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I am doing some research on small cell lung cancer and, from what I have found, many tumors show high levels of ASCL1, which is a regulator for neuroendocrine cell differentiation. However, no papers propose a mechanism for the higher levels of ASCL1. Instead, many of them refer to ASCL1 target genes with "amplified" enhancers and propose that ASCL1 may bind more frequently to these enhancer regions.

In general, if there are more places for the regulator to bind on an enhancer, is it possible that this is sufficient for the regulator to be more highly expressed?

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