Academic literature on the topic 'Chromoplexie'
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Journal articles on the topic "Chromoplexie"
Serbyn, Nataliia, Myrthe M. Smit, Vimathi S. Gummalla, Gregory J. Brunette, and David S. Pellman. "Abstract 6105: Unravelling the mechanistic basis of chromoplexy, a mutational process driving early cancer genome evolution." Cancer Research 83, no. 7_Supplement (April 4, 2023): 6105. http://dx.doi.org/10.1158/1538-7445.am2023-6105.
Full textBallas, Leslie K., Brian R. Hu, and David I. Quinn. "Chromoplexy and hypoxic microenvironment drives prostate cancer." Lancet Oncology 15, no. 13 (December 2014): 1419–21. http://dx.doi.org/10.1016/s1470-2045(14)71114-3.
Full textAshby, Cody, Michael A. Bauer, Yan Wang, Christopher P. Wardell, Ruslana G. Tytarenko, Purvi Patel, Erin Flynt, et al. "Chromothripsis and Chromoplexy Are Associated with DNA Instability and Adverse Clinical Outcome in Multiple Myeloma." Blood 132, Supplement 1 (November 29, 2018): 408. http://dx.doi.org/10.1182/blood-2018-99-117359.
Full textWang, Kendric, Yuzhuo Wang, and Colin C. Collins. "Chromoplexy: a new paradigm in genome remodeling and evolution." Asian Journal of Andrology 15, no. 6 (August 26, 2013): 711–12. http://dx.doi.org/10.1038/aja.2013.109.
Full textAshby, Cody, Eileen M. Boyle, Brian A. Walker, Michael A. Bauer, Katie Rose Ryan, Judith Dent, Anjan Thakurta, Erin Flynt, Faith E. Davies, and Gareth Morgan. "Chromoplexy and Chromothripsis Are Important Prognostically in Myeloma and Deregulate Gene Function By a Range of Mechanisms." Blood 134, Supplement_1 (November 13, 2019): 3767. http://dx.doi.org/10.1182/blood-2019-130335.
Full textPham, Minh-Tam N., Michael C. Haffner, Heather C. Wick, Jonathan B. Coulter, Anuj Gupta, Roshan V. Chikarmane, Harshath Gupta, Sarah Wheelan, William G. Nelson, and Srinivasan Yegnasubramanian. "Abstract 680: Topoisomerase 2 beta facilitates chromatin reorganization during Androgen Receptor induced transcription and contributes to chromoplexy in prostate cancer." Cancer Research 82, no. 12_Supplement (June 15, 2022): 680. http://dx.doi.org/10.1158/1538-7445.am2022-680.
Full textAnderson, Nathaniel D., Richard de Borja, Matthew D. Young, Fabio Fuligni, Andrej Rosic, Nicola D. Roberts, Simon Hajjar, et al. "Rearrangement bursts generate canonical gene fusions in bone and soft tissue tumors." Science 361, no. 6405 (August 30, 2018): eaam8419. http://dx.doi.org/10.1126/science.aam8419.
Full textShen, Michael M. "Chromoplexy: A New Category of Complex Rearrangements in the Cancer Genome." Cancer Cell 23, no. 5 (May 2013): 567–69. http://dx.doi.org/10.1016/j.ccr.2013.04.025.
Full textZhang, Cheng-Zhong, and David Pellman. "Cancer Genomic Rearrangements and Copy Number Alterations from Errors in Cell Division." Annual Review of Cancer Biology 6, no. 1 (April 11, 2022): 245–68. http://dx.doi.org/10.1146/annurev-cancerbio-070620-094029.
Full textMustafin, R. N. "Participation of retroelements in chromoanagenesis in cancer development." Siberian journal of oncology 23, no. 5 (November 15, 2024): 146–56. http://dx.doi.org/10.21294/1814-4861-2024-23-5-146-156.
Full textDissertations / Theses on the topic "Chromoplexie"
Heintzé, Maxime. "Rôles des mutations somatiques dans STAG2, TP53 et CDKN2A et de la chromoplexie dans l'oncogenèse du sarcome d'Ewing." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL093.
Full textEwing sarcoma is the second most frequent pediatric cancer of the bones and soft tissues. It is characterized by the presence of a chromosomal translocation that fuses a gene from the FET family with a transcription factor from the ETS family. In 85% of cases, the t(11;22)(q24;q12) translocation fusing the EWSR1 and FLI1 genes is observed, and in 10% of cases, the t(21;22)(q22;q12) translocation fusing EWSR1 with ERG can be found. These fusion proteins exert an aberrant oncogenic role. Somatic mutations in the STAG2, TP53 and CDKN2A genes are frequently found in patient tumors. In particular, STAG2, a gene involved in the cohesin complex, is increasingly observed to be mutated or inactivated in cancers today. A recently described phenomenon of genomic instability, known as chromoplexy, is now found in 18% of cancers. Chromoplexy involves multiple, generally balanced, rearrangements between several chromosomes, forming complex translocation loops. Interestingly, tumors from patients positive for the EWSR1-ERG fusion are almost always associated with chromoplexy.Understanding the role of additional somatic mutations and chromoplexy in the initiation of oncogenesis in this sarcoma is necessary to decipher the mechanisms of cellular transformation in this disease. To generate new study models, we endogenously induce EWSR1-ETS translocations associated with additional mutations in primary human mesenchymal stem cells (MSCs), a potential cellular origin of this sarcoma, using CRISPR-Cas9. To better understand the mechanism of chromoplexy, we hypothesized that the orientation of the EWSR1 and ERG genes on their respective chromosomes leads to the formation of a theoretical dicentric chromosome. This highly unstable chromosome may promote the formation of rearrangement loops, such as chromoplexy, to stabilize the genome.In this way, we were able to generate a novel, innovative model of Ewing sarcoma from primary human MSCs. These models showed the ability to develop tumors and metastases when injected in vivo into mice. These tumors recapitulated all the typical characteristics of Ewing sarcoma, including its characteristic morphology and the membrane expression of the CD99 marker. Moreover, the transcriptomic profiles of the tumors were highly similar to those of patient tumors.Subsequently, we used the EWSR1-ERG fusion to study chromoplexy. Through the use of specific inhibitors targeting DNA double-strand break repair pathways, we were able to promote the formation of rearrangement loops in model cells. From our results, we generated entirely new, original models presenting the EWSR1-ERG fusion, with or without chromoplexy, from primary human MSCs.This work confirms a potential mesenchymal origin for this sarcoma. We have shown that the endogenous induction of EWSR1-ETS fusions enables complete cellular transformation when associated with additional somatic mutations in the STAG2, TP53, and CDKN2A genes. Finally, we were able to partially understand the role of chromoplexy in the initiation of oncogenesis in Ewing sarcoma
Baca, Sylvan Charles. "The landscape of somatic mutations in primary prostate adenocarcinoma." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:10824.
Full textBook chapters on the topic "Chromoplexie"
Das, Bhaswatee, Bipasha Choudhury, Aditya Kumar, and Vishwa Jyoti Baruah. "Genomic Instability and DNA Repair in Cancer." In DNA - Damages and Repair Mechanisms. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95736.
Full textConference papers on the topic "Chromoplexie"
Demeulemeester, J., M. Tarabichi, MW Fittall, P. Van Loo, JO Korbel, and PJ Campbell. "4 Patterns of clustered mutational processes: Pan-Cancer analysis of chromothripsis, chromoplexy and kataegis." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.4.
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