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FHIT Gene Expression in Human Ovarian, Endometrial, and Cervical Cancer Cell Lines¹

Medicine Branch, Division of Clinical Sciences, National Cancer Institute, NIH, Rockville, Maryland 20850 [D. T. H., M. J. B.]; and Department of Obstetrics and Gynecology/Gynecological Oncology, Walter Reed Army Medical Center, Washington, District of Columbia 20307 [R. T., M. R.]

¹The fragile histidine triad (FHIT) gene, located at 3p14.2, has been shown to be altered in numerous epithelial cancers. Because previous studies have shown a loss of heterozygosity and cytogenetic abnormalities at the 3p region in ovarian, endometrial, and cervical carcinomas, we examined the status of the FHIT gene in 14 ovarian, 8 cervical, and 4 endometrial human cancer cell lines. RNA was isolated and subjected to reverse transcription-PCR to amplify the FHIT gene transcript. Sixty-three % (5 of 8) of cervical cell lines, 14% (2 of 14) of ovarian cell lines, and none (0 of 4) of the endometrial cell lines displayed aberrantly migrating FHIT transcripts. DNA sequencing demonstrated that the aberrantly migrating bands primarily lacked exons 5, 6, and 7 (with other exon losses also observed), resulting in shorter mRNA transcripts. Southern blot analysis of DNA from five of the cervical carcinomas demonstrated alterations in four of them, three of which had exhibited no normally sized FHIT transcripts. The results suggest that the expression of the FHIT gene may be altered in cervical tumor tissue, potentially implicating this gene in cervical tumorigenesis, whereas the involvement of this gene appears to be less important in the development of ovarian and endometrial cancer.

¹ The views expressed herein are those of the authors and are not intended to reflect the opinion or official policy of the Department of the Army, the Department of the Navy, the Department of Defense, or the U.S. Government.

² Visiting Fellow in the Oncology Research Faculty Development Program.

³ To whom requests for reprints should be addressed.

Received 1/14/97. Accepted 4/18/97.

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