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Jennifer Boylston

Mentor: Charles Brenner, Ph.D.
Lab Room: 4-339 BSB
Lab Phone: 319-384-4099

Loss of FHIT contributes to carcinogenesis in epithelial cells

The fragile histidine triad gene (FHIT) is located on the most fragile site in the human genome. FHIT gene deletions are among the earliest and most frequent events in carcinogenesis, particularly in carcinogen-exposed lung and stomach tissue. FHIT- cells accumulate additional genetic changes, leading to cancer. FHIT has been shown to be an authentic tumor suppressor in mouse models and by re-expressing the gene in FHIT deficient cancer cell lines. Re-expression of FHIT in cell culture causes cell death via initiation of apoptosis, but the precise mechanism remains unknown. FHIT protein functions as a nucleotide hydrolase, but a connection between this activity and apoptosis is outstanding. We do know that delivery of catalytically inactive FHIT mutants to cells induces apoptosis, while delivery of mutants deficient in substrate binding does not. My current work is designed to establish the mechanism by which FHIT-nucleotide complexes protect cells from neoplastic transformation.

Boylston J, Brenner C. "FHIT," Encyclopedia of Signaling Molecules, S. Choi, ed, chapter 68, part 7, pp. 613-616 (2012). DOI: 10.1007/978-1-4419-0461-4_68.

Honors and Awards

  • Cancer Biology Training Grant, Dartmouth College, 2008-2009