Sung Han Kim has completed his MD from Seoul National University of Medicine, Seoul, Korea and Postdoctoral studies from National Cancer Center, Goyang, Korea and Seoul National University of Medicine, Seoul , Korea. He is the Clinical Staff and Associate Researcher and Director of Jinsoo Chung, Prostate Cancer Center, National Cancer Center, Goyang, Korea. He has published more than 30 papers in reputed journals.
The study was aimed to identify targetable genes in PC from The Cancer Genome Atlas (TCGA), and to validate the significance of the genes identified in clinical studies using immunohistochemistry in PC patients’ prostatectomy microarray. Omics data and clinical data of 550 PC patients were obtained from TCGA. Several significant genes were identified from TCGA dataset having the most number of point mutation to exhibit significantly strong positive relationship in expression values with the most frequently mutated gene. Further validation of different expression values for the list of genes between tumor and normal lesions was performed to evaluate their prognostic significance using tissue microarray of 514 prostatectomy specimens by performing immunohistochemistry in clinical setting from a single cancer institution. Prognostic powers of these genes were investigated on the NCC dataset. Immunohistochemistry were performed on the genes associated with the most mutated gene. The gene markers’ prognostic factors were analyzed using Cox proportional hazard analysis with a significant p-value<0.05. FRG1B gene was found lineage-specific mutation with ESRP1, RAD51, and CHEK2 genes in the TCGA dataset. The union of samples with these three up-regulated markers with FRG1B mutation showed significant differences in disease-free survival compared to the samples without expression of two combinational series (p<0.05). Analysis of the clinicopathological factors related to three markers suggested that expression of ESRP1 was a significant risk factor for biochemical recurrence (BCR, HR 1.003) and cancer-specific survival (HR 1.048), even after adjusting for significant prognostic clinicopathological factors of BCR and CSS (p<0.05). On the other hand, CHEK2 was not significant in any BCR and CSS. RAD51 could not be evaluated because of its overall overexpressed in specimens. The study identified that ESRP1 was a potentially significant target gene of survival prognoses in PC.
Joanna Tracz has received his/her Bachelor’s degree in 2015 and completed his/her Master’s degree in Chemical Science in 2016 and Biological Science in 2017. Presently, She/he is a PhD student in Laboratory of Mass Spectrometry at the Polish Academy of Sciences. She/he is involved in project concerning the molecular mechanism of atherosclerosis progression in chronic kidney disease.
The major cause of mortality in patients with chronic kidney disease (CKD) is atherosclerosis related to traditional and non-traditional risk factors. However, the understanding of the molecular specificity that distinguishes the risk factors for classical cardiovascular disease (CVD) and CKD-related atherosclerosis (CKD-A) is far from complete. Although dyslipidemia is common in CKD patients, epidemiological data show that in CKD the link between cholesterol and its fractions is not as straightforward like in the general population. CKD is frequently accompanied by reduced of plasma HDL concentrations, and normal or even low serum total cholesterol and LDL concentrations. Normal HDL function is reverse cholesterol transport from peripheral cells and its transport to the liver. HDL protects of LDL against oxidation and suppress of systemic inflammation. Therefore, HDL deficiency is the key in perpetuating chronic inflammation and oxidative stress leading to atherosclerosis. On the other hand, it is suggested that lipid abnormalities in CKD are characterized by more qualitative abnormalities and may be related to HDL function rather than HDL deficiency. Mass spectrometry-based proteomic analysis is excellent, powerful tool for tracking molecular changes during progression of CKD. In this study we investigated the alterations in leukocytes protein accumulation in patients with CKD and classical cardiovascular disease (CVD) without CKD. Cells collected from patients in various stages of CKD, CVD patients without symptoms of kidney dysfunction and healthy volunteers (HVs), were analyzed by a label-free proteomic approach. Obtained cells were also analyzed in term of inflammation modulators and the oxidative status enzymes. Label-free quantitation analysis revealed characteristic proteins of particular stage of atherosclerotic plaque formation process and CKD progression. All proteomic data were subjected to bioinformatic analysis for identification of specific for CKD and CVD pathways. Further research should focus on precise profiling of metabolites and/or lipids present in cells during the atherosclerosis development.