Predictive value of ACEF II score for adverse prognosis in patients with coronary heart disease after percutaneous coronary intervention.

OBJECTIVE: To investigate the predictive value of age, creatinine and ejection fraction (ACEF) II score for the incidence of major adverse cardiovascular and cerebrovascular events (MACCEs) in patients with coronary heart disease (CHD) after percutaneous coronary intervention (PCI). METHODS: A total of 445 patients with CHD who underwent PCI were consecutively enrolled. The receiver operating characteristic (ROC) curve was used to analyse the power of the ACEF II score in predicting MACCE. Kaplan-Meier survival curves and log-rank tests were chosen for survival analysis of adverse prognosis between groups. Finally, multivariate Cox proportional risk regression analysis was used to investigate independent risk factors for MACCEs in patients with CHD after PCI. RESULTS: There was a significantly higher incidence of MACCEs in patients with high ACEF II scores. The area under the ROC curve of ACEF II score was 0.718, suggesting it had ideal predictive value for MACCE risks. The ACEF II score had a best cut-off value of 1.461 (sensitivity 79.4%, specificity 53.7%). Survival analysis indicated that patients in the high-score group had a significantly lower cumulative MACCE-free survival rate. Multivariate Cox regression analysis showed that ACEF II scores ≥1.461, Gensini scores ≥61.5, age, cardiac troponin I and previous PCI were independent risk factors of MACCE in patients with CHD after PCI, while the utilisation of statins was an independent protective factor. CONCLUSIONS: The ACEF II score has an ideal capacity for risk stratification in patients with CHD undergoing PCI and offers good predictive value for MACCE in the long term.

Association of Tumor Size With Prognosis in Patients With Resectable Endometrial Cancer: A SEER Database Analysis.

This study aimed to explore the relationship between tumor size (Ts) and prognosis in endometrial cancer (EC). A total of 52,208 patients with EC who underwent total hysterectomy were selected from the Surveillance, Epidemiology, and End Results Program database. Overall survival (OS) and endometrial cancer-specific survival (ESS) were chosen as survival outcomes. The Cox proportional hazards model was used to explore the effect of Ts on prognosis. The restricted cubic splines based on the Cox regression model were used to determine the nonlinear relationship between Ts and survival. When Ts was analyzed as a categorical variable, the risk of death increased with Ts, with the highest risk in patients with Ts > 9 cm with regard to all-cause death (ACD) (hazard ratio [HR] 1.317; 95% confidence interval [CI], 1.196-1.450; P < 0.001) and endometrial cancer-specific death (ESD) (HR, 1.378; 95% CI, 1.226-1.549; P < 0.001). As a continuous variable, Ts showed a nonlinear relationship with ACD (HR, 1.061; 95% CI, 1.053-1.069; P < 0.001) and ESD (HR, 1.062; 95% CI, 1.052-1.073; P < 0.001). The risk of mortality increased quickly with Ts when Ts was less than 7.5 cm and then leveled off when Ts was larger than 7.5 cm in all patients. Among patients with lymph node metastasis, the risk of poor prognosis decreased rapidly with Ts when Ts was less than 3.5 cm, and subsequently increased sharply with Ts when Ts ranged from 3.5 cm to 7.5 cm, and then increased slowly when Ts was larger than 7.5 cm (P < 0.001 for nonlinearity). There was a nonlinear relationship between Ts and prognosis in patients with EC. Clinicians should not ignore the impact of small tumors on prognosis in EC patients with lymph node metastasis.

YSL-12, a novel microtubule-destabilizing agent, exerts potent anti-tumor activity against colon cancer in vitro and in vivo.

PURPOSE: Microtubules play a central role in various fundamental cell functions and thus become an attractive target for cancer therapy. A novel compound YSL-12 is a combretastatin A-4 (CA-4) analogue with more stability. We investigated its anti-tumor activity and mechanisms in vitro and in vivo for the first time. METHODS: Cytotoxicity was evaluated by MTT method. In vitro microtubule polymerization assay was performed using a fluorescence-based method by multifunction fluorescence microplate reader. Intracellular microtubule network was detected by immunofluorescence method. Cell cycle analysis and apoptosis were measured by flow cytometry. Metabolic stability was recorded by liquid chromatography-ultraviolet detection and liquid chromatography-mass spectrometry. In vivo anti-tumor activity was assessed using HT-29 colon carcinoma xenografts established in BALB/c nude mice. RESULTS: YSL-12 displayed nanomolar-level cytotoxicity against various human cancer cell lines. A high selectivity toward normal cells and potent activity toward drug-resistant cells were also observed. YSL-12 was identified as tubulin polymerization inhibitor evidenced by effectively inhibits tubulin polymerization and heavily disrupted microtubule networks in living HT-29 cells. YSL-12 displayed potent disruption effect of pre-established tumor vasculature in vitro. In addition, YSL-12 treatment also caused cell cycle arrest in the G2/M phase and induced cell apoptosis in a dose-dependent manner. In vitro metabolic stability study revealed YSL-12 displayed considerable better stability than CA-4 in liver microsomes. In vivo, YSL-12 delayed tumor growth with 69.4 % growth inhibition. CONCLUSIONS: YSL-12 is a promising microtubule inhibitor that has great potential for the treatment of colon carcinoma in vitro and in vivo and worth being a candidate for further development of cancer therapy.

N­Myc downstream­regulated gene 2 suppresses proliferation and induces oncosis of OS­RC­2 human renal cancer cells.

V­myc avian myelocytomatosis viral oncogene homolog (Myc) regulates cell proliferation, differentiation and apoptosis in several types of cancer. N­myc downstream­regulated gene 2 (NDRG2) is known to exhibit reduced expression in renal cell carcinoma (RCC) tissues compared with adjacent non­neoplastic tissues and is an independent poor prognostic factor predicting survival in RCC. In the present study, green fluorescent protein (GFP)­NDRG2 and control GFP recombinant adenovirus plasmids were constructed and used to infect human renal cancer (OS­RC­2) cells. NDRG2 expression was measured using western blot analysis and the subcellular localization of NDRG2 was detected using confocal microscopy. The rate of proliferation of the cells was measured using colony formation and MTT assays, and the cell cycle was analyzed using flow cytometry. The results showed that the OS­RC­2 cells expressed little NDRG2 prior to infection with GFP­NDRG2 recombinant adenovirus; however, following infection, NDRG2 was found to be overexpressed, primarily in the mitochondria. The proliferation rate of the OS­RC­2 cells was reduced by NDRG2. Approximately 84.8% of the NDRG2­expressing cells were in S phase compared with 58.7% in the control virus­infected cells (P<0.05). In addition, the upregulation of NDRG2 induced a higher proportion of OS­RC­2 cells to undergo oncosis instead of apoptosis. In conclusion, the results from this study suggest that NDRG2 expressed in mitochondria may arrest renal cancer cells in S phase, decrease cell proliferation and induce oncosis. This indicates that NDRG2 is not only a biomarker, but may also be a therapeutic target for the treatment of RCC.