(6/n) @DFCI_CancerBio @DanaFarber @broadinstitute @GRO_Broad. So lucky to be in such an amazing research environment that supportive of cutting edge science. #epigenetics #CancerResearch #chromatin #methylation #topology.

(5/n) results in more transcription. Grateful for the amazing mentorship of @BradEBernstein and the wonderful collaboration involving @Anders_S_Hansen @GilbertRahme @chadi_elfarran and Viraat Y. Goel. So great to see this online! Thankful to the wonderful communities at . .

(4/n) and the FGF3 promoter. Interestingly, the contact frequency between the transcription start sites of the enhancer RNA (eRNA) and FGF3 was linearly correlated with the activity of FGF3 transcription, supporting an activity-by contact (ABC) model, where more contact . .

(3/n) region-capture micro-C (RCMC) assay, we precisely mapped the genome architecture and its remodeling as a result of CTCF disruption in the boundary region separating FGF3 and an enhancer regions. Our results show clear loop-dot interactions between the hijacked enhancer. .

(2/n) We previously reported that FGF3/4 are aberrantly activated by epigenetic reprogramming. We teased out the precise mechanism by which CTCF site methylation, and subsequent disruption of its binding, drives FGF3 expression. Using high resolution. .

(1/n) We used a model of gastrointestinal stromal tumors, a disease in which a sizable proportion is driven by epigenetic reprogramming by means of SDH deficiency. SDH-deficient GISTs are characterized with DNA hypermethylation at CpG sites, which spreads to CTCF binding sites. .

Extremely excited to share my main postdoctoral project, published today @MolecularCell (. We carefully investigated the precise role of CTCF binding sites in the FGF3/4 locus, teasing out the role of CTCF insulators either singly, or in combination. .