scholarly journals Endometriosis-Associated Ovarian Cancer: The Role of Oxidative Stress

10.5772/30541 ◽  
2012 ◽  
Author(s):  
Yoriko Yamashita ◽  
Shinya Toyokuni
Keyword(s):  
Oxidative Stress ◽  
Ovarian Cancer

scholarly journals The Role of Oxidative Stress in the Development of Cisplatin Resistance in Epithelial Ovarian Cancer

2013 ◽  
Vol 21 (4) ◽  
pp. 503-508 ◽  
Author(s):  
Jimmy Belotte ◽  
Nicole M. Fletcher ◽  
Awoniyi O. Awonuga ◽  
Mitchell Alexis ◽  
Husam M. Abu-Soud ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Cisplatin Resistance

The Role of Oxidative Stress in Ovarian Cancer

Cancer ◽  
2014 ◽  
pp. 41-50
Author(s):  
Matthew White ◽  
Joshua Cohen ◽  
Charles Hummel ◽  
Robert Burky ◽  
Ana Cruz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ovarian Cancer

scholarly journals Insights into the Role of Oxidative Stress in Ovarian Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-20
Author(s):  
Dan-Ni Ding ◽  
Liang-Zhen Xie ◽  
Ying Shen ◽  
Jia Li ◽  
Ying Guo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ovarian Cancer ◽  
Therapy Resistance ◽  
Genetic Alterations ◽  
The Body ◽  
Gynecological Malignancy ◽  
Microbial Infections ◽  
New Ideas ◽  
Exogenous Factors

Oxidative stress (OS) arises when the body is subjected to harmful endogenous or exogenous factors that overwhelm the antioxidant system. There is increasing evidence that OS is involved in a number of diseases, including ovarian cancer (OC). OC is the most lethal gynecological malignancy, and risk factors include genetic factors, age, infertility, nulliparity, microbial infections, obesity, smoking, etc. OS can promote the proliferation, metastasis, and therapy resistance of OC, while high levels of OS have cytotoxic effects and induce apoptosis in OC cells. This review focuses on the relationship between OS and the development of OC from four aspects: genetic alterations, signaling pathways, transcription factors, and the tumor microenvironment. Furthermore, strategies to target aberrant OS in OC are summarized and discussed, with a view to providing new ideas for clinical treatment.

Updates of the role of oxidative stress in the pathogenesis of ovarian cancer

2017 ◽  
Vol 145 (3) ◽  
pp. 595-602 ◽  
Author(s):  
Ghassan M. Saed ◽  
Michael P. Diamond ◽  
Nicole M. Fletcher
Keyword(s):  
Oxidative Stress ◽  
Ovarian Cancer

Abstract B49: The role of oxidative stress in the development of cisplatin resistance in epithelial ovarian cancer

2013 ◽  
Author(s):  
Jimmy Belotte ◽  
Nicole Fletcher ◽  
Awoniyi Awonuga ◽  
Mitchell Alexis ◽  
Husam Abu-soud ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Cisplatin Resistance

scholarly journals NCMP-16. THE ROLE OF p38 AND JNK MAPK PATHWAYS IN CISPLATIN CHEMOTHERAPY-RELATED COGNITIVE IMPAIRMENT

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii126-ii126
Author(s):  
Naomi Lomeli ◽  
Kaijun Di ◽  
Daniela Bota
Keyword(s):  
Oxidative Stress ◽  
Ovarian Cancer ◽  
Cognitive Impairment ◽  
Rat Model ◽  
Dendritic Spine ◽  
Hippocampal Neurons ◽  
Mapk Signaling ◽  
Spine Density

Abstract OBJECTIVES Chemotherapy-related cognitive impairment (CRCI) is an adverse sequela of cancer treatment commonly reported in cancer survivors. Cisplatin is used for the treatment of various malignancies including ovarian, testicular, head and neck cancers, and pediatric brain tumors. More than 30% of advanced ovarian cancer patients develop CRCI during and after platinum-based chemotherapy. We examined the role of p38 and c-Jun N-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) activation in cisplatin-induced CRCI, and whether the small molecule p38 MAPK inhibitor Neflamapimod and JNK inhibitor SP600125, can prevent cisplatin-induced neuronal damage. The p38 and JNK MAPK signaling pathways are involved in various stress response pathways in the CNS including oxidative stress. METHODS The effect of cisplatin on cognition in an ovarian cancer female rat model was assessed by novel object recognition (NOR). Hippocampal glutathione levels were measured post-behavioral testing. P38 and JNK MAPK signaling activation were assessed in the neural cell lines PC12 and SH-SY5Y by Western blot. Cultured hippocampal neurons were pretreated with Neflamapimod or SP600125 followed by cisplatin for 24 hours, and dendritic spine density and branch length were quantified. RESULTS Cisplatin increased phospho-p38 and phospho-JNK MAPK protein levels in PC12 and SH-SY5Y cells. Cisplatin reduced dendritic branching and spine density, which was prevented by Neflamapimod and SP600125 pre-treatment in hippocampal neurons, in vitro. Chronic cisplatin treatment decreased hippocampal glutathione levels and impaired cognitive function in the ovarian cancer rat model. DISCUSSION The cognitive deficits caused by cisplatin results in part from dendritic damage and neural apoptosis, which is mediated by oxidative stress and the p38 and JNK MAPK pathways. P38 and JNK MAPK inhibition mitigated cisplatin-induced dendritic spine loss and branching in vitro. Next, we will examine whether Neflamapimod and SP600125 administration in an ovarian cancer rat model is safe and if they can prevent cognitive impairment.

792: Role of Oxidative Stress in Tumorigenic Potential of Bladder Cancer Cells

2005 ◽  
Vol 173 (4S) ◽  
pp. 214-215 ◽  
Author(s):  
Daniel Cho ◽  
Xiao Fang Ha ◽  
J. Andre Melendez ◽  
Louis J. Giorgi ◽  
Badar M. Mian
Keyword(s):  
Oxidative Stress ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Tumorigenic Potential ◽  
Bladder Cancer Cells
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