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. 2014 Jan 1;28(1):58–70. doi: 10.1101/gad.232009.113

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© 2014 Kelly et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 3.0 Unported), as described at http://creativecommons.org/licenses/by-nc/3.0/.

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Figure 6. — A proposed model in which c-MYC-driven lymphoma cells that are highly dependent on MCL-1 for their sustained expansion can no longer survive once MCL-1 expression is reduced and the balance between this prosurvival protein and the p53 proapoptotic targets PUMA/NOXA is disturbed. The c-MYC-driven lymphoma cells that have acquired p53 mutations display an accelerated lymphoma progression. These lymphomas express less PUMA/NOXA, and, consequently, less MCL-1 expression is required to maintain the lymphoma progression. Despite this, we showed that targeting of MCL-1 in lymphomas with p53 mutations was sufficient to result in tumor regression. Note that the mouse protein nomenclature is used.