FHIT as tumor suppressor: mechanisms and therapeutic opportunities.
Chromosomal abnormalities including homozygous deletions and loss of heterozygosity at 3p l4.2 are commonly observed in most human tumors, including lung, breast and kidney cancers. This region also contains the most common human fragile site FRA3B, a familial kidney cancer-associated translocation breakpoint and papilloma virus integration sites. The FHIT gene is a tumor suppressor, which is frequently inactivated by mentioned genomic alterations at 3pl4.2. In the last few years considerable amount of data describing inactivation of FHIT in a variety of human malignancies and demonstrating the tumor suppressor potential of Fhit has accumulated. However, these have not yet led to major advances in uncovering the precise molecular mechanism of Fhit action. This review focuses on the most recent progress in understanding of Fhit function as a tumor suppressor and opportunities for gene cancer therapy with Fhit.
Pekarsky
Yuri
Y
Kimmel Cancer Center; Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Palamarchuk
Alexey
A
Huebner
Kay
K
Croce
Carlo M
CM
D017766:Acid Anhydride Hydrolases; D000818:Animals; D002471:Cell Transformation, Neoplastic; D002869:Chromosome Aberrations; D002893:Chromosomes, Human, Pair 3 / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor / Q000502:physiology*; D006801:Humans; D019656:Loss of Heterozygosity; D051379:Mice; D018345:Mice, Knockout; D009363:Neoplasm Proteins / Q000502:physiology*; D009369:Neoplasms / Q000378:metabolism* / Q000628:therapy*; D000099170:Bis(5'-adenosyl)triphosphatase
D017766:Acid Anhydride Hydrolases; D009363:Neoplasm Proteins; D000099170:Bis(5'-adenosyl)triphosphatase