FHIT基因研究进展

林亚华 叶巧滔

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FHIT基因研究进展

    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。;
  • 中图分类号: Q334+.13

Advances of FHIT gene

  • CLC number: 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。
  • [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.
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出版历程
  • 收稿日期:  2001-04-25

FHIT基因研究进展

    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。
  • 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

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。

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