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https://www.selleckchem.com/products/pf-3758309.html BACKGROUND Until recently, patients who have the same type and stage of cancer all receive the same treatment. It has been established, however, that individuals with the same disease respond differently to the same therapy. Further, each tumor undergoes genetic changes that cause cancer to grow and metastasize. The changes that occur in one person's cancer may not occur in others with the same cancer type. These differences also lead to different responses to treatment. Precision medicine, also known as personalized medicine, is a strategy that allows the selection of a treatment based on the patient's genetic makeup. In the case of cancer, the treatment is tailored to take into account the genetic changes that may occur in an individual's tumor. Precision medicine, therefore, could be defined in terms of the targets involved in targeted therapy. METHODS A literature search in electronic data bases using keywords "cancer targeted therapy, personalized medicine and cancer combination therapies" was conducted erapies. Acute lung injury (ALI) is caused by severe infection, and urgently needs effective treatments or validated pharmacological targets. Formyl peptide receptor 2 (Fpr2) plays essential roles in immune responses and inflammatory diseases. In the present study, Fpr2 expression was markedly increased in lung tissues of lipopolysaccharide (LPS)-challenged mice, and these effects were confirmed in LPS-stimulated macrophages. Then, the in vitro analysis suggested that Fpr2 knockdown significantly decreased LPS-induced inflammatory response in macrophages. Notably, the in vivo experiments indicated that Fpr2 deficiency alleviated ALI in LPS-treated mice, as evidenced by the improved histological changes in lung, reduced protein concentrations in bronchoalveolar lavage fluid (BALF) and decreased neutrophil infiltration. In addition, LPS-induced pulmonary inflammation was ameliorated by Fpr2 knockout, which was p

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