scholarly journals Reactive Oxygen Species-Mediated Mechanisms of Action of Targeted Cancer Therapy

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Hanna-Riikka Teppo ◽  
Ylermi Soini ◽  
Peeter Karihtala
Keyword(s):  
Reactive Oxygen Species ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Kinase Inhibitors ◽  
Reactive Oxygen ◽  
Current Evidence ◽  
Cancer Therapies ◽  
Oxygen Species ◽  
Mediated Effects ◽  
Targeted Cancer Therapies

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.

scholarly journals Diarrhea Induced by Small Molecule Tyrosine Kinase Inhibitors Compared With Chemotherapy: Potential Role of the Microbiome

2020 ◽  
Vol 19 ◽  
pp. 153473542092849
Author(s):  
Kate R. Secombe ◽  
Ysabella Z. A. Van Sebille ◽  
Bronwen J. Mayo ◽  
Janet K. Coller ◽  
Rachel J. Gibson ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Small Molecule ◽  
Kinase Inhibitors ◽  
Treatment Modalities ◽  
Research Approach ◽  
Cancer Therapies ◽  
Current State ◽  
Targeted Cancer Therapies

Small molecule receptor tyrosine kinase inhibitors (SM-TKIs) are among a group of targeted cancer therapies, intended to be more specific to cancer cells compared with treatments, such as chemotherapy, hence reducing adverse events. Unfortunately, many patients report high levels of diarrhea, the pathogenesis of which remains under investigation. In this article, we compare the current state of knowledge of the pathogenesis of chemotherapy-induced diarrhea (CID) in comparison to SM-TKI–induced diarrhea, and investigate how a similar research approach in both areas may be beneficial. To this end, we review evidence that both treatment modalities may interact with the gut microbiome, and as such the microbiome should be investigated for its ability to reduce the risk of diarrhea.

scholarly journals Activation of the Cytoplasmic c-Abl Tyrosine Kinase by Reactive Oxygen Species

2000 ◽  
Vol 275 (23) ◽  
pp. 17237-17240 ◽  
Author(s):  
Xiangao Sun ◽  
Pradip Majumder ◽  
Hisashi Shioya ◽  
Frank Wu ◽  
Shailendra Kumar ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Tyrosine Kinase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Abl Tyrosine Kinase

scholarly journals PAC1 regulates receptor tyrosine kinase transactivation in a reactive oxygen species-dependent manner

Peptides ◽  
2019 ◽  
Vol 120 ◽  
pp. 170017
Author(s):  
Terry W. Moody ◽  
Lingaku Lee ◽  
Tatiana Iordanskaia ◽  
Irene Ramos-Alvarez ◽  
Paola Moreno ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Reactive Oxygen ◽  
Dependent Manner ◽  
Oxygen Species

Current evidence on thyroid related adverse events in patients treated with protein tyrosine kinase inhibitors

2019 ◽  
Vol 51 (4) ◽  
pp. 562-569
Author(s):  
Katalin Gabora ◽  
Andra Piciu ◽  
Iulian Claudiu Bădulescu ◽  
Maria Iulia Larg ◽  
Ioan-Adrian Stoian ◽  
...  
Keyword(s):  
Adverse Events ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Protein Tyrosine Kinase ◽  
Kinase Inhibitors ◽  
Current Evidence ◽  
Protein Tyrosine

scholarly journals The Involvement of the Tyrosine Kinase c-Src in the Regulation of Reactive Oxygen Species Generation Mediated by NADPH Oxidase-1

2008 ◽  
Vol 19 (7) ◽  
pp. 2984-2994 ◽  
Author(s):  
Davide Gianni ◽  
Ben Bohl ◽  
Sara A. Courtneidge ◽  
Gary M. Bokoch
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Tyrosine Kinase ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Tumor Formation ◽  
Ros Generation ◽  
Oxygen Species ◽  
Human Colon Carcinoma Cell ◽  
Kinase C

NADPH oxidase (Nox) family enzymes are one of the main sources of cellular reactive oxygen species (ROS), which have been shown to function as second messenger molecules. To date, seven members of this family have been reported, including Nox1-5 and Duox1 and -2. With the exception of Nox2, the regulation of the Nox enzymes is still poorly understood. Nox1 is highly expressed in the colon, and it requires two cytosolic regulators, NoxO1 and NoxA1, as well as the binding of Rac1 GTPase, for its activity. In this study, we investigate the role of the tyrosine kinase c-Src in the regulation of ROS formation by Nox1. We show that c-Src induces Nox1-mediated ROS generation in the HT29 human colon carcinoma cell line through a Rac-dependent mechanism. Treatment of HT29 cells with the Src inhibitor PP2, expression of a kinase-inactive form of c-Src, and c-Src depletion by small interfering RNA (siRNA) reduce both ROS generation and the levels of active Rac1. This is associated with decreased Src-mediated phosphorylation and activation of the Rac1-guanine nucleotide exchange factor Vav2. Consistent with this, Vav2 siRNA that specifically reduces endogenous Vav2 protein is able to dramatically decrease Nox1-dependent ROS generation and abolish c-Src-induced Nox1 activity. Together, these results establish c-Src as an important regulator of Nox1 activity, and they may provide insight into the mechanisms of tumor formation in colon cancers.

Apoptosis in Heart and Skeletal Muscle

2002 ◽  
Vol 27 (4) ◽  
pp. 349-395 ◽  
Author(s):  
Andy J. Primeau ◽  
Peter J. Adhihetty ◽  
David A. Hood
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Cell Death ◽  
Mitochondrial Permeability Transition ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Permeability Transition ◽  
Current Evidence ◽  
Oxygen Species ◽  
Cellular Mechanisms

Apoptosis, or programmed cell death, is now recognized to be an important cellular event during normal development and in the progression of specific diseases. Apoptosis can be triggered by stimuli initiating outside of the cell, or within the mitochondria, leading to the activation of caspases and subsequent cell death. Although apoptosis has been widely studied in a variety of tissues over the last 5 years, skeletal muscle and heart have been relatively ignored in this regard. Research on apoptosis in cardiac muscle has recently taken on a higher profile as the recognition emerges that it may be an important contributor to specific cardiac pathologies, particularly in response to ischemia-reperfusion in which reactive oxygen species are formed. In skeletal muscle, very few studies have been done under specific physiological (e.g., exercise) and pathophysiological (e.g., dystrophies, denervation, myopathies) conditions. Skeletal muscle is unique in that it is mutli-nucleated, and evidence suggests that it can undergo individual myonuclear apoptosis as well as complete cell death. This review discusses the basic cellular mechanisms of apoptosis, as well as the current evidence of this process in cardiac and skeletal muscle. The need for more work in this area is highlighted, particularly in exercise and training. Key words: transcription factors, reactive oxygen species, mitochondria, caspase, mitochondrial permeability transition

scholarly journals The Arabidopsis SIAMESE-RELATED Cyclin-Dependent Kinase Inhibitors SMR5 and SMR7 Regulate the DNA Damage Checkpoint in Response to Reactive Oxygen Species

2014 ◽  
Vol 26 (1) ◽  
pp. 296-309 ◽  
Author(s):  
Dalong Yi ◽  
Claire Lessa Alvim Kamei ◽  
Toon Cools ◽  
Sandy Vanderauwera ◽  
Naoki Takahashi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Kinase Inhibitors ◽  
Reactive Oxygen ◽  
Dna Damage Checkpoint ◽  
Oxygen Species ◽  
Cyclin Dependent Kinase
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