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Some genetic alterations of glutathione S-transferase omega 2 (GSTO2) have been reported to increase the risk of many malignancies, including hepatocellular carcinoma (HCC); however, their prognostic capability remained unresolved in HCC patients treated with transarterial chemoembolization (TACE). To fill this gap, we genotyped three well-defined polymorphisms in GSTO2 to assess whether they can predict overall survival among 228 HCC patients under TACE treatment. The median follow-up time and survival time were 22.0 months (range 3.0-60.0) and 19.2 months, respectively. Only one of three polymorphisms examined, rs157077, was significantly associated with overall survival of TACE-treated HCC (P = 0.003), and its mutant allele conferred a higher risk of death than its wild homozygotes (hazard ratio 1.58, 95 % confidence interval 1.17-2.14). Moreover, carriers of this mutant allele had higher tissue GSTO2 expression, reinforcing the prognostic capability of GSTO2 rs157077 for HCC, especially in combination with age and tumor-node-metastasis (TNM) stage. Taken together, we for the first time provided evidence supporting the prognostic role of GSTO2 in the progression of TACE-treated HCC.

Background: High mobility group box 1 (HMGB1), a versatile protein with intranuclear and extracellular functions, plays an important role in a variety of human cancers. However, the clinical/prognostic significance of HMGB1 expression in human bladder urothelial carcinoma (BUC) remains unclear. The aim of this study was to investigate the HMGB1 expression in human BUC with regard to its clinical and prognostic significance. Patients and methods: HMGB1 mRNA and protein expressions in tumor and paired normal bladder tissues were detected in 20 BUC cases by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. HMGB1 protein expression in 165 primary BUC tissues was evaluated by immunohistochemistry (IHC), and its correlations with clinicopathological characteristics and prognosis were also analyzed. Student's t-test, X2 test, Kaplan-Meier plots, and Cox proportional hazard regression model were performed to analyze the data. Results: By using qRT-PCR and Western blot, the upregulated expression of HMGB1 mRNA and protein was detected in BUC, compared with paired normal tissue (P＜0.05). By using IHC, high HMGB1 expression was examined in 84 of 165 (51.0%) BUC cases. High HMGB1 expression was significantly correlated with poorer differentiation and higher T and N classification (all P＜0.05). Univariate analysis showed that high HMGB1 expression was significantly associated with a shortened patients' overall survival (OS) and disease-free survival (DFS; both P＜0.001). In different subgroups of BUC patients, HMGB1 expression was a prognostic factor in patients with different histological grades or T classification (all P＜0.05), pN- (both P＜0.001) for OS and DFS, and pT1/pN- (P＜0.05) for OS. HMGB1 expression, as well as pT and pN status, was an independent prognostic factor for both OS (P=0.001, hazard ratio [HR] =2.973, 95% confidence interval [CI] =1.550-5.704) and DFS (P＜0.001, HR =3.019, 95% CI =1.902-4.792) in multivariate analysis. Conclusion: Overexpression of HMGB1 may be a new independent molecular marker for the poor prognosis of patients with BUC. [ABSTRACT FROM AUTHOR]

Background: Pyruvate kinase M2 (PKM2) is a key regulator of the Warburg effect and has critical functions in glycolysis, contributing to the Warburg effect, tumor growth, angiogenesis, cell division, metastasis, and apoptosis. The high expression of PKM2 in various solid tumors renders it a potential biomarker of tumorigenesis and tumor invasion, but the expression and role of PKM2 in bladder cancer have not been studied extensively. Patients and methods: Western blot and immunohistochemistry (IHC) were used to measure the expression of PKM2, and quantitative real-time polymerase chain reaction (PCR) was performed to determine PKM2 mRNA levels. The relationships between PKM2 expression and clinicopathological parameters and prognosis were analyzed using the Kaplan-Meier plots and a Cox proportional hazards regression model. Results: Compared with paired adjacent normal bladder tissues, PKM2 mRNA and protein levels were found to be higher in urothelial carcinoma of the bladder (UCB) samples by realtime PCR and Western blot. By IHC, high expression of PKM2 was seen in 117 of 215 UCBs (54.4%) and in eight of 90 adjacent normal bladder tissues (8.9%). The expression of PKM2 was significantly associated with grade, stage, and lymph node status (P＜0.001). In the univariate survival analysis, a significant association between PKM2 expression and shorter patient survival was observed (P＜0.001). In different subsets of UCB patients, we found that PKM2 expression was a prognostic factor in patients with G2 (P=0.009), G3 (P＜0.001), pTa/pTis (P=0.006), pT1, pT2-4, and pN-disease (P＜0.001). Importantly, PKM2 expression (P=0.003), with tumor histological grade (P＜0.001), pT (P＜0.001), and pN status (P=0.005), was a significant independent prognostic parameter in the multivariate analysis. Conclusion: PKM2 protein and mRNA are upregulated in UCBs and may serve as molecular markers for a poor prognosis in patients with UCB. [ABSTRACT FROM AUTHOR]

