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Inflammation and lung cancer: Oxidative stress, ROS, and DNA damage

Title
Inflammation and lung cancer: Oxidative stress, ROS, and DNA damage
Type
Chapter or Part of a Book
Year
2017
Authors
Gomes, M
(Author)
Other
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Teixeira, AL
(Author)
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Coelho, A
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Araújo, A
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Rui Medeiros
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ICBAS
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Book
Pages: 215-223
ISBN: 9781498735469; 9781498735452
Indexing
Other information
Authenticus ID: P-00T-WQY
Abstract (EN): Cancer is the leading cause of death in the world, accounting for more than 25% of all deaths in developed countries, and lung cancer is the most common cause of cancer-related death in the world. The predominant risk factor for this cancer is smoking, accounting for approximately 90% of these lung cancer deaths. Furthermore, lung cancer risk is associated with several indicators of inflammation. The inflammation process is a complex response to stimuli involving the interplay of host cells and signaling molecules, such as angiogenesis factors and chemokines. Inhalation of air pollutants and microorganisms results in lung injury and generation of reactive oxygen species/reactive nitrogen species (ROS/RNS), leading to a cascade of signaling events that trigger the production of proinflammatory cytokines. Inflammation is the primary reaction of a tissue to eliminate pathogenic insult and injured tissue components in order to restore normal physiological functions or replace the irreparable tissue with scar tissue. Cancer and inflammation are closely linked, and many inflammatory conditions increase the risk of cancer development. Matrix metalloproteins are clearly important effectors in inflammation both in physiological situations, such as tissue repair, and in pathological inflammatory conditions and cancer. A better understanding of the role of ROS/RNS in lung inflammation and cancer is probable to inspire new strategies for lung cancer prevention and treatment. © 2016 by Taylor & Francis Group, LLC.
Language: English
Type (Professor's evaluation): Scientific
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Gomes, M; Teixeira, AL; Coelho, A; Rui Medeiros; Araújo, A
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