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Epigenomic annotation of noncoding mutations identifies mutated pathways in primary liver cancer

Fig 1

Models for regulatory element involvement in cancer.

In the trans-model of cancer enhancers, somatic mutation to a chromatin modifier gene, here MLL3/4 (red pentagon), results in that chromatin modifier binding more tightly to a DNA-bound transcription factor (yellow oval) and aberrantly creates a persistently open chromatin state, up-regulating the target gene. In the cis-model of cancer enhancers, a somatic mutation to a noncoding regulatory element (orange bar) creates the same open chromatin state, perhaps by creating a binding site for a transcription factor that is recruited to the locus and facilitates opening local chromatin.

Fig 1