口腔癌及癌前病变中脆性组氨酸三联体基因的表达及其意义

南方医科大学学报 ›› 2005, Vol. 25 ›› Issue (05): 584-586.

口腔癌及癌前病变中脆性组氨酸三联体基因的表达及其意义

殷操¹, 沈丽佳², 谢思明², 阮萍², 姚希²

1. 广东省口腔医院, 广东, 广州, 510280;
2. 暨南大学医学院口腔医学系, 广东, 广州, 510632

出版日期:2005-05-20 发布日期:2005-05-20
基金资助:
收稿日期:2004-11-5。
作者简介:殷操(1965- ),男,硕士,广东省口腔医院口腔粘膜病科主任,副主任医师,联系电话:020-84427024;E-mail:yin9731@hotmail.com

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

YIN Cao¹, SHEN Li-jia², XIE Si-ming², RUAN Ping², YAO Xi²

1. 广东省口腔医院, 广东, 广州, 510280;
2. 暨南大学医学院口腔医学系, 广东, 广州, 510632

Online:2005-05-20 Published:2005-05-20

摘要/Abstract

摘要： 目的检测抑癌基因脆性组氨酸三联体基因(FHIT)在口腔鳞状细胞癌(OSCC)及癌前病变中的表达情况,并探讨其在口腔癌发生过程中的作用及其意义.方法采用SP免疫组化方法检测64例OSCC、9例口腔癌前病变、12例正常粘膜中FHIT蛋白情况的表达.结果正常粘膜的FHIT蛋白100%(12/12)高表达;癌前病变组中均为中度和高表达,与正常组相比无统计学差异;64例OSCC中,例为阴性表达、8例低表达、4例中度和高度表达;OSCC中FHIT蛋白缺乏或减少的比率为17%(11/64),与正常组、癌前病变组相比有显著差异,而与OSCC的分化程度无关.结论 FHIT在口腔鳞癌的发生过程中起着一定的作用.

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.

中图分类号:

R781

殷操¹, 沈丽佳², 谢思明², 阮萍², 姚希². 口腔癌及癌前病变中脆性组氨酸三联体基因的表达及其意义[J]. 南方医科大学学报, 2005, 25(05): 584-586.

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.

参考文献

[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.