A signal is only as meaningful as the cell that reads it. Growth factors, cytokines, and metabolic cues never act alone. Each cell receives them through its own regulatory layers, a resident transcription factor network and chromatin state, and these decode the input and build the machinery that reaches the genome.

No two cell states read alike. One signal is refracted into many programs of gene expression. Yet distant cells can also converge on the same program, as when metastatic or therapy-resistant cells co-opt the logic of development and regeneration. The signal proposes. Context decides.

Shifts in the chromatin landscape make familiar signals read anew, pushing cells from one identity into another as a tissue repairs, remodels, or transforms.

We work to crack this code: how context gives signals meaning, how cell state holds their identity, and how metastatic cells exploit both to thrive in tissues that are not their own.