Background: P2Y12 Reaction Units (PRU) is an index of platelet activity after treatment with clopidogrel. Apart from the reactions of the P2Y12 fit in dual antiplatelet therapy (DAPT) with clopidogrel after percutaneous coronary intervention (PCI), cardiovascular events actually occur in some patients, probably due to dysfunction of genetic cytochrome P450 2C19 (CYP2C19), which is the major metabolic enzymes clopidogrel. As a test to predict patient’s CYP2C19 phenotypes may be less flexibility common in everyday clinical practice, the purpose of this study was to test whether the measured levels of several cytokines in patients presenting with Prus desired in DAPT with clopidogrel can be a substitute for testing CYP2C19 phenotypes.
Methods: We analyzed the relationship between the PRU, serum levels of 51 cytokines and CYP2C19 phenotypes in 22 patients receiving DAPT with aspirin and clopidogrel after PCI.
Results: Seventeen, 18, and 19 of 22 patients showed PRU ≤ 208, 230 ≤ PRU and PRU ≤ 262, respectively. Approximately 60% of patients have a dysfunction of genetic metabolism of CYP2C19, and serum levels of interleukin-18 independently increased in patients (p = 0.024 for patients with PRU ≤ 208, p = 0.021 by PRU ≤ 230, and p = 0.020 by PRU ≤ 262) , Area under the curve in the plot receiver operating characteristic curve for serum levels of interleukin-18 was 0.94, 0.96, and 0.90 in the non-extensive metabolizer patients with PRU ≤ 208, 230 ≤ PRU and PRU ≤ 262, respectively -masing.
Conclusion: Serum levels of interleukin-18 may be a predictor for diagnosing patients receiving DAPT unwanted by clopidogrel, CYP2C19 may be due to genetic dysfunction regardless of the P2Y12 reaction fits after PCI.
Serum interleukin-18 levels as a predictor for patients with genetic dysfunction of cytochrome P450 2C19 in dual antiplatelet therapy with clopidogrel
Genetic alteration of interleukin-17 and related genes in human prostate cancer.
Interleukin-17 (IL-17) has been shown to promote the development of hormone-naive prostate cancer (HNPC) and castration-resistant prostate cancer (CRPC) and lymph node metastasis in mouse models. changes in the gene IL-17 family of cytokines and their downstream genes in human prostate cancer has not been investigated. We studied 7 dataset archived at cBioPortal and ask gene changes in a total of 1303 cases of human prostate cancer. 35 genes examined, including IL-17 family of cytokines and receptors, IL-17 gene-downstream, and genes associated with IL-17 gene-downstream.
We found that 34/35 (97%) genes have a more significant change in metastatic prostate cancer (the rate of change ranging from 3.42% to 13.01%) of primary prostate cancer (the rate of change ranging from 0.40% to 2.96%). 15/35 (43%) genes have a more significant change in the prime of HNPC primary CRPC. 34/35 (97%) genes have a more significant change in CRPC metastases from primary HNPC. Only three genes (S100A7, S100A8 and S100A9) have a more significant change in CRPC metastases from CRPC primer.
Description: ?-Interleukin II (44-56), (C68H113N19O19) is a peptide with the sequence NH2-ILE-LEU-ASN-GLY-ILE-ASN-ASN-TYR-LYS-ASN-PRO-LYS-LEU-COOH, MW= 1500.7.
Description: ?-Interleukin II (44-56), (C68H113N19O19) is a peptide with the sequence NH2-ILE-LEU-ASN-GLY-ILE-ASN-ASN-TYR-LYS-ASN-PRO-LYS-LEU-COOH, MW= 1500.7.
Description: ?-Interleukin II (44-56), (C68H113N19O19) is a peptide with the sequence NH2-ILE-LEU-ASN-GLY-ILE-ASN-ASN-TYR-LYS-ASN-PRO-LYS-LEU-COOH, MW= 1500.7.
Custom Peptide Synthesis (>70% antigen grade; mass spec, hplc (mg-kg size, price based upon peptide size: 2-100 aa)
The changes in gene amplification most genes (97%), whereas the gene deletion, missense mutations, and truncating mutations are very rare. 7/35 (20%) genes have a more significant change in the primary neuroendocrine prostate cancer (NEPC) of primary adenocarcinoma (AC). 23/35 (66%) genes have a more significant change in NEPC metastasis of AC metastasis. Only three genes (S100A7, S100A8 and S100A9) have a more significant change in NEPC metastasis of AC metastases with neuroendocrine features. Most of the changes in NEPC metastasis gene is a gene amplification (80%), whereas the gene deletion, missense mutations, and truncating mutations are very rare.
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