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. Author manuscript; available in PMC: 2012 Nov 1.
Published in final edited form as: Semin Cancer Biol. 2011 Sep 18;21(5):335–346. doi: 10.1016/j.semcancer.2011.09.008

Fig. 5.

Fig. 5

Targeting DNA Damage Response proteins. Exogenous and endogenous stress can activate the DNA damage sensor ATM, which is frequently mutated or deleted in primary MCL. ATM in turn activates p53, which stops cell cycle progression and activates DNA repair mechanisms. Pharmacologic inhibitors of MDM2, which degrades p53; and PARP, which aids in DNA repair, are shown in blue.