FRA3B and other common fragile sites: the weakest links (original) (raw)
Cohen, A. J. et al. Hereditary renal-cell carcinoma associated with a chromosomal translocation. N. Engl. J. Med.301, 592–595 (1979). CASPubMed Google Scholar
Glover, T. W., Berger, C., Coyle, J. & Echo, B. DNA polymerase-α inhibition by aphidicolin induces gaps and breaks at common fragile sites in human chromosomes. Hum. Genet.67, 136–142 (1984).Reports that the breaks and gaps induced by aphidicolin represent a new class of fragile sites: the common fragile sites. CASPubMed Google Scholar
Yunis, J. J. & Soreng, A. L. Constitutive fragile sites and cancer. Science226, 1199–1204 (1984).Notes that locations of about half of the common fragile sites seem cytogenetically to coincide with locations of specific chromosome translocations that are associated with human cancers and might be near proto-oncogenes. CASPubMed Google Scholar
Ohta, M. 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. Cell84, 587–597 (1996).Reports the cloning of theFHITgene, the t(3;8) translocation, theFRA3Bfragile site and homozygous deletions in cancer cells. CAS Google Scholar
Zimonjic, D. B. et al. Positions of chromosome 3p14.2 fragile sites (FRA3B) within the FHIT gene. Cancer Res.57, 1166–1170 (1997). CASPubMed Google Scholar
Huebner, K., Sozzi, G., Brenner, C., Pierotti, M. A. & Croce, C. M. Fhit loss in lung cancer: diagnostic & therapeutic implications. Adv. Oncol.15, 3–10 (1999). Google Scholar
Croce, C. M., Sozzi, G. & Huebner, K. Role of FHIT in human cancer. J. Clin. Oncol.17, 1618–1624 (1999). CASPubMed Google Scholar
Siprashvili, Z. et al. Replacement of Fhit in cancer cells suppresses tumorigenicity. Proc. Natl Acad. Sci. USA94, 13771–13776 (1997).The first report of suppression of cancer-cell tumorigenicity by overexpression of exogenousFhit. CASPubMed Google Scholar
Sard, L. et al. The tumour-suppressor gene FHIT is involved in the regulation of apoptosis and in cell cycle control. Proc. Natl Acad. Sci. USA96, 8489–8492 (1999). CASPubMed Google Scholar
Ji, L. et al. Induction of apoptosis and inhibition of tumorigenicity & tumour growth by adenovirus vector-mediated fragile histidine triad (FHIT) gene overexpression. Cancer Res.59, 3333–3339 (1999).The first report of induction of apoptosis in cancer cells that are transfected with an adenovirus that encodesFHIT. CASPubMed Google Scholar
Richards, R. I. Fragile and unstable chromosomes in cancer: causes and consequences. Trends Genet.17, 339–345 (2001). CASPubMed Google Scholar
Glover, T. W. in Genetic Instabilities and Neurological Diseases (eds Wells, R. D & Warren, S. T.) 75–83 (Academic, San Diego, 1998). Google Scholar
Kuwano, A. & Kajii, T. Synergistic effect of aphidicolin and ethanol on the induction of common fragile sites. Hum. Genet.75, 75–78 (1987). CASPubMed Google Scholar
Dan, S., Cologne, J. B. & Nefushi, K. Effect of radiation and cigarette smoke on expression of FUdR-inducible common fragile sites in human peripheral lymphocytes. Mutat. Res.334, 197–203 (1995). Google Scholar
Glover, T. W. & Stein, C. K. Chromosome breakage and recombination at fragile sites. Am. J. Hum. Genet.43, 265–273 (1988). CASPubMedPubMed Central Google Scholar
Wang, N. D., Testa, J. R. & Smith, D. I. Determination of the specificity of aphidicolin-induced breakage of the human 3p14.2 fragile site. Genomics17, 341–347 (1993). CASPubMed Google Scholar
Rassool, F. V. et al. Preferential integration of marker DNA into the chromosomal fragile site at 3p14: an approach to cloning fragile sites. Proc. Natl Acad. Sci. USA88, 6657–6661 (1991). CASPubMed Google Scholar
