Indeed, the methylation Tofacitinib Citrate Sigma status of the estrogen receptor and p15INK4B can predict relapse risk in AML patients in clinical remission.26 Futher studies will be required to explore the correlation between SLC6A6 methylation status at diagnosis and prognosis. SLC6A6 is a membrane bound sodium and chloride dependent taurine transporter that has been implicated in retinal and kidney development.27,28 This gene is abundant in proliferating lymphocytes and is a downstream target of p53 and WT1 (Wilms tumor suppressor gene).28,29 Interestingly, an estrogen receptor binding site has been identified in the promoter of the SCL6A6 gene and it has been suggested that taurine uptake is regulated by estrogen via SLC6A6.30 The estrogen receptor is a LEF1 target gene that we showed to be up-regulated in the favourable risk group (Fig.

1E) suggesting that SLC6A6 may function downstream of LEF1.31 Of the genes shown to have significant CpG island methylation, only a small proportion demonstrated a corresponding change in expression levels indicating that additional factors control gene expression levels. While the highest correlation between methylation and expression observed was between decreased methylation and increased expression, a significant proportion of genes were observed to show either increased methylation and increased expression or decreased expression and decreased methylation. This questions the dogma that increased promoter methylation results in gene suppression. A number of studies have recently emerged challenging this dogma suggesting that the mechanisms by which methylation impacts on gene expression have still to be completely characterized.

32�C34 The current studies using integration of global methylation and expression analysis will further increase our understanding of epigenetic regulation of gene expression. In conclusion, we ha
Molecularly targeted therapies are transforming the treatment of cancer at various levels.1 Small molecule inhibitors that target the cancer dependent enzymes raise the possibility of rational approaches to cancer therapy. The wealth of molecular information from the recent genomics technologies offer a remarkable opportunity for new target discovery.2,3 Systems level view of perturbed networks or pathways can provide promising therapeutic strategies.

Glioma is known as a highly cellular tumor with poorly differentiated, round or pleomorphic cells that are occasionally multinucleated, nuclear atypia, anaplasia, endothelial proliferation and pseudopalisading necrosis. Multiple genetic level changes involve in the development of primary Entinostat and secondary gliomas. Hence, inhibitions of multiple targets are essential to control the rapidly growing tumour cells.4 There are two major oncogenic pathways such as PI3K pathway and MAPK pathway.