Journal of investigative medicine : the official publication of the American Federation for Clinical Research
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With the continued failures of both early diagnosis and treatment options for pancreatic cancer, it is now time to comprehensively evaluate the role of the immune system on the development and progression of pancreatic cancer. It is important to develop strategies that harness the molecules and cells of the immune system to treat this disease. ⋯ We hypothesize that the role of the immune system in tumor development and progression is tissue specific. Our hope is that better understanding of this process will lead to better treatments for this devastating disease.
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Oxidative stress and free radicals have been indicated to be associated with increased risk of various cancers. Paraoxonase 1 (PON1) gene, encoding PON1 protein, plays an important role as an endogenous free-radical scavenging molecule. The aim of the present study was to determine whether genetic polymorphisms of the PON1 gene are associated with the risk and prognosis of non-small cell lung cancer (NSCLC). ⋯ The Q192R polymorphism of the PON1 gene may be associated with the risk and prognosis of NSCLC in a Chinese Han population.
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This study investigated the prognostic value of neutrophil gelatinase-associated lipocalin (NGAL) in patients with ST-segment elevation myocardial infarction (STEMI). ⋯ High NGAL levels may be associated with poor prognosis after PCI in patients with STEMI. However, further studies with larger numbers of patients and longer follow-up are required to evaluate the usefulness of plasma NGAL level for predicting prognosis of STEMI.
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The fat mass and obesity-associated (FTO) gene has recently attracted attention as one of the obesity-related genes. Obesity-related gene polymorphisms may be associated with the development of atherothrombosis in relation to platelets. The present study investigated the association between FTO gene polymorphisms (rs1558902, T/A) and hematological parameters, in particular the platelet counts. ⋯ The subjects with the A-allele (n = 73) showed significantly higher platelet counts than those without the A-allele (mean [SD], 237 [58] vs 217 [57] × 10/L, P < 0.05). Even when multiple-adjusted analyses were performed, the platelet counts continued to differ significantly and independently of other variables, including obesity-related parameters such as the index of insulin resistance or high-sensitivity C-reactive protein, between the subjects with and without the A-allele. The FTO gene polymorphisms may be associated with the minor but significant modulation of platelet counts in this population.