2/ Oncogene amplifications are common across cancers and frequently carry along non-coding DNA sequences. We find that these sequences undergo selection.pic.twitter.com/x43z6QwonZ
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2/ Oncogene amplifications are common across cancers and frequently carry along non-coding DNA sequences. We find that these sequences undergo selection.pic.twitter.com/x43z6QwonZ
3/ Focusing initially on glioblastoma, we found that a non-coding region upstream of EGFR is nearly always co-amplified with the gene. This region contains two enhancers elements that regulate EGFR.pic.twitter.com/mI36O2ICOT
4/ EGFR amplifications occur as circular extrachromosomal DNA (ecDNA), which are common across many types of cancer. We see that the ecDNA amplifications are loaded with regulatory elements.pic.twitter.com/k86jDqk2ZR
5/ We see massive rewiring of the chromatin topology on the ecDNA. Compared to the unamplified locus (top), amplified EGFR (bottom) co-opts nearly all neighboring enhancers, even those beyond the TAD boundary!pic.twitter.com/hezkwoTgHB
6/ We show through a CRISPRi screen that nearly all of the co-opted enhancers contribute to glioblastoma growth. This indicates that not just the oncogene, but the entire locus i.e. the “onco-locus” is a driver.pic.twitter.com/DAawwG1Ny3
7/ Looking at focal amplifications across 7 different cancers, we found that enhancer selection is common. The enhancers are often active in the tissue of origin. This suggests that these enhancers were present when the amplification first arose.pic.twitter.com/PziGJ5BH8P
8/ Many thanks to all of our fabulous collaborators, @MatLupien , Stephen Mack , @StephAngers , @BrainSurgn1989 , @axiotlinc , Brian Rubin, Shashi Shetty and all the other co-authors.
Heard about this work for awhile now from Nergiz. Amazing science, congratulations!
Congratulations! Awesome work!
Congrats to all. Fantastic work.
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