and the FHIT gene, straddling FRA3B, characterized. The gene is inactivated by deletions in cancer-derived cell lines and primary tumors and Fhit protein is absent or reduced in lung, stomach, kidney, and cervical carcinomas, consistent with function as a tumor suppressor. FRA3B thus fulfills the prophecy that fragile site alterations contribute to the neoplastic process through inactivation of a tumor suppressor gene.

Original languageEnglish (US)
Pages (from-to)7-31
Number of pages25
JournalAnnual Review of Genetics
StatePublished - 1998


  • Diadenosine polyphosphate hydrolases
  • Environmental carcinogens
  • Fragile sites
  • HIT gene family
  • Kidney carcinoma
  • Lung carcinoma
  • Tumor suppressor

ASJC Scopus subject areas

  • Genetics


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