Coquelle, A., Toledo, F., Stern, S., Bieth, A. & Debatisse, M. A new role for hypoxia in tumour progression: induction of fragile site triggering genomic rearrangements and formation of complex DMs & HSRs. Mol. Cell2, 259–265 (1998). CASPubMed Google Scholar
Inoue, H. et al. Sequence of the FRA3B common fragile region: implications for the mechanism of FHIT deletion. Proc. Natl Acad. Sci. USA94, 14584–14589 (1997). CASPubMed Google Scholar
Mimori, K. et al. Cancer specific chromosome alterations in the constitutive fragile region, FRA3B. Proc. Natl Acad. Sci. USA96, 7456–7461 (1999). CASPubMed Google Scholar
Mishmar, D. et al. Molecular characterization of a common fragile site (FRA7H) on human chromosome 7 by the cloning of a simian virus 40 integration site. Proc. Natl Acad. Sci. USA95, 8141–8146 (1998).Reports cloning and characterization ofFRA7H. CASPubMed Google Scholar
Huang, H. et al. Frequent deletions within FRA7G at 7q31.2 in invasive epithelial ovarian cancer. Genes Chromosom. Cancer24, 48–55 (1999). CASPubMed Google Scholar
Tatarelli, C., Linnenbach, A., Mimori, K. & Croce, C. M. Characterization of the human testin gene localized in the FRA7G region at 7q31.2. Genomics68, 1–12 (2000).References22and23report the cloning and partial characterization ofFRA7G. CASPubMed Google Scholar
Ried, K. et al. Common chromosomal fragile site FRA16D sequence: identification of the FOR gene spanning FRA16D and homozygous deletions and translocation breakpoints in cancer cells. Hum. Mol. Genet.9, 1651–1663 (2000). CASPubMed Google Scholar
Arlt, M. F., Miller, D. E., Beer, D. G. & Glover, T. W. Molecular characterization of FRAXB and comparative common fragile site instability in cancer cells. Genes Chromosom. Cancer33, 82–92 (2002).Identification and sequencing of theFRAXBregion, and characterization of deletions inFRAXBin oesophageal cancer cells. CASPubMed Google Scholar
Glover, T. W. et al. The murine Fhit gene is highly similar to its human ortholog and maps to a common fragile site region. Cancer Res.58, 3409–3414 (1998).Reports that the mouse orthologue ofFhitalso encompasses a fragile site:Fra14A2. CASPubMed Google Scholar
Shiraishi, T. et al. Sequence conservation at human and mouse orthologous common fragile regions, FRA3B/FHIT and Fra14A2/Fhit. Proc. Natl Acad. Sci. USA98, 5722–5727 (2001).The first comparison of orthologous fragile-site sequences of two species, mouse and human. CASPubMed Google Scholar
Laird, C., Jaffe, E. Karpsen, G., Lamb, M. & Nelson, R. Fragile sites in human chromsomes as regions of late-replicating DNA. Trends Genet.3, 274–281 (1987).Indicates that fragile sites replicate late in the cell cycle and that, during replication stress, condensation of sequences might not be complete, causing the appearance of a fragile site. CAS Google Scholar
Le Beau, M. M. et al. Replication of a common fragile site, FRA3B, occurs late in S phase and is delayed further upon induction: implications for the mechanism of fragile site induction. Hum. Mol. Genet.7, 755–761 (1998).Reports that delay of replication ofFRA3Bby aphidicolin causes fragile-site expression as gaps and breaks. CASPubMed Google Scholar
Li, F. P. et al. Clinical and genetic studies of renal cell carcinomas in a family with a constitutional chromosome 3;8 translocation. Ann. Intern. Med.118, 106–111 (1993). CASPubMed Google Scholar
Croce, C. M. Role of chromosome translocations in neoplasia. Cell49, 155–156 (1987). CASPubMed Google Scholar
Rowley, J. D. Chromosome translocations: dangerous liaisons revisited. Nature Rev. Cancer1, 245–250 (2001). CAS Google Scholar
