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FHIT gene abnormalities in both benign and malignant thyroid tumours
1Department of Biological and Medical Research (MBC-03), King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia.
Summary
The FHIT gene, a tumor suppressor, shows alterations in various thyroid tumors, suggesting its inactivation is an early event in thyroid neoplasm development. Its absence in follicular thyroid carcinoma indicates other tumor suppressor genes may be involved.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The FHIT gene, located at 3p14.2, is a candidate tumor suppressor gene frequently deleted in human cancers.
- Loss of heterozygosity (LOH) at 3p14.2 is common in follicular thyroid carcinoma (FTC).
Purpose of the Study:
- To investigate the role of the FHIT gene in thyroid tumorigenesis.
- To identify genetic alterations in FHIT within various thyroid tumor types.
Main Methods:
- Analysis of 57 thyroid tumor specimens and 2 thyroid carcinoma cell lines.
- Techniques included RT-PCR, sequencing, SSCP, and Southern blot analysis.
Main Results:
- Truncated FHIT transcripts were detected in benign adenomas (38%), papillary carcinomas (23%), anaplastic carcinomas (40%), and cell lines.
- Intragenic homozygous deletions of FHIT were found in two papillary thyroid carcinoma specimens.
- FHIT gene alterations were absent in follicular thyroid carcinoma specimens.
Conclusions:
- FHIT gene inactivation appears to be an early event in the pathogenesis of some thyroid neoplasms.
- The absence of FHIT defects in FTC suggests the involvement of other tumor suppressor genes in its development.