Gene/Protein Disease Symptom Drug Enzyme Compound
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 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity, a worldwide epidemic, confers increased risk for multiple serious conditions, including cancer, and is increasingly recognized as a growing cause of preventable cancer risk. Chronic inflammation, a well-known mediator of cancer, is a central characteristic of obesity, leading to many of its complications, and obesity-induced inflammation confers additional cancer risk beyond obesity itself. Multiple mechanisms facilitate this strong association between cancer and obesity. Adipose tissue is an important endocrine organ, secreting several hormones, including leptin and adiponectin, and chemokines that can regulate tumor behavior, inflammation, and the tumor microenvironment. Excessive adipose expansion during obesity causes adipose dysfunction and inflammation to increase systemic levels of proinflammatory factors. Cells from adipose tissue, such as cancer-associated adipocytes and adipose-derived stem cells, enter the cancer microenvironment to enhance protumoral effects. Dysregulated metabolism that stems from obesity, including insulin resistance, hyperglycemia, and dyslipidemia, can further impact tumor growth and development. This review describes how adipose tissue becomes inflamed in obesity, summarizes ways these mechanisms impact cancer development, and discusses their role in four adipose-associated cancers that demonstrate elevated incidence or mortality in obesity.
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PMID:Obesity, Inflammation, and Cancer. 2719 54

HMG-CoA reductase inhibitors (known as statins) are commonly prescribed worldwide for the management of coronary heart disease and the underlying dyslipidemia. This class of drugs has been shown to infer a significant decrease in the risk of cardiovascular morbidity and mortality. Only recently though have the beneficial effects of statins in other diseases such as non-alcoholic steatohepatitis been highlighted. Importantly, also, multiple studies have revealed that statin use was associated with lower cancer-associated mortality across multiple types of cancers. This work aims to review those studies with a particular focus on liver cancer. We also provide a review of the proposed mechanisms of action describing how statins can induce chemo-preventive and antitumor effects.
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PMID:Hepatocellular Carcinoma and Statins. 3320 Sep 23

Metabolic complications affect over 50% of solid organ transplant recipients. These include post-transplant diabetes, non-alcoholic fatty liver disease, dyslipidemia, and obesity. Pre-existing metabolic disease is further exacerbated with immunosuppression and post-transplant weight gain. Patients transition from a state of cachexia induced by end-organ disease to a pro-anabolic state after transplant due to weight gain, sedentary lifestyle and suboptimal dietary habits in the setting of immunosuppression. Specific immunosuppressants have different metabolic effects, though all the foundation/maintenance immunosuppressants (CNIs, mTOR inhibitors) increase the risk of metabolic disease. In this comprehensive review, we summarize the emerging knowledge of the molecular pathogenesis of these different metabolic complications, and the potential genetic contribution (recipient +/- donor) to these conditions. These metabolic complications impact both graft and patient survival, particularly increasing the risk of cardiovascular and cancer-associated mortality. The current evidence for prevention and therapeutic management of post-transplant metabolic conditions is provided while highlighting gaps for future avenues in translational research.
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PMID:Metabolic Consequences of Solid Organ Transplantation. 3324 13