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A study of patients with NSCLC [ 26] is consistent with this assumption: the 8-week rate of disease control, defined as no disease progression, performed better in predicting survival than did the 8-week rate of CR/PR.
Additionally, in a recent multicenter study of CPB and cancer progression performed by Suzuki et. al. in 74 patients with metastatic cancer who underwent open-heart surgery with and without CPB, no significant difference was observed in cancer-specific mortality (26.7% and 24.1%, respectively, p=0.8) [ 7].
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To identify the putative oncogene involved in urothelial carcinoma progression we performed bioinformatics guided experimental investigation targeting chromosome 19q13.
As measurements of atherosclerotic progression, we performed two ultrasound methods, namely brachial artery flow-mediated dilation (FMD), an endothelial function assessment quantitatively reflecting the endothelium-dependent vasodilation responses following hyperemia, and measurement of carotid intima-media thickness (IMT).
Monitoring of disease progression was performed by tracking bacterial dissemination to the internal organs and blood.
All measures of disease progression were performed blind by independent investigators to avoid subjective bias.
To investigate if Fe-SP exerts anti-proliferative effects and disturbances of cell cycle progression we performed a BrdU incorporation assay.
To determine whether the increase of cell number was caused by the promotion of cell cycle progression, we performed BrdU incorporation experiments.
To investigate the role of Sema3E in mediating invasiveness and/or migratory ability during tumor progression, we performed gain and loss of function studies in OEC cells.
To investigate the mechanism by which ECT2 is related to cell cycle progression, we performed FACS analysis of shECT2-transfected cells.
To assess the status of E2F-1 during melanoma progression, we performed Western Blot analysis in non-metastatic and metastatic melanoma cell lines.
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