MTI Seminar Series. Jason Carroll Live Q&A ‘Mechanisms of estrogen receptor activity in breast cancer’ - Shared screen with gallery view
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Related to your one million dollar question on how ER redistributes in poor-prognosis breast cancer.Recently, it’s been postulated that chromatin remodellers can regulate the availability of free TFs in the cells by exposing high-affinity DNA sequences that would drive redistribution of TFs to new sites.Given that you have identified components of NuRD complex, which is involved in metastasis of breast cancer, do you think that gain or loss of remodelling activity of these enzymes in poor-prognosis breast cancers can drive repositioning of ER? (Or any other chromatin remodeller for that matter)?
is the integration of RIMEseq with CRISPR screening a good way of narrowing down hits from CRISPR screens, or do you find that there is not a lot overlap between the two?