Background: The effects of the estimated glomerular filtration rate (eGFR) and cystatin C on clinical outcomes on intracerebral hemorrhage (ICH) remain unclear. We investigated the associations of eGFR and cystatin C with 3-month functional outcome and all-cause mortality in acute ICH patients. Methods: A total of 365 patients with acute ICH were enrolled. Serum creatinine and cystatin C levels were measured within 24 h of admission. Outcomes at 3-month were evaluated by interviews with patients or their family members. Poor functional outcome was defined as a modified Rankin Scale score ≥ 3. Results: During the 3-month follow-up, 154 patients experienced poor functional outcome, and 48 patients died from all causes. Low eGFR level was associated with poor outcome (adjusted OR 8.95; 95% CI 2.13-37.66; p-trend = 0.045) and all-cause mortality (adjusted hazards ratio (HR) 5.10; 95% CI 2.00-13.03; p-trend = 0.001). Additionally, a high cystatin C level was also found to be associated with all-cause mortality (adjusted HR 4.01; 95% CI 1.09- 14.72; p-trend = 0.015). However, no significant association between cystatin C and poor functional outcome was observed (p-trend = 0.615). Conclusions: Low eGFR at baseline predicts poor functional outcome and all-cause mortality at 3-month in acute ICH patients. Also, high cystatin C was associated with increased risk of mortality but not with poor functional outcome. [ABSTRACT FROM AUTHOR]

Some genetic alterations of glutathione S-transferase omega 2 (GSTO2) have been reported to increase the risk of many malignancies, including hepatocellular carcinoma (HCC); however, their prognostic capability remained unresolved in HCC patients treated with transarterial chemoembolization (TACE). To fill this gap, we genotyped three well-defined polymorphisms in GSTO2 to assess whether they can predict overall survival among 228 HCC patients under TACE treatment. The median follow-up time and survival time were 22.0 months (range 3.0-60.0) and 19.2 months, respectively. Only one of three polymorphisms examined, rs157077, was significantly associated with overall survival of TACE-treated HCC ( P = 0.003), and its mutant allele conferred a higher risk of death than its wild homozygotes (hazard ratio 1.58, 95 % confidence interval 1.17-2.14). Moreover, carriers of this mutant allele had higher tissue GSTO2 expression, reinforcing the prognostic capability of GSTO2 rs157077 for HCC, especially in combination with age and tumor-node-metastasis (TNM) stage. Taken together, we for the first time provided evidence supporting the prognostic role of GSTO2 in the progression of TACE-treated HCC. [ABSTRACT FROM AUTHOR]

Background Monocyte and monocyte to high-density lipoprotein ratio (MHR) recently emerged as markers of inflammation and have been reported to be novel prognostic indicators of cardiovascular diseases. We investigated the association of monocyte and MHR with hospital discharge and 3-month outcome after acute intracerebral hemorrhage (ICH). Methods A total of 316 patients with acute ICH were enrolled from November 2011 to March 2014. Demographic characteristics, lifestyle risk factors, medical history, admission laboratory parameters, and monocyte level were recorded. Clinical outcome was disability or death (defined as having a modified Rankin Scale score ≥ 2) upon discharge or at 3 months. Results 202 patients (63.9%) experienced disability or death at hospital discharge, and 176 patients (55.7%) at 3 months post-ICH. Admission monocyte level was associated with clinical outcome at 3 months (adjusted OR, 4.17; 95% CI, 1.45–12.00; P -trend = 0.028) when highest and lowest quartiles were compared. However, no significant association was found between monocyte and discharge outcome ( P -trend = 0.102). Compared to the lowest category of MHR, the highest category was associated with a 3.87-fold increase in the odds of disability or death at discharge (95% CI, 1.17–12.76; P -trend = 0.045) and 3.08-fold increased odds of disability or death at 3-month (95% CI, 1.05–9.08; P -trend = 0.024). Conclusions In patients with acute ICH, higher MHR was associated with increased risk of disability or death at discharge and at 3 months post-ICH, however higher monocyte was only associated with increased risk of 3-month disability or death. [ABSTRACT FROM AUTHOR]