[1]林亚华,叶巧滔.FHIT基因研究进展[J].国际放射医学核医学杂志,2001,25(6):275-279.
 LIN Ya-hua,YE Qiao-tao.Advances of FHIT gene[J].International Journal of Radiation Medicine and Nuclear Medicine,2001,25(6):275-279.
点击复制

FHIT基因研究进展(/HTML)
分享到:

《国际放射医学核医学杂志》[ISSN:1673-4114/CN:12-1381/R]

卷:
25
期数:
2001年第6期
页码:
275-279
栏目:
综述
出版日期:
1900-01-01

文章信息/Info

Title:
Advances of FHIT gene
作者:
林亚华1 叶巧滔2
1. 200433 上海, 第二军医大学海医系放射医学教研室;
2. 352102 福建 宁德, 中国人民解放军第442医院外科
Author(s):
LIN Ya-hua1 YE Qiao-tao2
1. Department of Radiation & nuclear medicine of The Second Military Medical University, Shanghai 200433, China;
2. Deprtment of Surgery, The 442 nd Hospital of PLA, Ningde Fujian 352102, China
关键词:
FHIT基因肿瘤抑制基因细胞凋亡肿瘤辐射
Keywords:
FHIT genetumor suppressor geneapoptosisneoplasmradiation
分类号:
Q334+.13
摘要:
FHIT基因是定位于染色体3p14.2区域的候选肿瘤抑制基因,在许多肿瘤,特别是环境致癌物引起的上皮肿瘤中经常发生改变,在辐射引起的癌症中也有改变,参与细胞周期和细胞凋亡的调控,但其作用的机理尚未完全阐明。
Abstract:
The FHIT gene located at chromosome 3p14.2 is a putative tumor suppressor gene. It is frequently altered in many tumors, particularly in tumors resulting from exposing to environmental carcinogens.In tumor that is caused by radiation, the FHIT gene is also altered. It is involved in the regulation of apoptosis and in cell cycle control. However, its mechanism is not completely clarified.

参考文献/References:

[1] Ohta M, Inoue H, Cotticelli WG, 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):587-597.
[2] Sard L, Accornero P, Tornielli S, et al.The tumorsuppressor gene FHIT is involved in the regulation of apoptosis and in cell cycle control[J].Proc Natl Acad Sci USA, 1999, 96(15):8489-8492.
[3] Ji L, Fang B, Yen N, et al.Induction of apoptosis and inhibition of tumorigenicity and tumor growth by adenovirus vector-mediated fragile histidine triad (FHIT) gene overexpression[J].Cancer Res, 1999, 59(14):3333-3339.
[4] Barnes LD, Garrison PN, Siprashvili Z, et al.Fhit, a putative tumor suppressor in humans, is a dinucleoside 5’, 5’’’-P1, P3-triphosphate hydrolase[J].Biochemistry, 1996, 35(36):11529-11535.
[5] Siprashvili Z, Sozzi G, Barnes LD, et al.Replacement of Fhit in cancer cells suppresses tumorigenicity[J].Proc Natl Acad Sci USA, 1997, 94(25):13771-13776.
[6] Pace HC, Garrison PN, Robinson AK, et al.Genetic, biochemical, and crystallographic characterization of Fhit-substrate complexes as the active signaling form of Fhit[J].Proc Natl Acad Sci USA, 1998, 95(10):5484-5489.
[7] Morikawa H, Nakagawa Y, Hashimoto K, et al.Frequent altered expression of fragile histidine triad protein in human colorectal adenomas[J].Biochcm Biophys Res Comrmn, 2000, 278(1):205-210.
[8] Otterson GA, Xiao GH, Geradts J, et al.Protein expression and functional analysis of the FHIT gene in human tumor cells[J].J Natl Cancer Inst, 1998, 90(6):426-432.
[9] Pekarsky Y, Campiglio M, Siprashvili Z, et al.Nitrilase and Fhit homologs are encoded as fusion proteins in Drosophila melanogaster and Caenorhabditis elegans[J].Proc Natl Acad Sci USA, 1998, 95(15):8744-8749.
[10] Garinis GA, Gorgoulis VG, Mariatos G, et al.Association of allelic loss at the FHIT locus and p53 alterations with tumour kinetics and chromesomal instability in non-small cell lung carcinomas (NSCLCs)[J].JPathol, 2001, 193(1):55-65.
[11] Gemma A, Hagiwara K, Ke Y, et al.FHIT mutations in human primary gastric cancer[J].Cancer Res, 1997, 57(8):1435-1437.
[12] Sozzi G, Veronese ML, Negrini M, et al.The FHIT gene 3p14.2 is abnormal in lung cancer[J].Cell, 1996, 85(1):17-26.
[13] Sozzi G, Sard L, De Gregorio L, et al.Association between cigarette smoking and FHIT gene alterations in lung cancer[J].Cancer Res, 1997, 57(11):2121-2123.
[14] Nelson HH, Wiencke JK, Gunn L, et al.Chromosome 3p14 alterations in lung cancer evidence that FHIT exon deletion is a target of tobacco carcinogens and asbestos[J].Cancer Res, 1998, 58(9):1804-1807.
[15] Fang JM, Arlt MF, Burgess AC, et al.Translocation breakpoints in FHIT and FRA3B in both homologs of chromosome 3 in an esophageal adenocarcinoma[J].Genes Chromosomes Cancer, 2001, 30(3):292-298.
[16] Campiglio M, Pekarsky Y, Menard S, et al.FHIT loss of function in human primary breast cancer correlates with advanced stage of the disease[J].Cancer Res, 1999, 59(16):3866-3869.
[17] Huiping C, Jonasson JG, Agnarsson BA, et al.Analysis of the fragile histidine triad (FHIT) gene in lobular breast cancer[J].Eur J Cancer, 2000, 36(12):1552-1557.
[18] Baffa R, Gomella LG, Vecchione A, et al.Loss of FHIT expression in transitional cell carcinoma of the urinary hladder[J].Am J Pathol, 2000, 156(2):419-424.
[19] Louhelainen J, Wijkstrom H, Hemminki K, et al.Multiple regions with allelic loss at chromosome 3 in superficial multifocal bladder tumors[J].Int J Oncol, 2001, 18(1):201-210.
[20] Dano L, Guilly MN, Muleris M, et al.CGH analysis of radon-induced rat lung tumors indicates similarities with human lung cancers[J].Genes Chromosomes Cancer, 2000, 29(1):1-8.

备注/Memo

备注/Memo:
收稿日期:2001-4-25。
作者简介:林亚华(1973-),男,福建莆田人,硕士研究生,主要从事辐射致癌机理的研究;叶巧滔(1975-),女,福建古田人,中国人民解放军第422医院外科护师。
更新日期/Last Update: 1900-01-01