Inflammation and Lung Cancer

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506 g
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241x160x17 mm
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Steven M. Dubinett is Professor of Medicine and Pathology at the David Geffen School of Medicine at UCLA, Senior Associate Dean for Translational Research at UCLA, as well as the Director of the UCLA Lung Cancer Research Program. Building on original discoveries relevant to inflammation in the pathogenesis of lung cancer, he has developed a translational research program which now utilizes these laboratory-based discoveries in the translational research. Dr. Dubinett has received continuous peer-reviewed federal funding for translational lung cancer research for more than 20 years.
Presents the inflammatory tumor microenvironment in lung cancer
Inflammation and Lung Cancer: The relationship to COPD.- Inflammation and Lung Cancer: The role of EMT.- Inflammation and Lung Cancer: Molecular pathology.- Inflammation and Lung Cancer: Prevention.- Inflammation and Lung Cancer: The Link to Angiogenesis.- Inflammation and Lung Cancer: Eicosanoids.- Inflammation and Lung Cancer: Addressing Inflammation with Immunotherapy.
In recent years there have been various discoveries connecting inflammation and lung cancer and clearly there is growing interest in this area of cancer research. The link between unresolved inflammation and cancer has been well established with estimates that 15% of cancer deaths are inflammation-related. Evidence for this link includes the following: a) some inflammatory diseases are associated with increased risk of cancer development; b) inflammatory mediators are present surrounding and within most tumors; c) overexpression of inflammatory cytokines increases cancer development and progression in murine studies; d) inhibition of inflammatory mediators decreases cancer development and progression; and e) the use of non-steroidal anti-inflammatory drugs (NSAIDs) has been found to decrease cancer incidence and delay progression. The volume will present aspects of the inflammatory tumor microenvironment (TME), its many roles in tumor progression and metastasis, including creation of a hypoxic environment, increased angiogenesis and invasion, changes in expression of micro-RNAs (miRNAs) and an increase in a stem cell phenotype. The book will also cover the mechanisms of inflammatory mediators. Chronic overexpression of inflammatory mediators in the TME, as seen in smokers and patients with non-small cell lung cancer (NSCLC), can also lead to increased tumor initiation, progression, invasion and metastasis. The volume will provide a comprehensive perspective of the latest findings and summaries of progress made regarding inflammation and its connection to lung cancer.

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