Scientists at Thomas Jefferson University in Philadelphia, the University Hospital of Iceland in Reykjavik, and the National Human Genome Research Institute in Bethesda have found further evidence linking damage to the tumor suppressor gene FHIT to the development of breast cancer.
In a study of 92 Icelandic women, the researchers, led by Kay Huebner, Ph.D., professor of microbiology and immunology at Jefferson Medical College and a member of Jefferson's Kimmel Cancer Center, showed reduced levels of Fhit, the protein for which FHIT encodes, both in women with sporadic breast cancer and those with hereditary breast cancer who carry a BRCA2 mutation, a gene predisposing them to develop the disease. Among the 58 sporadic and 34 BRCA2-associated breast cancers, Dr. Huebner's team reports a "significant association" between damage to the FHIT gene at its most fragile area and a reduced expression of the Fhit protein.
She reports her team's work April 13 at the American Association for Cancer Research meeting in Philadelphia.
"Genetic alterations at this most common fragile site in the FHIT gene lead to reduced Fhit protein expression in sporadic cancers and in a much larger fraction of BRCA2-associated familial cancer," Dr. Huebner explains. "This is consistent with the idea that loss of BRCA2 function affects the stability of the FHIT site."
An improved understanding of the FHIT gene may lead to the identification of individuals predisposed to some of the most common human cancers, the development of new drugs that may arrest the growth of cancer cells, and prevention of some of the most common cancers.
In 1996, Dr. Huebner and Carlo M. Croce, M.D., director of the Kimmel
Cancer Center, and professor and chair of microbiology and immunology at
Jefferson Medical College, identified and characterized FHIT . The investigators
found that the FHIT gene is located in the human genome's most fragile area, on
Contact: Steve Benowitz
Thomas Jefferson University