Project description:Cell lines representing human T-ALL were analyzed to compare GATA3low ETP-ALL (i.e. PER-117) with "typical" T-ALL. Moreover, changes in global gene expression were assessed comparing GATA3low ETP-ALL (i.e. PER-117) and GATA3high ETP-ALL (i.e. Loucy) upon treatment with Decitabine, a hypomethylating agent.
Project description:Cell lines representing human T-ALL were analyzed to compare GATA3low ETP-ALL (i.e. PER-117) with "typical" T-ALL. Moreover, changes in global gene expression were assessed comparing GATA3low ETP-ALL (i.e. PER-117) and GATA3high ETP-ALL (i.e. Loucy) upon treatment with Decitabine, a hypomethylating agent. Analysis of 6 human cell lines representing "typical" T-ALL (BE13, Jurkat, Molt4, RPM18402) and ETP-ALL (Loucy, PER-117). Additionally, global gene expression was assessed before and after treatment of ETP-ALL cell lines with Decitabine
Project description:Yersinia pestis is a lethal pathogen responsible for millions of human deaths in three worldwide pandemics.The global acetylome analyses of Y. pestis grown under conditions mimicking two typical niches, i.e., the mammalian host (Mh) and the flea vector (Fv), were performed.
Project description:STAG2/LMO2 subtype in T-ALL was investigated through integrative genomic analysis. H3K27ac HiChIP was used to investigate the impact of LMO2::STAG2 translocations in MOLT-14 and PER-117 cell lines. ChIP-seq was used to explore the effects of STAG2 inactivation by using gene-edited MOLT-14 and PF382 cell lines.
Project description:STAG2/LMO2 subtype in T-ALL was investigated through integrative genomic analysis. H3K27ac HiChIP was used to investigate the impact of LMO2::STAG2 translocations in MOLT-14 and PER-117 cell lines. ChIP-seq was used to explore the effects of STAG2 inactivation by using gene-edited MOLT-14 and PF382 cell lines.
Project description:Comparing control and LPS-administered with either 40 mg/kg LPS for early time points (ETP) or 10 mg/kg for late time points (LTP). In ETP, 7-7 animals were sacrificed at 1.5 and at 6 hours after LPS administration. In LTP, 7-7 animals were sacrificed at 24 and 48 hours after the endotoxin injection. In both ETP and LTP 7 mice were received equal volume of saline to use as negative control. Four animals were selected for miRNA microArray analysis based on their proinflammatory (TNF-α and IL-6) mRNA expression levels.
Project description:Integrative analysis of global RNASeq and proteomic data comparing human colorectal cancer (CRC) cell lines to primary tumors and normal tissues.
Project description:Early T-cell precursor acute lymphoblastic leukaemia (ETP ALL) is an aggressive malignancy of unknown genetic basis. We performed whole genome sequencing of tumour and normal DNA from 12 children with ETP ALL and assessed the frequency of somatic alterations in 52 ETP and 42 non-ETP T-ALL samples by sequencing and DNA copy number analysis. ETP ALL was characterised by a high frequency of activating mutations in genes regulating cytokine receptor and Ras signalling (67% of cases; NRAS, KRAS, FLT3, IL7R, JAK3, JAK1, SH2B3 and BRAF); alterations disrupting haemopoietic development (58%; GATA3, ETV6, RUNX1, IKZF1, EP300); and inactivating mutations in histone modifying genes (48%; EZH2, EED, SUZ12, SETD2 and EP300). We also identified new targets of mutation including DNM2, ECT2L and RELN. Ten of 12 ETP ALL cases harboured chromosomal rearrangements, several of which complex and resulted in the expression of novel chimeric in-frame fusion genes disrupting haemopoietic regulators. Thus, similar to myeloid malignancies, mutations that drive proliferation, impair differentiation and disrupt histone modification are hallmarks of ETP ALL. Moreover, the global transcriptional profile of ETP ALL was similar to that of normal and myeloid leukaemia haemopoietic stem cells. These findings suggest that addition of myeloid-directed therapies might improve the poor outcome of ETP ALL. Gene expression profiling was performed on 52 single diagnosis tumor samples. No control or reference samples were included.
Project description:Early T-cell precursor acute lymphoblastic leukaemia (ETP ALL) is an aggressive malignancy of unknown genetic basis. We performed whole genome sequencing of tumour and normal DNA from 12 children with ETP ALL and assessed the frequency of somatic alterations in 52 ETP and 42 non-ETP T-ALL samples by sequencing and DNA copy number analysis. ETP ALL was characterised by a high frequency of activating mutations in genes regulating cytokine receptor and Ras signalling (67% of cases; NRAS, KRAS, FLT3, IL7R, JAK3, JAK1, SH2B3 and BRAF); alterations disrupting haemopoietic development (58%; GATA3, ETV6, RUNX1, IKZF1, EP300); and inactivating mutations in histone modifying genes (48%; EZH2, EED, SUZ12, SETD2 and EP300). We also identified new targets of mutation including DNM2, ECT2L and RELN. Ten of 12 ETP ALL cases harboured chromosomal rearrangements, several of which complex and resulted in the expression of novel chimeric in-frame fusion genes disrupting haemopoietic regulators. Thus, similar to myeloid malignancies, mutations that drive proliferation, impair differentiation and disrupt histone modification are hallmarks of ETP ALL. Moreover, the global transcriptional profile of ETP ALL was similar to that of normal and myeloid leukaemia haemopoietic stem cells. These findings suggest that addition of myeloid-directed therapies might improve the poor outcome of ETP ALL.
