Expression and significance of fragile histidine triad in oral cancer and precancerous lesions

Abstract

Abstract: Objective To detect the expression of fragile histidine triad (FHIT) in oral cancer and oral precancerous lesions and investigate the relationship between the FHIT expression and the histopathological changes.Methods Immunohistochemical staining by SP methods was utilized to detect the expression of FHIT in 64 cases of oral squamous cell carcinoma, 39 oral precancerous lesions and 12 normal oral mucosa specimens.Results The positivity rate of FHIT in normal oral membrane was 100% (12/12), and medium and high FHIT expression levels were detected in oral precancerous lesions but without significant difference from that in normal oral mucosa. In 64 oral squamous cell carcinoma specimens, 3 were negative for FHIT expression, 8 had low expression, and the other 43 had moderate and high expression. The rate of negative or low FHIT expression in the oral squamous cell carcinoma was 17% (11/64), which was significantly different from that in the normal oral mucosa and oral precancerous lesions, but the rate was not correlated to the differentiation of the cancer.Conclusion The tumor suppressor gene FHIT plays a role in the pathogenesis of oral squamous cell carcinoma.

CLC Number:

R781

YIN Cao¹, SHEN Li-jia², XIE Si-ming², RUAN Ping², YAO Xi². Expression and significance of fragile histidine triad in oral cancer and precancerous lesions[J]. Journal of Southern Medical University, 2005, 25(05): 584-586.

References

[1] Ohta M, Inoue H, Cotticelli MG, et al. The FHIT gene, spanning the chromosome 3p14.2 fragile site and renal carcinoma associated t (3;8) breakpoint, is abnormal in digestive tract cancers[J]. Cell, 1996,84(4): 587-97.
[2] MurphyGA, HallidayD, MclennanAG, et al. The Fhit tumor suppressor protein regulates the intracellular concentration of diadenosine triphosphate but not diadenosine tetraphosphate [J].Cancer Res, 2000, 60(9): 2342-4.
[3] 蔡清萍,王强,王梁华,等.人胰腺癌细胞FHIT基因转染对肿瘤坏死因子敏感性的影响[J].中华实验外科杂志,2002,19(2):1634.Cai QP, Wang Q, Wang LH, et al. Effects of FHIT gene transfection into human pancreatic adenocarcinoma cells on tumor necrosis factor sensitivity[J]. Chin J Exp Surg, 2002, 19(2): 163-4.
[4] Sard L, Accornero P, Tornielli S, et al. The tumor-suppressor gene FHIT is involved in the regulation of apoptosis and in cell cycle control [J]. Proc Natl Acad Sci USA, 1999, 6: 8489-92.
[5] Uzawa N, Akanuma D, Negishi A, et al. Homozygous deletions on the short arm of chromosome 3 in human oral squamous cell carcinomas [J]. Oral Oncol, 2001, 37(4): 351-6.
[6] Kannan K, Munirajan AK, Bhuvarahamurthy V, et al. FHIT gene mutations and single nucleotide polymorphism in Indian oral and cervical squamous cell carcinomas[J]. Oral Oncol, 2000, 36(2): 189-93.
[7] Tanimoto K, Hayashi S, Tsuchiya E, et al. Abnormalities of the FHIT gene in human oral carcinogenesis [J]. Br J Cancer, 2000, 82(4): 838-43.
[8] van Heerden WF, Swart T J, Robson B, et al. FHIT RNA and protein expression in oral squamous cell carcinomas [J]. Anticancer Res,2001, 21 (4A): 2425-8.
[9] van Heerden WF, Swart TJ, Van Heerden MB, et al. Fhit protein expression in oral epithelium: immunohistochemical evaluation of three antisera[J]. Anticancer Res, 2001, 21 (4A): 2419-23.
[10] Chang KW, Kao SY, Tzeng RJ, et al. Multiple molecular alterations of FHIT in betel-associated oral carcinoma [J]. J Pathol, 2002, 196(3): 300-6.
[11] Lee JI, Soria JC, Hassan K. Loss of fhit expression is a predictor of poor outcome in tongue cancer[J].Cancer Res, 2001, 61(3): 837-41.