Knudson, A. G. Mutation and cancer: statistical study of retinoblastoma. Proc. Natl Acad. Sci. USA68, 820–823 (1971). Google Scholar
Knudson, A. G., Hethcote, H. W. & Brown, B. W. Mutation and childhood cancer: a probabilistic model for the incidence of retinoblastoma. Proc. Natl Acad. Sci. USA72, 5116–5120 (1975). PubMed Google Scholar
Sozzi, G. et al. The FHIT gene at 3p14.2 is abnormal in lung cancer. Cell85, 17–26 (1996). CASPubMed Google Scholar
Werner, N. S. et al. Differentail susceptibility of renal carcinoma cell lines to tumour suppression by exogenous Fhit expression. Cancer Res.60, 2780–2785 (2000). CASPubMed Google Scholar
Otterson, G. A. et al. Protein expression and functional analysis of the FHIT gene in human tumour cells. J. Natl Cancer Inst.90, 426–432 (1998). CASPubMed Google Scholar
Wu, R., Connolly, D. C., Dunn, R. L. & Cho, K. R. Restored expression of fragile histidine triad protein and tumorigenicity of cervical carcinoma cells. J. Natl Cancer Inst.92, 338–344 (2000).Reports lack of suppression of tumorigenicity of some cancer cells afterFHITtransfections. CASPubMed Google Scholar
Ishii, H. et al. Effect of adenoviral transduction of FHIT into esophageal cancer cells. Cancer Res.61, 1578–1589 (2001). CASPubMed Google Scholar
Dumon, K. R. et al. FHIT expression delays tumour development and induces apoptosis in human pancreatic cancer. Cancer Res.61, 4827–4836 (2001). CASPubMed Google Scholar
Kholodnyuk, I. D., Szeles, A., Yang, Y., Klein, G. & Imreh, S. Inactivation of the human fragile histidine triad gene at 3p14.2 in monochromosomal human/mouse microcell hybrid-derived severe combined immunodeficient mouse tumours. Cancer Res.60, 7119–7125 (2000). CASPubMed Google Scholar
Barnes, L. D. et al. Fhit, a putative tumour suppressor in humans, is a dinucleoside 5,5′-P1,P3-triphosphate hydrolase. Biochemistry35, 11529–11535 (1996). CAS Google Scholar
Pace, H. C. et al. Genetic, biochemical and crystallographic definition of a substrate analog complex with the fragile histidine triad protein as the active signalling form of Fhit. Proc. Natl Acad. Sci. USA95, 5484–5489 (1998). CASPubMed Google Scholar
Pekarsky, Y. et al. Nitrilase and Fhit homologs are encoded as fusion proteins in Drosophila melanogaster and Caenorhabditis elegans. Proc. Natl Acad. Sci. USA95, 8744–8749 (1998). CASPubMed Google Scholar
Brenner, C., Bieganowski, P., Pace, H. C. & Huebner, K. The histidine triad superfamily of nucleotide-binding proteins. J. Cell. Physiol.181, 179–187 (1999). CASPubMedPubMed Central Google Scholar
Murphy, G. A., Halliday, D. & McLennan, A. G. The Fhit tumour suppressor protein regulates the intracellular concentration of diadenosine triphosphate but not diadenosine tetraphosphate. Cancer Res.60, 2342–2344 (2000). CASPubMed Google Scholar
Pace, H. C. & Brenner, C. The nitrilase superfamily: classification, structure and functions. Genome Biol.2, 0001.1–0001.9 (2001). Google Scholar
Chaudhuri, A. R. et al. The tumour suppressor protein Fhit. J. Biol. Chem.274, 24378–24382 (1999). CASPubMed Google Scholar
Pekarsky, Y. et al. The murine Fhit locus: isolation, characterization and expression in normal and tumour cells. Cancer Res.58, 3401–3408 (1998). CASPubMed Google Scholar
Fong, L. Y. Y. et al. Muir–Torre-like syndrome in Fhit deficient mice. Proc. Natl Acad. Sci. USA97, 4742–4747 (2000).Reports the development ofFhitknockout mice, their exquisite carcinogen susceptibility and development of a carcinogen-induced Muir–Torre-like syndrome. CASPubMed Google Scholar
