Korean J Gynecol Oncol.  2007 Jun;18(2):139-145.

Promoter hypermethylation and loss of heterozygosity of FHIT genes in squamous cell carcinoma of uterine cervix

Affiliations
  • 1Department of Obstetrics and Gynecology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. bgkim@smc.samsung.co.kr

Abstract


OBJECTIVE
This study was to investigate the status of hypermethylation and loss of heterozygosity (LOH) in chromosome 3p tumor-suppressor gene for cervical carcinoma.
METHODS
We examined the promoter methylation status of the chromosome 3p gene, fragile histidine triad (FHIT), in 37 samples of cervical squamous cell carcinoma and corresponding noncancerous tissues using a methylation-specific polymerase chain reaction. We also analyzed the 37 paired samples for LOH at two loci on chromosome 3p.
RESULTS
Promoter hypermethylation in FHIT was detected in 24% of tumors, whereas no hypermethylation was detected in the corresponding noncancerous tissues. LOH in the regions of FHIT was observed in 10% of informative cases. There were no correlations between LOH and promoter hypermethylation for the gene. FHIT hypermethylation was associated with small tumors and, when adjusted for tumor size, correlated significantly with more frequent lymph node metastasis.
CONCLUSION
Promoter hypermethylation and LOH of FHIT gene may play a role in cervical carcinogenesis. In addition, hypermethylation of FHIT may be associated with the status (aggressiveness) of cervical carcinoma.

Keyword

Promoter hypermethylation; Loss of heterozygosity; FHIT; Cervical squamous cell carcinoma

MeSH Terms

Carcinogenesis
Carcinoma, Squamous Cell*
Cervix Uteri*
Female
Histidine
Loss of Heterozygosity*
Lymph Nodes
Methylation
Neoplasm Metastasis
Polymerase Chain Reaction
Histidine
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