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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 2597581, 18 pages
Review Article

Oxidative Stress Gene Expression Profile Correlates with Cancer Patient Poor Prognosis: Identification of Crucial Pathways Might Select Novel Therapeutic Approaches

Experimental Pharmacology Unit, Istituto Nazionale Tumori Fondazione G. Pascale-IRCCS, Naples, Italy

Correspondence should be addressed to Alessandra Leone;

Received 15 March 2017; Accepted 30 May 2017; Published 9 July 2017

Academic Editor: Lars Bräutigam

Copyright © 2017 Alessandra Leone et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The role of altered redox status and high reactive oxygen species (ROS) is still controversial in cancer development and progression. Intracellular levels of ROS are elevated in cancer cells suggesting a role in cancer initiation and progression; on the contrary, ROS elevated levels may induce programmed cell death and have been associated with cancer suppression. Thus, it is crucial to consider the double-face of ROS, for novel therapeutic strategies targeting redox regulatory mechanisms. In this review, in order to derive cancer-type specific oxidative stress genes’ profile and their potential prognostic role, we integrated a publicly available oxidative stress gene signature with patient survival data from the Cancer Genome Atlas database. Overall, we found several genes statistically significant associated with poor prognosis in the examined six tumor types. Among them, FoxM1 and thioredoxin reductase1 expression showed the same pattern in four out of six cancers, suggesting their specific critical role in cancer-related oxidative stress adaptation. Our analysis also unveiled an enriched cellular network, highlighting specific pathways, in which many genes are strictly correlated. Finally, we discussed novel findings on the correlation between oxidative stress and cancer stem cells in order to define those pathways to be prioritized in drug development.