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A new role for hypoxia in tumor progression: induction of fragile site triggering genomic rearrangements and formation of complex DMs and HSRs.
Coquelle A, Toledo F, Stern S, Bieth A, Debatisse M. Coquelle A, et al. Mol Cell. 1998 Aug;2(2):259-65. doi: 10.1016/s1097-2765(00)80137-9. Mol Cell. 1998. PMID: 9734364
Here, we report direct evidence for a causal relationship between hypoxia, induction of fragile sites, and gene amplification. ...This pathway operates efficiently for DMs bearing different sequences, suggesting a model of hypoxia-driven formation of the HSRs contai …
Here, we report direct evidence for a causal relationship between hypoxia, induction of fragile sites, and gene amplification. ...Thi …
Induction of multiple double-strand breaks within an hsr by meganucleaseI-SceI expression or fragile site activation leads to formation of double minutes and other chromosomal rearrangements.
Coquelle A, Rozier L, Dutrillaux B, Debatisse M. Coquelle A, et al. Oncogene. 2002 Oct 31;21(50):7671-9. doi: 10.1038/sj.onc.1205880. Oncogene. 2002. PMID: 12400009
This demonstrates, for the first time, a direct relationship between double-strand breaks and inversions. Finally, we show that activation of fragile sites by aphidicolin or hypoxia in hsr-containing cells also generates dmin and a variety of chromosomal rearrangeme …
This demonstrates, for the first time, a direct relationship between double-strand breaks and inversions. Finally, we show that activ …
Does interference between replication and transcription contribute to genomic instability in cancer cells?
Tuduri S, Crabbe L, Tourrière H, Coquelle A, Pasero P. Tuduri S, et al. Among authors: coquelle a. Cell Cycle. 2010 May 15;9(10):1886-92. doi: 10.4161/cc.9.10.11539. Epub 2010 May 15. Cell Cycle. 2010. PMID: 20495385 Free article.
Enhanced flexibility and aphidicolin-induced DNA breaks near mammalian replication origins: implications for replicon mapping and chromosome fragility.
Toledo F, Coquelle A, Svetlova E, Debatisse M. Toledo F, et al. Among authors: coquelle a. Nucleic Acids Res. 2000 Dec 1;28(23):4805-13. doi: 10.1093/nar/28.23.4805. Nucleic Acids Res. 2000. PMID: 11095694 Free PMC article.
Gene amplification mechanisms: the role of fragile sites.
Debatisse M, Coquelle A, Toledo F, Buttin G. Debatisse M, et al. Among authors: coquelle a. Recent Results Cancer Res. 1998;154:216-26. doi: 10.1007/978-3-642-46870-4_13. Recent Results Cancer Res. 1998. PMID: 10027002
We studied the early stages of gene amplification in a Chinese hamster cell line and identified two distinct amplification mechanisms, both relying on an unequal segregation of gene copies at mitosis. In some cases, a sequence containing the selected gene is looped …
We studied the early stages of gene amplification in a Chinese hamster cell line and identified two distinct amplification mechanisms …
Expression of fragile sites triggers intrachromosomal mammalian gene amplification and sets boundaries to early amplicons.
Coquelle A, Pipiras E, Toledo F, Buttin G, Debatisse M. Coquelle A, et al. Cell. 1997 Apr 18;89(2):215-25. doi: 10.1016/s0092-8674(00)80201-9. Cell. 1997. PMID: 9108477
We demonstrate a dual role for fragile sites in intrachromosomal amplification: a site telomeric to the selected gene is involved in initiation, while a centromeric site defines the size and organization of early amplified units. The positions of fragile site …
We demonstrate a dual role for fragile sites in intrachromosomal amplification: a site telomeric to the selected gene is invol …
Interstitial deletions and intrachromosomal amplification initiated from a double-strand break targeted to a mammalian chromosome.
Pipiras E, Coquelle A, Bieth A, Debatisse M. Pipiras E, et al. Among authors: coquelle a. EMBO J. 1998 Jan 2;17(1):325-33. doi: 10.1093/emboj/17.1.325. EMBO J. 1998. PMID: 9427766 Free PMC article.
Using the properties of the I-SceI nuclease to introduce a localized double-strand break (DSB) in a mammalian chromosome carrying its target sequence, we demonstrate here that both types of mutations can be initiated by non-conservative DSB repair pathways. ...Takin …
Using the properties of the I-SceI nuclease to introduce a localized double-strand break (DSB) in a mammalian chromosome carry …
Topoisomerase I suppresses genomic instability by preventing interference between replication and transcription.
Tuduri S, Crabbé L, Conti C, Tourrière H, Holtgreve-Grez H, Jauch A, Pantesco V, De Vos J, Thomas A, Theillet C, Pommier Y, Tazi J, Coquelle A, Pasero P. Tuduri S, et al. Among authors: coquelle a. Nat Cell Biol. 2009 Nov;11(11):1315-24. doi: 10.1038/ncb1984. Epub 2009 Oct 18. Nat Cell Biol. 2009. PMID: 19838172 Free PMC article.
New Topoisomerase I mutations are associated with resistance to camptothecin.
Gongora C, Vezzio-Vie N, Tuduri S, Denis V, Causse A, Auzanneau C, Collod-Beroud G, Coquelle A, Pasero P, Pourquier P, Martineau P, Del Rio M. Gongora C, et al. Among authors: coquelle a. Mol Cancer. 2011 May 27;10:64. doi: 10.1186/1476-4598-10-64. Mol Cancer. 2011. PMID: 21619602 Free PMC article.
Non-homologous end-joining genes are not inactivated in human radiation-induced sarcomas with genomic instability.
Lefèvre SH, Coquelle A, Gonin-Laurent N, Cör A, Vogt N, Chauveinc L, Anract P, Dutrillaux B, Chevillard S, Malfoy B. Lefèvre SH, et al. Among authors: coquelle a. J Radiat Res. 2005 Jun;46(2):223-31. doi: 10.1269/jrr.46.223. J Radiat Res. 2005. PMID: 15988141
We analyzed the loss of heterozygosity (LOH) and the presence of mutations for a series of genes implicated in DSB repair by non-homologous end-joining in five radiation-induced sarcomas devoid of both active Tp53 and Rb1. ...
We analyzed the loss of heterozygosity (LOH) and the presence of mutations for a series of genes implicated in DSB repair by non-homo …
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