Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

34 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The functional interplay between the t(9;22)-associated fusion proteins BCR/ABL and ABL/BCR in Philadelphia chromosome positive acute lymphatic leukemia

ABSTRACT: p96ABL/BCR fusion protein plays an important role in the pathogenesis of Ph+ ALL Isolation of murine bone marrow stem cells, transduction of the cells with the desired construct, tranplantation of the cells into lethaly irradiated mice, isolation of RNA from the spleens 12 days after the transplantation, investigation of gene expression profile

ORGANISM(S): Mus musculus

SUBMITTER: Anahita Rafiei

PROVIDER: E-GEOD-57515 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiling of microdissected tumor cells of nodular lymphocyte predominant Hodgkin lymphomas and T-cell/histiocyte rich B cell lymphoma

Project description:Tumor cells were microdissected from frozen sections of NLPHL and THRLBCL. RNA was amplified using the NUGEN One-direct kit. Samples were compared to tonsilar germinal center CD77 B cells. 30 microdissected tumour samples were compared with 5 sorted CD77 samples.

2013-12-01 | E-GEOD-47044 | biostudies-arrayexpress

Activating c-KIT mutations confers oncogenic cooperativity and rescue RUNX1-ETO induced DNA-damage in human cells

Project description:REtr causes genomic instability in U937 cells. Activated forms of c-KIT, like c-KIT(N822K), rescues the Retr induced genomic instability by increasing the rate of DNA repair by homologous recombination Human U937 cells were transduced with retroviral vectors encoding REtr or c-KIT(N822K), expanded in culture and FACS selected prior to molecular analysis

2014-07-29 | E-GEOD-57658 | biostudies-arrayexpress

Macrophages in T cell/histiocyte rich B cell lymphoma strongly express metal-binding proteins and show a bi-activated phenotype

Project description:In a supervised principal component analysis, histiocytes from TCHRBCL were most closely related to epithelioid cells from NLPHL, with both types of cells expressing genes related to proinflammatory and regulatory macrophage activity. 39 microdissected histiocyte samples were compared with 9 sorted monocyte samples

2013-08-01 | E-GEOD-42495 | biostudies-arrayexpress

Infection of Myeloid Angiogenic Cells (MACs) with Bartonella henselae (B.h.) induces a chord formation phenotype in vitro.

Project description:Myeloid Angiogenic Cells (MACs) were infected with the intracellular, bacterial pathogen Bartonella henselae (B.h.). Infected cells were seeded onto Matrigel coated plates. While uninfected cells showed no phenotypic changes and died over time, infected cells showed strong phenotypic changes and developed into complex 2D chord networks over the course of long term culture (eg 49d). To examine the changes in gene expression associated with the development of the B.h.dependent chord formation phenotype, RNA was isolated from MACs shortly after isolation (d4) and from cells of the chord structures (+B.h. Matrigel). As primary endothelial cells are also know to form chord networks when cultured on Matrigel, a sample of human umbilical vein endothelial cells (HUVECs) cultured on Matrigel for 12hr was also included in the analysis as a control. myeloid angiogenic cells (MACs) from three donors were compared d4 after isolation with MACs infected with Bartonella henselae and cultured on Matrigel coated plates for up to 49 days, 1 sample from human umbilical cord vein endothelial cells (HUVECs) cultured for 12hr on Matrigel coated plates were also included as a control.

2015-04-23 | E-GEOD-55170 | biostudies-arrayexpress

MicroRNA Profiling of Laser-Microdissected Hepatocellular Carcinoma Reveals an Oncogenic Phenotype of the Tumor Capsule

Project description:Tumor cells were microdissected from FFPE sections of hepatocellular carcinoma (HCC) samples. Samples were compared between different localisations either within or around the tumor. miRNA was labeled with the Affymetrix FlashTag Biotin HSR RNA Labeling Kit 6 microdissected hepatocellular carcinoma samples were compared to four different tumor localisations (LC: cirrhotic septa of the tumor-adjacent liver; LP: tumor-adjacent liver parenchyma;TC: fibrinous capsule of the tumor; TP: tumor parenchyma)

2015-01-14 | E-GEOD-54537 | biostudies-arrayexpress

Feasibility of global microRNA analysis from fine-needle biopsy FFPE material in patients with hepatocellular carcinoma treated with sorafenib

Project description:Tumor cells were microdissected from FFPE sections of hepatocellular carcinoma (HCC) samples. micro RNA expression were correlated to clinical outcome and sorafenib-therapy. miRNA was labeled with the Affymetrix FlashTag Biotin HSR RNA Labeling Kit 20 microdissected hepatocellular carcinoma samples with detailed clinical data

2014-07-29 | E-GEOD-56059 | biostudies-arrayexpress

Expression data from Hodgkin lymphoma cell lines L-428 and L-1236: L-428 and L-1236 cells were transduced with tGFP-EBF1 or as control tGFP-only.

