The emphasis in anticancer drug discovery has always been on finding a drug with great antitumor potential but few side-effects. This can be achieved if the drug is specific for a molecular site found only in tumor cells. Here, we find the enhancer of zeste homolog 2 (EZH2) to be highly overexpressed in lung and other cancers, and show that EZH2 is integral to proliferation in cancer cells. Quantitative real-time PCR analysis revealed higher expression of EZH2 in clinical bladder cancer tissues than in corresponding non-neoplastic tissues (P < 0.0001), and we confirmed that a wide range of cancers also overexpress EZH2, using cDNA microarray analysis. Immunohistochemical analysis showed positive staining for EZH2 in 14 of 29 cases of bladder cancer, 135 of 292 cases of non-small-cell lung cancer (NSCLC), and 214 of 245 cases of colorectal cancer, whereas no significant staining was observed in various normal tissues. We found elevated expression of EZH2 to be associated with poor prognosis for patients with NSCLC (P = 0.0239). In lung and bladder cancer cells overexpressing EZH2, suppression of EZH2 using specific siRNAs inhibited incorporation of BrdU and resulted in significant suppression of cell growth, even though no significant effect was observed in the normal cell strain CCD-18Co, which has undetectable EZH2. Because EZH2 expression was scarcely detectable in all normal tissues we examined, EZH2 shows promise as a tumor-specific therapeutic target. Furthermore, as elevated levels of EZH2 are associated with poor prognosis of patients with NSCLC, its overexpression in resected specimens could prove a useful molecular marker, indicating the necessity for a more extensive follow-up in some lung cancer patients after surgical treatment. (Cancer Sci 2011; 102: 1298-1305

BackgroundTo improve the diagnostic accuracy for hepatic tumors on the liver surface,

The scaffold-free isogenic artificial tracheas produced by a bio-3D printer could be utilized as tracheal grafts in rats.

The E-PASS score system was a useful predictor of postoperative complications and mortality, especially in patients with advanced age.

Current scaffold‐based tissue engineering approaches are subject to several limitations, such as design inflexibility, poor cytocompatibility, toxicity, and post‐transplant degradation. Thus, scaffold‐free tissue‐engineered structures can be a promising solution to overcome the issues associated with classical scaffold‐based materials in clinical transplantation. The present study seeks to optimize the culture conditions and cell combinations used to generate scaffold‐free structures using a Bio‐3D printing system. Human cartilage cells, human fibroblasts, human umbilical vein endothelial cells, and human mesenchymal stem cells from bone marrow are aggregated into spheroids and placed into a Bio‐3D printing system with dedicated needles positioned according to 3D configuration data, to develop scaffold‐free trachea‐like tubes. Culturing the Bio‐3D‐printed structures with proper flow of specific medium in a bioreactor facilitates the rearrangement and self‐organization of cells, improving physical strength and tissue function. The Bio‐3D‐printed tissue forms small‐diameter trachea‐like tubes that are implanted into rats with the support of catheters. It is confirmed that the tubes are viable in vivo and that the tracheal epithelium and capillaries proliferate. This tissue‐engineered, scaffold‐free, tubular structure can represent a significant step toward clinical application of bioengineered organs.