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, 2007). Placing tumors into these two classes is now possible with a routine clinical test with fine needle biopsy where 15 genes are profiled on a microfluidics platform (Harbour and Chen, 2013). As described earlier, the presence of BAP1 mutations is also strongly correlated with likelihood of metastasis. BAP1 mutations are usually sporadic and are found in approximately 85% of class 2 (metastatic) tumors and http://www.selleckchem.com/products/PLX-4032.html with neural crest-like http://www.selleck.cn/products/BEZ235.html features have been identified for both uveal and cutaneous melanoma (Thies et?al., 2004). The polycomb repressive deubiquitinase (PR-DUB) complex of which BAP1 is a component catalyzes the removal of monoubiquitin moieties from histone H2A in opposition to the ubiquitinating activity of the PRC1 complex. Loss of BAP1 in mammalian cells results in abnormal ubiquitination of histone H2A and that this can be reversed with histone deacetylase (HDAC) inhibitors (Landreville et?al., 2012). Further, HDAC inhibitors revert primary class 2 UM cells to a differentiated class 1 phenotype and restore to normal levels the expression of melanocyte differentiation genes that are down-regulated by BAP1 depletion. Inhibitors of HDACs also induce morphological changes that are consistent with melanocyte differentiation. Given the important role of BAP1 in tumor progression and metastasis, there may be a role for HDAC inhibitors in preventing the progression of http://www.selleckchem.com/products/AZD2281(Olaparib).html micro-metastatic disease or in combination with other therapies for advanced disease (Landreville et?al., 2012). An exciting development in the UM research arena that has the potential to significantly enhance our understanding of UM biology is the inclusion of UM in the NIH/NCI TCGA Rare Tumor Project. The cancer genome atlas (TCGA) was designed as a collaborative effort to create a comprehensive collection of maps that chart genomic changes that occur in each type of cancer, with a specific plan to comprehensively molecularly characterize up to 500 melanomas. The TCGA program was further expanded in March 2012 with rollout and promulgation of the TCGA Rare Tumor Project, the goal of which is to characterize at least 50 qualifying cases for each of ten or so uncommon malignancies into its well-established overall TCGA effort (i.e., inclusion of approximately 1/10 the number of cases allocated to the principal TCGA tumor types). A UM TCGA Disease Working Group (DWG) was configured in January 2013, and receipt of all UM specimens was complete by December 31, 2013.