In addition, novel splice isoforms were observed for the lncRNA MALAT1. MALAT1 codes for an 8.7 kb transcript, which high throughput screening generates a 7.5 kb RNA that localizes to nuclear speckles, and a 61 nucleotide tRNA-like cytoplasmic molecule of unknown function produced by 39 processing. Splice isoforms have not been observed in studies showing Northern blots for MALAT1. However, spliced ESTs in the MALAT1 gene locus that overlap with apparent spliced exons in our study have been isolated. The different isoforms found in iPSCs and neurons suggest that MALAT1 produces alternative transcripts in a cell type specific manner that could potentially modulate its role in pre-mRNA processing. Such an effect would be consistent with the role of nuclear speckles, cell type specific nuclear organization, and nuclear architecture on the differentiation of neurons and other cell types. CP-690550 cancer is a disease characterized by DNA damage and widespread deregulation of cell signaling and gene transcription. Genes with roles in cancer can be broadly grouped into oncogenes, tumor supressors, and DNA damage-associated genes. Oncogenes promote cancer by over-expression or hyper-activation. The molecular pathways leading to oncogenesis and tumor progression are diverse. Much progress has been made in the past 30 years in defining these pathways at the level of signal transduction involving protein-to-protein interaction. However, signal transduction leads through the chain of events to transcriptional regulation of a specific set of genes. With the advent of global gene expression profiling technology within the last ten years, we can now more readily examine oncogenic pathways at the level of gene transcription. Through the use of experimental models such as cell cultures or transgenic mice, one may turn up the expression or activity of a specific gene and observe which genes are regulated as a result. Here an oncogenic pathway signature will be defined to mean a set of genes that show a specific pattern of up- or down-regulation when a given pathway associated with oncogenesis is activated. Oncogenic signatures observed experimentally have potential use for inferring pathway deregulation in human tumors. In a seminal study by Lamb et al., a set of genes induced by cyclin D1 in an in vitro model were found to be co-expressed as a group with cyclin D1 mRNA in multiple expression profile datasets of human tumors of various types. In a recent study by Bild et al., gene signatures of Myc, Ras, E2F3, Src, and beta-catenin defined in vitro were used to predict Ras mutation status in human lung tumors and to predict the response of a panel of breast cancer cell lines to Src or Ras inhibitors. In another study by Creighton et al., a signature of the MAP kinase pathway was defined from gene expression profiles of ErbB-2, EGFR, Raf, and MEK in MCF-7 cells; this MAPK signature was found to share extensive similarities with signatures of ER-negative human breast cancer, which commonly has hyper-activated MAPK.