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Epigenetic balance in DLBCL.

Cancer therapies are usually designed to directly target and block the activity of oncogenic drivers. Loss of tumor suppressors contributes equally to tumor development, but they are almost impossible to target therapeutically. Understanding which molecular changes derive from altered tumor-suppressor activity provides opportunities to identify indirect therapeutic targets where inhibition will counterbalance and “correct” these changes. In diffuse large B-cell lymphoma (DLBCL), it is possible to partially correct the epigenetic phenotype derived from the loss of histone-methyl transferase (HMT) KMT2D activity by inhibiting the histonedemethylase (HDT) KDM5.