STEM CELLS 2006;24:506 -513

Human chromosome 14q32.2 carries a cluster of imprinted genes including paternally expressed genes (PEGs) such as DLK1 and RTL1 and maternally expressed genes (MEGs) such as MEG3 (also known as GTL2), RTL1as (RTL1 antisense) and MEG8 (refs. 1,2), together with the intergenic differentially methylated region (IG-DMR) and the MEG3-DMR. Consistent with this, paternal and maternal uniparental disomy for chromosome 14 (upd(14)pat and upd(14)mat) cause distinct phenotypes. We studied eight individuals (cases 1-8) with a upd(14)pat-like phenotype and three individuals (cases 9-11) with a upd(14)mat-like phenotype in the absence of upd(14) and identified various deletions and epimutations affecting the imprinted region. The results, together with recent mouse data, imply that the IG-DMR has an important cis-acting regulatory function on the maternally inherited chromosome and that excessive RTL1 expression and decreased DLK1 and RTL1 expression are relevant to upd(14)pat-like and upd(14)mat-like phenotypes, respectively.

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Enhancer of zeste homologue 2 (EZH2), a member of the polycomb group protein family, plays a crucial role in the regulation of embryonic development and has been associated with the regulation of the cell cycle. Recently, several studies have shown that EZH2 is highly expressed in aggressive tumours, including human breast cancer, prostate cancer, and lymphomas. We thus analysed EZH2 expression using real-time reverse transcription -polymerase chain reaction, and correlated its expression status with various clinicopathological parameters in 66 patients with hepatocellular carcinoma (HCC). We found high expression of EZH2 in human liver cancer cell lines. Furthermore, EZH2 gene-expression levels in tumour tissue specimens (0.3470.52) were significantly higher (Po0.0001) than those in the corresponding nontumour tissue specimens (0.0770.09). The incidence of cancer cell invasion into the portal vein was significantly higher (Po0.001) in the high EZH2 expression group (26 of the 33, 79%) than in the low expression group (13 of the 33, 39%). However, there was no significant difference in the disease-free survival rate between the two groups. The findings of this study indicate that EZH2 mRNA expression was upregulated in human HCC and may play an important role in tumour progression, especially by facilitating portal vein invasion. British Journal of Cancer (2005) Polycomb group (PcG) proteins are known to maintain the silenced state of several developmentally regulated genes and to control the transcriptional memory of a cell (Laible et al, 1997;van der Vlag et al, 1999). Dysregulation of this gene-silencing machinery may lead to cancer (Jacobs et al, 1999;Satijin and Otte, 1999). Recently, enhancer of zeste homologue 2 (EZH2), a member of the PcG protein family, has been linked to the aggressiveness of human cancers, including lymphomas ) provided biological evidence that overexpression of EZH2 promotes oncogenic transformation. In breast epithelial cells, they observed that high expression of EZH2 induced anchorage-independent growth and cell invasion, behaviours that are hallmarks of cancer. Moreover, they found that higher expression levels of EZH2 protein were strongly associated with decreased disease-free survival and decreased overall survival for patients with breast cancer. In addition, Varambally et al (2002) reported that EZH2 was overexpressed in metastatic prostate cancer and that inhibition of EZH2 blocked prostate cell growth. EZH2 expression has also been demonstrated to have prognostic significance in patients with prostate cancer (Sellers and Loda, 2002;Varambally et al, 2002;Rhodes et al, 2003;Foster et al, 2004). Therefore, the role of EZH2 in tumour development and progression has recently become a subject of increased interest (Tonini et al, 2004). To the best of our knowledge, however, the clinicopathological and prognostic significance of the EZH2 geneexpression status has not previously been examined in digestive organ cancers. The present study thus focused on examining the relationsh...

These findings suggest that low-energy laser irradiation stimulates the velocity of tooth movement via induction of RANK and RANKL.