Project description:RNA extracted from diagnostic tumor samples of 126 patients affected by cHL was analyzed on the nCounter system using the PanCancer Immune Profiling Panel.
Project description:To determine whether the polyamide-Chl conjugate 1R-Chl would cause similar changes in global gene expression in K562 cells, affymetrix gene chip analysis was performed using 1R-Chl. Through class comparison analysis, 1R-Chl affected the levels of transcription and genes of interest were determined. Experiment Overall Design: K562 cells were incubated with 1R-Chl (at 250 nM) or in the absence of polyamide, in triplicate for 24 h before RNA purification and microarray analysis at The Scripps Research Institute microarray facility. Affymetrix U133A Plus 2.0 GeneChips were hybridized in groups of three for each of the two groups. The Affymetrix probe set data were imported into BRB Arraytools (3.5.0 Beta 2), selecting the U133 chips used in the experiment and leaving all filters off.
Project description:Herein we describe a case with histological, immunohistochemical and molecular features of GTAKA showing widespread leptomeningeal dissemination.
Project description:Herein we describe a case with histological, immunohistochemical and molecular features of GTAKA showing widespread leptomeningeal dissemination.
Project description:To determine whether the polyamide-Chl conjugate 1R-Chl would cause similar changes in global gene expression in K562 cells, affymetrix gene chip analysis was performed using 1R-Chl. Through class comparison analysis, 1R-Chl affected the levels of transcription and genes of interest were determined. Keywords: Treatment response
Project description:FOXO1 is highly expressed in normal B cells and in most types of non-Hodgkinl lymphoma. In Hodgkin and Reed-Sternberg cells of classical Hodgkin lymphoma(cHL) expression of FOXO1 is low or absent. We overexpressed constitutively active mutant of FOXO1 fused in frame with estrogen receptor ligand-binding domain (FOXO1(3A)ER), which can be activated by 4-Hydroxytamoxifen (4-OHT), in cHL cell lines KM-H2 and L428. Activation of the FOXO1 with 4-OHT resulted in inhibition of proliferation and apoptosis. Using gene-expression array we found that FOXO1 activates transcription of known and potential tumor suppressor genes: CDKN1B, PMAIP1, BCL2L11, TNFSF10, FBXO32, CBLB). Of note, FOXO1 repressed transcription of several cytokines and cytokine receptors, which are known tobe involved in pathogenesis of cHL (e.g. CCL5, CXCR5, TNFRSF8). Taken togather our data indicate important role of FOXO1 repression in pathogenesis of cHL.
Project description:Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) with leptomeningeal dissemination and ZMIZ1::RET fusion
Project description:The number of peripheral blood (PB) circulating tumor cells (CTCs) predicts risk of transformation in smoldering multiple myeloma (MM) and survival in active MM. Growing evidence suggests that as the tumor progresses and the microenvironment becomes hypoxic, clonal plasma cells (PCs) constantly invade new regions of the bone marrow (BM) through induced systemic recirculation. Of note, the frequency of CTCs is typically low and thus, it could be hypothesized that the dissemination of MM is made by few tumor cells with unique features that induce them to egress the BM and spread the disease through PB. This hypothesis has not been demonstrated because the molecular profile of CTCs in MM has not been investigated. We used gene expression profiling (GEP) arrays to identify gene regulatory networks related to disease dissemination by comparing the molecular profile of CTCs with patient-matched BM clonal PCs.
Project description:The number of peripheral blood (PB) circulating tumor cells (CTCs) predicts risk of transformation in smoldering multiple myeloma (MM) and survival in active MM. Growing evidence suggests that as the tumor progresses and the microenvironment becomes hypoxic, clonal plasma cells (PCs) constantly invade new regions of the bone marrow (BM) through induced systemic recirculation. Of note, the frequency of CTCs is typically low and thus, it could be hypothesized that the dissemination of MM is made by few tumor cells with unique features that induce them to egress the BM and spread the disease through PB. This hypothesis has not been demonstrated because the molecular profile of CTCs in MM has not been investigated. We used gene expression profiling (GEP) arrays to identify gene regulatory networks related to disease dissemination by comparing the molecular profile of CTCs with patient-matched BM clonal PCs.
Project description:Characteristic extinguishing of B-cell phenotype in cHL is believed to be a result of transcription factor network deregulation due to the overexpression of repressor proteins ID2 and ABF-1. KLF4 is a versatile transcription factor, participating in regulation of differentiation processes in various tissues. Epigenetic silencing of KLF4 in cHL hints that KLF4 is involved in the complex mechanism of extinguishing of B-cell phenotype in cHL. To clarify this issue we investigated transcriptome changes, induced by KLF4 activation in two cHL cell lines KM-H2 and L428.