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Role of FHIT in Human Cancer

From the The Kimmel Cancer Center, Jefferson Medical College, Philadelphia, PA, and Istituto Nazionale dei Tumori, Milan, Italy.

Address reprint requests to Carlo M. Croce, MD, Thomas Jefferson Medical College, 233 South 10th St, BLSB, Rm 1050, Philadelphia, PA 19107-5799.

ABSTRACT

ABSTRACT: Through investigation of hemizygous and homozygous deletions in common human cancers, including lung cancer, we have cloned and characterized a gene at chromosome region 3p14.2, FHIT, that is inactivated in epithelial tumors, particularly in tumors resulting from exposure to environmental carcinogens. In some tumors, particularly those associated with environmental carcinogens, alterations in the FHIT gene occur quite early in the development of cancer. In other cancers, Fhit inactivation seems to be a later event, possibly associated with progression to more aggressive neoplasias. Thus, detection of Fhit expression by immunohistochemistry in premalignant and malignant tissues may provide important diagnostic and prognostic information.

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