Role of Oxidative Stress in Pathophysiology of Diseases 2020
DOI: 10.1007/978-981-15-1568-2_14
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Oxidative Stress and Inflammation Can Fuel Cancer

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Cited by 27 publications
(20 citation statements)
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“…In addition, tumor-promoting inflammation was also inhibited by CORM-2, as demonstrated by the reduction of serous levels of inflammatory markers (i.e., tumor necrosis factor alpha, IL-1β, and IL-6) in orthotopic lung cancer mice [ 70 ]. Intriguingly, growing body of literature has reported the involvement of ROS in the development of both genomic instability and inflammation [ 5 , 9 , 105 ]. Because CO-RMs have been documented as potent candidates in a variety of diseases owing to their broad activities, particularly anti-inflammation and antioxidant [ 20 , 25 ], it is rationale to believe that ROS may be an important signaling by which CO-RMs regulate two enabling characteristics of cancers.…”
Section: Mechanisms Behind the Anticancer Activities Of Co-rms: An Outlook From Ros Biology And Medicinementioning
confidence: 99%
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“…In addition, tumor-promoting inflammation was also inhibited by CORM-2, as demonstrated by the reduction of serous levels of inflammatory markers (i.e., tumor necrosis factor alpha, IL-1β, and IL-6) in orthotopic lung cancer mice [ 70 ]. Intriguingly, growing body of literature has reported the involvement of ROS in the development of both genomic instability and inflammation [ 5 , 9 , 105 ]. Because CO-RMs have been documented as potent candidates in a variety of diseases owing to their broad activities, particularly anti-inflammation and antioxidant [ 20 , 25 ], it is rationale to believe that ROS may be an important signaling by which CO-RMs regulate two enabling characteristics of cancers.…”
Section: Mechanisms Behind the Anticancer Activities Of Co-rms: An Outlook From Ros Biology And Medicinementioning
confidence: 99%
“…Despite of remaining ambiguous, the discovery of the involvement of oxidative stress during the course of cancer can be considered a noticeable milestone in cancer biology. A series of reviews has reported that the disturbance of redox balance may result in numerous oncogenic cellular events, such as genome instability and mutations, uncontrolled cell proliferation, evasion of cell death, angiogenesis, invasiveness, and metastasis, among others [ [4] , [5] , [6] ]. On the other hand, chronic inflammation has also been shown to involve in multiple steps in carcinogenesis [ 7 , 8 ].…”
Section: Introductionmentioning
confidence: 99%
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“…The macrophages that dominate the chronic inflammatory microenvironment produce increased levels of ROS and RNI, which in turn interact with the DNA of proliferating epithelial cells and generate permanent genetic mutations leading to the malignant transformation. Excessive ROS/RNI production during the process of oxidative metabolism has been reported to promote the synthesis and secretion of inflammation-promoting cytokines such as tumor necrosis factor (TNF)-α, interferon-gamma (IFN-γ), and interleukin (IL)-6 [64,65]. Moreover, other inflammatory mediators such as chemokines, growth factors, and eicosanoids in tumor microenvironments contribute to inflammation-triggered tumor progression and metastasis via modulating the immune response, inhibiting apoptosis, inducing cell proliferation, and promoting the accumulation of oncogenic mutations [66].…”
Section: Esophagealmentioning
confidence: 99%
“…Excess ROS can cause cellular damage by reacting with cellular components such as proteins, lipids, or DNA [ 3 ]. In the human body, oxidative stress plays a crucial role in the onset of several diseases including cancer, diabetes, cardiovascular and respiratory diseases [ 4 , 5 ]. Oxidative stress can both be a cause and a consequence of inflammation.…”
Section: Introductionmentioning
confidence: 99%