Hanna-Riikka Teppo, Ylermi Soini, and Peeter Karihtala, “Reactive Oxygen Species-Mediated Mechanisms of Action of Targeted Cancer Therapy,” Oxidative Medicine and Cellular Longevity, vol. 2017, Article ID 1485283, 11 pages, 2017. doi:10.1155/2017/1485283
Reactive oxygen species-mediated mechanisms of action of targeted cancer therapy
|Author:||Teppo, Hanna-Riikka1; Soini, Ylermi1; Karihtala, Peeter2|
1Department of Pathology, Medical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland
2Department of Oncology and Radiotherapy, Medical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland
|Online Access:||PDF Full Text (PDF, 1.5 MB)|
|Persistent link:|| http://urn.fi/urn:nbn:fi-fe201708228172
|Publish Date:|| 2017-08-22
Targeted cancer therapies, involving tyrosine kinase inhibitors and monoclonal antibodies, for example, have recently led to substantial prolongation of survival in many metastatic cancers. Compared with traditional chemotherapy and radiotherapy, where reactive oxygen species (ROS) have been directly linked to the mediation of cytotoxic effects and adverse events, the field of oxidative stress regulation is still emerging in targeted cancer therapies. Here, we provide a comprehensive review regarding the current evidence of ROS-mediated effects of antibodies and tyrosine kinase inhibitors, use of which has been indicated in the treatment of solid malignancies and lymphomas. It can be concluded that there is rapidly emerging evidence of ROS-mediated effects of some of these compounds, which is also relevant in the context of drug resistance and how to overcome it.
Oxidative medicine and cellular longevity
|Type of Publication:||
A2 Review article in a scientific journal
|Field of Science:||
Copyright © 2017 Hanna-Riikka Teppo 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.