Common fragile site profiling in epithelial and erythroid cells reveals that most recurrent cancer deletions lie in fragile sites hosting large genes

Cell Reports

Volumn 4, Issue 3, 2013, Pages 420-428

  LeTallec, Benoît ^a,b,c   Millot, GaëlArmel ^a,b,c   Blin, MarionEsther ^a,b,c   Brison, Olivier ^a,b,c   Dutrillaux, Bernard ^d   Debatisse, Michelle ^a,b,c  

^a INSTITUT CURIE   (France)

^b SORBONNE UNIVERSITÉ   (France)

^c Institut Curie   (France)

^d MUSÉUM NATIONAL D'HISTOIRE NATURELLE   (France)

Author keywords

[No Author keywords available]

Indexed keywords

ARTICLE; BREAST CANCER; CANCER CELL CULTURE; CHROMOSOME ANALYSIS; CHROMOSOME BREAKAGE; CHROMOSOME FRAGILE SITE; CHROMOSOME FRAGILITY; COLORECTAL CANCER; COMPARATIVE STUDY; CONTROLLED STUDY; EPITHELIUM CELL; ERYTHROID CELL; FIBROBLAST; GENE DELETION; GENE LENGTH; GENE LOCUS; GENE MAPPING; GENETIC ASSOCIATION; GENETIC CONSERVATION; GENETIC PARAMETERS; GENETIC PREDISPOSITION; GENETIC TRANSCRIPTION; HUMAN; HUMAN CELL; LYMPHOCYTE; MOUSE; NONHUMAN; PRIORITY JOURNAL; TUMOR GENE;

CELL LINE, TUMOR; CHROMOSOME FRAGILE SITES; EPITHELIAL CELLS; ERYTHROID CELLS; HCT116 CELLS; HUMANS; K562 CELLS; NEOPLASMS; TRANSCRIPTION, GENETIC;

EID: 84881615685     PISSN: None     EISSN: 22111247     Source Type: Journal    
DOI: 10.1016/j.celrep.2013.07.003     Document Type: Article

References (24)

