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Review
FHIT as Tumor Suppressor: Mechanisms and Therapeutic Opportunities
Yuri Pekarsky, Alexey Palamarchuk, Kay Huebner and Carlo M. Croce
volume 1 | issue 3
May/June 2002Pages: 232-235
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Chromosomal abnormalities including homozygous deletions and loss of heterozygosity at 3p14.2 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 3p14.2. 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.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDFIf the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.