The loss of function of D-l(3)mbt causes hyperplasia and transformation of the neural cells resulting in brain tumors in Drososophila. L3MBTL1 the human paralog FG 4592 of L3MBTL4 has been proposed as a target gene in the myeloid malignancies associated with 20q deletions. The four human L3MBTL proteins shares MBT repeats involved in transcriptional repression and chromatin

remodeling. The MBT repeat is capable of methyl-lysine histone recognition. The presence of MBT repeats in L3MBTL4 suggest that it could also interact with chromatin. We hypothesized that L3MBTL4 loss-of-function could play a role in cellular transformation. We established genomic profiles by array comparative genomic hybridization and search for mutations by sequencing analysis on large set of primary breast tumors. Our results demonstrate that L3MBTL4 is targeted by losses and mutations suggesting that it could be a tumor suppressor gene. Poster No. 18 PTPIP51 is Expressed in Human Keratinocyte Carcinoma, Prostate Carcinoma and Glioblastoma Philipp Koch 1 , Meike Petri1, Albrecht Stenzinger1, Agnieszka Paradowska2, Monika Wimmer1 1 Institute of Anatomy

and Cell Biology, Justus-Liebig-University Giessen, selleck inhibitor Giessen, Germany, 2 Department of Urology and Pediatric Urology, Justus-Liebig-University Giessen, Giessen, Germany The novel protein PTPIP51 (protein tyrosine phosphatase interacting PRKACG protein 51) shows a tissue-specific expression pattern and is associated with cellular differentiation and apoptosis in several mammalian tissues. Overexpression of the full-length protein enhances apoptosis. PTPIP51 is a positive regulator of the MAPK on Raf level. Various carcinoma express PTPIP51. Here we demonstrate the expression profile of PTPIP51 in human keratinocyte carcinoma (KC), prostate carcinoma (PCa) and in glioblastoma multiforme (GBM). Paraffin embedded sections of KC, PCa and GBM were Selleck EVP4593 analyzed by immunohistochemistry and in situ hybridization. RT-PCR was performed on cryo samples. For PCa, and benign prostate hyperplasia (BPH)

as reference, bisulfite DNA treatment, followed by sequencing of PCR products was performed in order to analyze CpG methylation within the promoter region on the ptpip51 gene. PTPIP51 mRNA and protein was detected in all investigated tumor tissues. Basal cell carcinoma (BCC), squamous cell carcinoma (SCC), Bowen’s disease (BD) and keratoacanthoma (KA) displayed a specific localization pattern of PTPIP51 in malignant keratinocytes. For SCC, BD and KA a mainly membranous localization was investigated, whereas BCC showed an either cytoplasmic or predominantly membranous expression. Tumor cells of the PCa express PTPIP51, however a stronger expression of PTPIP51 is present in nerve fibres, immune cells and in smooth muscle and endothelial cells of vessels.