1. Alsop A.E., Taylor K., Zhang J., Gabra H., Paige A.J., Edwards P.A. Homozygous deletions may be markers of nearby heterozygous mutations: The complex deletion at FRA16D in the HCT116 colon cancer cell line removes exons of WWOX. Genes Chromosomes Cancer 2008, 47:437-447.
2. Barlow J.H., Faryabi R.B., Callén E., Wong N., Malhowski A., Chen H.T., Gutierrez-Cruz G., Sun H.W., McKinnon P., Wright G., et al. Identification of early replicating fragile sites that contribute to genome instability. Cell 2013, 152:620-632.
3. Beroukhim R., Mermel C.H., Porter D., Wei G., Raychaudhuri S., Donovan J., Barretina J., Boehm J.S., Dobson J., Urashima M., et al. The landscape of somatic copy-number alteration across human cancers. Nature 2010, 463:899-905.
4. Bignell G.R., Greenman C.D., Davies H., Butler A.P., Edkins S., Andrews J.M., Buck G., Chen L., Beare D., Latimer C., et al. Signatures of mutation and selection in the cancer genome. Nature 2010, 463:893-898.
5. Coquelle A., Pipiras E., Toledo F., Buttin G., Debatisse M. Expression of fragile sites triggers intrachromosomal mammalian gene amplification and sets boundaries to early amplicons. Cell 1997, 89:215-225.
6. De S., Michor F. DNA replication timing and long-range DNA interactions predict mutational landscapes of cancer genomes. Nat. Biotechnol. 2011, 29:1103-1108.
7. Debatisse M., Le Tallec B., Letessier A., Dutrillaux B., Brison O. Common fragile sites: mechanisms of instability revisited. Trends Genet. 2012, 28:22-32.
8. Dereli-Öz A., Versini G., Halazonetis T.D. Studies of genomic copy number changes in human cancers reveal signatures of DNA replication stress. Mol. Oncol. 2011, 5:308-314.
9. Djebali S., Davis C.A., Merkel A., Dobin A., Lassmann T., Mortazavi A., Tanzer A., Lagarde J., Lin W., Schlesinger F., et al. Landscape of transcription in human cells. Nature 2012, 489:101-108.
10. Durkin S.G., Glover T.W. Chromosome fragile sites. Annu. Rev. Genet. 2007, 41:169-192.
11. Hansen R.S., Thomas S., Sandstrom R., Canfield T.K., Thurman R.E., Weaver M., Dorschner M.O., Gartler S.M., Stamatoyannopoulos J.A. Sequencing newly replicated DNA reveals widespread plasticity in human replication timing. Proc. Natl. Acad. Sci. USA 2010, 107:139-144.
12. Helmrich A., Ballarino M., Tora L. Collisions between replication and transcription complexes cause common fragile site instability at the longest human genes. Mol. Cell 2011, 44:966-977.
13. Iliopoulos D., Guler G., Han S.Y., Druck T., Ottey M., McCorkell K.A., Huebner K. Roles of FHIT and WWOX fragile genes in cancer. Cancer Lett. 2006, 232:27-36.
14. Le Tallec B., Dutrillaux B., Lachages A.M., Millot G.A., Brison O., Debatisse M. Molecular profiling of common fragile sites in human fibroblasts. Nat. Struct. Mol. Biol. 2011, 18:1421-1423.
15. Letessier A., Millot G.A., Koundrioukoff S., Lachagès A.M., Vogt N., Hansen R.S., Malfoy B., Brison O., Debatisse M. Cell-type-specific replication initiation programs set fragility of the FRA3B fragile site. Nature 2011, 470:120-123.
16. McAvoy S., Ganapathiraju S.C., Ducharme-Smith A.L., Pritchett J.R., Kosari F., Perez D.S., Zhu Y., James C.D., Smith D.I. Non-random inactivation of large common fragile site genes in different cancers. Cytogenet. Genome Res. 2007, 118:260-269.
17. Méchali M. Eukaryotic DNA replication origins: many choices for appropriate answers. Nat. Rev. Mol. Cell Biol. 2010, 11:728-738.
18. Mrasek K., Schoder C., Teichmann A.C., Behr K., Franze B., Wilhelm K., Blaurock N., Claussen U., Liehr T., Weise A. Global screening and extended nomenclature for 230 aphidicolin-inducible fragile sites, including 61 yet unreported ones. Int. J. Oncol. 2010, 36:929-940.
19. Murano I., Kuwano A., Kajii T. Fibroblast-specific common fragile sites induced by aphidicolin. Hum. Genet. 1989, 83:45-48.
20. Ryba T., Hiratani I., Lu J., Itoh M., Kulik M., Zhang J., Schulz T.C., Robins A.J., Dalton S., Gilbert D.M. Evolutionarily conserved replication timing profiles predict long-range chromatin interactions and distinguish closely related cell types. Genome Res. 2010, 20:761-770.
21. Saldivar J.C., Miuma S., Bene J., Hosseini S.A., Shibata H., Sun J., Wheeler L.J., Mathews C.K., Huebner K. Initiation of genome instability and preneoplastic processes through loss of Fhit expression. PLoS Genet. 2012, 8:e1003077.
22. Schepeler T., Lamy P., Laurberg J.R., Fristrup N., Reinert T., Bartkova J., Tropia L., Bartek J., Halazonetis T.D., Pan C.C., et al. A high resolution genomic portrait of bladder cancer: correlation between genomic aberrations and the DNA damage response. Oncogene 2012, Published online August 27, 2012. 10.1038/onc.2012.381.
23. Smith D.I., McAvoy S., Zhu Y., Perez D.S. Large common fragile site genes and cancer. Semin. Cancer Biol. 2007, 17:31-41.
24. Solimini N.L., Xu Q., Mermel C.H., Liang A.C., Schlabach M.R., Luo J., Burrows A.E., Anselmo A.N., Bredemeyer A.L., Li M.Z., et al. Recurrent hemizygous deletions in cancers may optimize proliferative potential. Science 2012, 337:104-109.