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10.1200/JCO.2016.67.4283 http://scihub22266oqcxt.onion/10.1200/JCO.2016.67.4283 C5562428!5562428!27903155     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Oncol 2016 ; 34 (35): 4270-6 Nephropedia Template TP {{tp|p=27903155|t=2016. Obesity and Cancer Mechanisms: Tumor Microenvironment and Inflammation |pdf=|usr=}}{{27903155}} gab.com Text Obesity and Cancer Mechanisms: Tumor Microenvironment and Inflammation JO: J Clin Oncol http://www.kidney.de/pget.php?&tw=1&pmid=27903155 #FOAvip Purpose: There is growing evidence that inflammation is a central and reversible mechanism through which obesity promotes cancer risk and progression. Methods: We review recent findings regarding obesity-associated alterations in the microenvironment and the local and systemic mechanisms through which these changes support tumor growth. Results: Locally, hyperadiposity is associated with altered adipose tissue function, adipocyte death, and chronic low-grade inflammation. Most individuals who are obese harbor inflamed adipose tissue, which resembles chronically injured tissue, with immune cell infiltration and remodeling. Within this distinctly altered local environment, several pathophysiologic changes are found that may promote breast and other cancers. Consistently, adipose tissue inflammation is associated with a worse prognosis in patients with breast and tongue cancers. Systemically, the metabolic syndrome, including dyslipidemia and insulin resistance, occurs in the setting of adipose inflammation and operates in concert with local mechanisms to sustain the inflamed microenvironment and promote tumor growth. Importantly, adipose inflammation and its protumor consequences can be found in some individuals who are not considered to be obese or overweight by body mass index. Conclusion: The tumor-promoting effects of obesity occur at the local level via adipose inflammation and associated alterations in the microenvironment, as well as systemically via circulating metabolic and inflammatory mediators associated with adipose inflammation. Accurately characterizing the obese state and identifying patients at increased risk for cancer development and progression will likely require more precise assessments than body mass index alone. Biomarkers of adipose tissue inflammation would help to identify high-risk populations. Moreover, adipose inflammation is a reversible process and represents a novel therapeutic target that warrants further study to break the obesity-cancer link. Twit Text FOAVip Obesity and Cancer Mechanisms: Tumor Microenvironment and Inflammation ????J Clin Oncol http://www.kidney.de/pget.php?&tw=1&pmid=27903155 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27903155 #FOAvip English Wikipedia <ref>{{Cite pmid|27903155}}</ref> Obesity and Cancer Mechanisms: Tumor Microenvironment and Inflammation #MMPMID27903155 Iyengar NM; Gucalp A; Dannenberg AJ; Hudis CA J Clin Oncol 2016[Dec]; 34 (35): 4270-6 PMID27903155show ga Purpose: There is growing evidence that inflammation is a central and reversible mechanism through which obesity promotes cancer risk and progression. Methods: We review recent findings regarding obesity-associated alterations in the microenvironment and the local and systemic mechanisms through which these changes support tumor growth. Results: Locally, hyperadiposity is associated with altered adipose tissue function, adipocyte death, and chronic low-grade inflammation. Most individuals who are obese harbor inflamed adipose tissue, which resembles chronically injured tissue, with immune cell infiltration and remodeling. Within this distinctly altered local environment, several pathophysiologic changes are found that may promote breast and other cancers. Consistently, adipose tissue inflammation is associated with a worse prognosis in patients with breast and tongue cancers. Systemically, the metabolic syndrome, including dyslipidemia and insulin resistance, occurs in the setting of adipose inflammation and operates in concert with local mechanisms to sustain the inflamed microenvironment and promote tumor growth. Importantly, adipose inflammation and its protumor consequences can be found in some individuals who are not considered to be obese or overweight by body mass index. Conclusion: The tumor-promoting effects of obesity occur at the local level via adipose inflammation and associated alterations in the microenvironment, as well as systemically via circulating metabolic and inflammatory mediators associated with adipose inflammation. Accurately characterizing the obese state and identifying patients at increased risk for cancer development and progression will likely require more precise assessments than body mass index alone. Biomarkers of adipose tissue inflammation would help to identify high-risk populations. Moreover, adipose inflammation is a reversible process and represents a novel therapeutic target that warrants further study to break the obesity-cancer link. äObesity and Cancer Mechanisms: Tumor Microenvironment and Inflammation(epmc).pdf DeepDyve Pubget Overpricing