Zanesi, N. et al. The tumour spectrum in Fhit deficient mice. Proc. Natl Acad. Sci. USA98,10250–10255 (2001).Provides evidence thatFhitmight be a one-hit tumour suppressor, at least in some mouse tissues. CASPubMed Google Scholar
Fero, M. L., Randel, E., Gurley, K. E., Roberts, J. M. & Kemp, C. J. The murine gene p27Kip1 is haplo-insufficient for tumour suppression. Nature396, 177–180 (1998). CASPubMedPubMed Central Google Scholar
Hilgers, W. et al. Genomic FHIT analysis in RER+ and RER− adenocarcinomas of the pancreas. Genes Chromosom. Cancer27, 239–243 (2000). CASPubMed Google Scholar
Mimori, K. et al. Absence of Msh2 protein expression is associated with alteration in the FHIT locus and Fhit protein expression in colorectal carcinoma. Cancer Res.61, 7379–7382 (2001). PubMed Google Scholar
Hansan, L.-E., Sparen, P. & Nyren, O. Increasing incidence of both major histological types of esophageal carcinomas among men in Sweden. Int. J. Cancer54, 402–407 (1993). Google Scholar
Mori, M. et al. Altered expression of Fhit in carcinoma and precarcinomatous lesions of the esophagus. Cancer Res.60, 1177–1182 (2000). CASPubMed Google Scholar
Michael, D., Beer, D. G., Wilke, C. W., Miller, D. E. & Glover, T. W. Frequent deletions of FHIT and FRA3B in Barrett's metaplasia and esophageal adenocarcinomas. Oncogene15, 1553–1559 (1997). Google Scholar
Schrump, D. S., Chen, G. A., Consuli, U., Jin, X. & Roth, J. A. Inhibition of esophageal cancer proliferation by adenovirally mediated delivery of p16INK4. Cancer Gene Ther.3, 357–364 (1996). CASPubMed Google Scholar
Dumon, K. R. et al. FHIT gene therapy prevents tumour development in Fhit-deficient mice. Proc. Natl Acad. Sci. USA98, 3346–3351 (2001).Reports prevention ofin vivocarcinogen-induced cancers in mice by infection withFhit-encoding adenoviruses. CASPubMed Google Scholar
Hellman, A. et al. Replication delay along FRA7H, a common fragile site on human chromosome 7, leads to chromosomal instability. Mol. Cell Biol.20, 4420–4427 (2000). CASPubMedPubMed Central Google Scholar
Hurlstone, A. F. et al. Analysis of the CAVEOLIN-1 gene at human chromosome 7q31.1 in primary tumours and tumour-derived cell lines. Oncogene18, 1881–1890 (1999). CASPubMed Google Scholar
Bednarek, A. K. et al. WWOX, a novel WW domain-containing protein mapping to human chromosome 16q23.3–24.1, a region frequently affected in breast cancer. Cancer Res.60, 2140–2145 (2000).Reports the cloning and preliminary characterization of theWWOXgene. CASPubMed Google Scholar
Paige, A. J. W. et al. A 700-kb physical map of a region of 16q23.2 homozygously deleted in multiple cancers and spanning the common fragile site FRA16D. Cancer Res.60, 1690–1697 (2000).Reports homozygous deletions inWWOXin cancer cells. CASPubMed Google Scholar
Mangelsdorf, M. et al. Chromosomal fragile site FRA16D and DNA instability in cancer. Cancer Res.60, 1683–1689 (2000).Reports thatWWOXencompassesFRA16D. CASPubMed Google Scholar
Chang, N.-S. et al. Hyaluronidase induction of a WW domain-containing oxidoreductase that enhances tumour necrosis factor cytotoxicity. J. Biol. Chem.276, 3361–3370 (2001). CASPubMed Google Scholar
Paige, A. J. W. et al. WWOX: a candidate tumour suppressor gene involved in multiple tumour types. Proc. Natl Acad. Sci. USA98, 11417–11422 (2001).ReportsWWOXdeletion in primary ovarian carcinoma. CASPubMed Google Scholar
Bednarek, A. K. et al. WWOX, the FRA16D gene, behaves as a suppressor of tumor growth. Cancer Res. (in the press). Reports that WWOX inhibits tumorigenicity of a breast cancer cell linein vivo.
