TY  - JOUR
A1  - Helfinger, Valeska
A1  - Schröder, Katrin
T1  - Redox control in cancer development and progression
T2  - Molecular Aspects of Medicine
N2  - Cancer is the leading cause of death worldwide after cardiovascular diseases. This has been the case for the last few decades despite there being an increase in the number of cancer treatments. One reason for the apparent lack of drug effectiveness might be, at least in part, due to unspecificity for tumors; which often leads to substantial side effects. One way to improve the treatment of cancer is to increase the specificity of the treatment in accordance with the concept of individualized medicine. This will help to prevent further progression of an existing cancer or even to reduce the tumor burden. Alternatively it would be much more attractive and efficient to prevent the development of cancer in the first place. Therefore, it is important to understand the risk factors and the mechanisms of carcinogenesis in detail. One such risk factor, often associated with tumorigenesis and tumor progression, is an increased abundance of reactive oxygen species (ROS) arising from an imbalance of ROS-producing and -eliminating components. A surplus of ROS can induce oxidative damage of macromolecules including proteins, lipids and DNA. In contrast, ROS are essential for an adequate signal transduction and are known to regulate crucial cellular processes like cellular quiescence, differentiation and even apoptosis. Therefore, regulated ROS-formation at physiological levels can inhibit tumor formation and progression. With this review we provide an overview on the current knowledge of redox control in cancer development and progression.
KW  - Reactive oxygen species
KW  - Cancer development
KW  - Cancer progression
KW  - Redox-sensitive transcription factor
KW  - Antioxidants
KW  - Redox dependent epigenetic modifications
Y1  - 2018
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/77429
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-774295
SN  - 0098-2997
VL  - 63
SP  - 88
EP  - 98
PB  - Elsevier
CY  - Amsterdam
ER  -