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View full-text article in PMC

. 2020 Oct 13;12(10):2951. doi: 10.3390/cancers12102951

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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The proposed model of action of NPM-ALK and RAF1 inhibitions on autophagy flux and cells outcome. The pharmacological inactivation of the NPM-ALK oncogene in NPM-ALK+ ALCL was previously shown to induce a cytoprotective autophagic flux. This status was shown to be associated with the downregulation of miR-7-5p levels and the increased expression of one of its targets: RAF1. When pharmacological or molecular tools allowing RAF1 inactivation were used in combination with NPM-ALK inhibition, the autophagy flux was potentiated and associated with increased cell death, therefore, highlighting the superiority of the co-treatment to kill NPM-ALK+ lymphoma cells.