Krummel, K. A., Roberts, L. R., Kawakami, M., Glover, T. W. & Smith, D. I. The characterization of the common fragile site FRA16D and its involvement in multiple myeloma translocations. Genomics69, 37–46 (2000). CASPubMed Google Scholar
Yakicier, M. C. et al. Identification of homozygous deletions at chromosome 16q23 in aflatoxin B1 exposed hepatocellular carcinoma. Oncogene20, 5232–5238 (2001). CASPubMed Google Scholar
Ingvarsson, S. et al. Reduced Fhit expression in familial and sporadic breast carcinomas. Cancer Res.59, 2682–2689 (1999). CASPubMed Google Scholar
Burke, L. et al. Allelic deletion analysis of the FHIT gene predicts poor survival in non-small cell lung cancer. Cancer Res.58, 2533–2536 (1998). CASPubMed Google Scholar
Tomizawa, Y. et al. Clinicopathological significance of Fhit protein expression in stage 1 non-small cell lung carcinoma. Cancer Res.58, 5478–5483 (1998). CASPubMed Google Scholar
Ingvarsson, S., Sigbjornsdottir, B. I., Huiping, C., Jonasson, J. G. & Agnarsson, B. A. Alterations of the FHIT gene in breast cancer: association with tumour progression and patient survival. Cancer Detect. Prev.25, 318–324 (2001). Google Scholar
Capuzzi, D. et al. Fhit expression in gastric adenocarcinoma: correlation with disease stage and survival. Cancer88, 24–34 (1999). Google Scholar
Lee, J. I. et al. Loss of Fhit expression is a predictor of poor outcome in tongue cancer. Cancer Res.61, 837–841 (2001). CASPubMed Google Scholar
Krivak, T. C. et al. Abnormal fragile histidine triad (FHIT) expression in advanced cervical carcinoma: a poor prognostic factor. Cancer Res.61, 4382–4385 (2001). CASPubMed Google Scholar
Yoshino, K. et al. FHIT alterations in cancerous and non-cancerous cervical epithelium. Int. J. Cancer85, 6–13 (2000). CASPubMed Google Scholar
Connolly, D. C. et al. Loss of Fhit expression in invasive cervical carcinomas and intraepithelial lesions associated with invasive disease. Clin. Cancer Res.6, 3505–3510 (2000). CASPubMed Google Scholar
Mao, L. et al. Clonal genetic alterations in the lungs of current and former smokers. J. Natl Cancer Inst.89, 857–862 (1997).Shows that deletions in 3p at theFHITlocus occur in histologically normal lung cells of smokers. CASPubMed Google Scholar
Tseng, J. E. et al. Loss of Fhit is frequent in stage I non-small cell lung cancer and in the lungs of chronic smokers. Cancer Res.59, 4798–4803 (1999).Biopsies of 43% of chronic smokers show decreasedFhitexpression. CASPubMed Google Scholar
Wistuba, I. I. et al. Molecular damage in the bronchial epithelium of current and former smokers. J. Natl Cancer Inst.89, 1366–1373 (1997). CASPubMedPubMed Central Google Scholar
Ramesh, R. et al. Successful treatment of primary and disseminated human lung cancers by systemic delivery of tumour suppressor genes using an improved liposome vector. Mol Ther3, 337–350 (2001). CASPubMed Google Scholar