Project description:The transcription factor network in Hodgkin lymphoma (HL) represents a unique composition of proteins found in no other hematopoietic cell. An aberrant downregulation of the B cell transcription factor EBF1 is observed in the B cell-derived Hodgkin and Reed/Sternberg (HRS) tumor cells. Herein, we elucidated the consequences of the down regulation of this factor in HL. To obtain a more comprehensive overview of EBF1 regulated genes in cHL cell lines, we performed a gene chip analysis comparing gene expression in tGFP-EBF1-transduced L-1236 and L-428 cells compared to samples transduced with vectors encoding only tGFP. 12 total samples were analyzed. Three independent samples were analyzed per condition and cell line.We generated the following pairwise comparisons using Bioconductor: tGFP-EBF1 L-428 < tGFP L-428; tGFP-EBF1 L-1236 < tGFP L-1236. Genes with an FDR≤ 5 % and a fold-change ≥ 2.0 and ≤ -2.0 were selected.

2012-11-01 | E-GEOD-41493 | biostudies-arrayexpress

Expression data from Hodgkin lymphoma cell lines UHO-1 and L-1236 transduced with shRNAs against GATA-3 or non-functional control shRNAs

Project description:The transcription factor network in Hodgkin lymphoma (HL) represents a unique composition of proteins found in no other hematopoietic cell. Among these factors, an aberrant expression of the T cell transcription factor GATA-3 is observed in the B cell-derived Hodgkin and Reed/Sternberg (HRS) tumor cells. Herein, we elucidated the regulation and function of this factor in HL To obtain a more comprehensive overview of GATA-3 regulated genes in cHL cell lines, we performed a gene chip analysis comparing gene expression in GATA-3-specific shRNA-transduced L-1236 and U-HO1 cells compared to samples transduced with vectors encoding scrambled shRNAs. 12 Total samples were analyzed. Three independent samples were analyzed per condition and cell line.We generated the following pairwise comparisons using Bioconductor: shRNA Gata-3 UHO-1 < control shRNA UHO-1; shRNA Gata-3 L1236 < control shRNA L-1236. Genes with an FDR≤ 25% and a fold-change ≥ 1.5 and ≤ -1.5 were selected.

2010-07-24 | E-GEOD-22550 | biostudies-arrayexpress

Protein Kinase CK2: A Targetable BCR-ABL Partner in Philadelphia Positive Leukemias.

Project description:BCR-ABL-mediated leukemias, either Chronic Myeloid Leukemia (CML) or Philadelphia positive Acute Lymphoblastic Leukemia (ALL), are the paradigm of targeted molecular therapy of cancer due to the impressive clinical responses obtained with BCR-ABL specific tyrosine kinase inhibitors (TKIs). However, BCR-ABL TKIs do not allow completely eradicating both CML and ALL. Furthermore, ALL therapy is associated with much worse responses to TKIs than those observed in CML. The identification of additional pathways that mediate BCR-ABL leukemogenesis is indeed mandatory to achieve synthetic lethality together with TKI. Here, we review the role of BCR-ABL/protein kinase CK2 interaction in BCR-ABL leukemias, with potentially relevant implications for therapy.

| S-EPMC4710905 | biostudies-literature

The functional interplay between the t(9;22)-associated fusion proteins BCR/ABL and ABL/BCR in Philadelphia chromosome-positive acute lymphatic leukemia.

Project description:The hallmark of Philadelphia chromosome positive (Ph(+)) leukemia is the BCR/ABL kinase, which is successfully targeted by selective ATP competitors. However, inhibition of BCR/ABL alone is unable to eradicate Ph(+) leukemia. The t(9;22) is a reciprocal translocation which encodes not only for the der22 (Philadelphia chromosome) related BCR/ABL, but also for der9 related ABL/BCR fusion proteins, which can be detected in 65% of patients with chronic myeloid leukemia (CML) and 100% of patients with Ph+ acute lymphatic leukemia (ALL). ABL/BCRs are oncogenes able to influence the lineage commitment of hematopoietic progenitors. Aim of this study was to further disclose the role of p96(ABL/BCR) for the pathogenesis of Ph(+) ALL. The co-expression of p96(ABL/BCR) enhanced the kinase activity and as a consequence, the transformation potential of p185(BCR/ABL). Targeting p96(ABL/BCR) by RNAi inhibited growth of Ph(+) ALL cell lines and Ph(+) ALL patient-derived long-term cultures (PD-LTCs). Our in vitro and in vivo stem cell studies further revealed a functional hierarchy of p96(ABL/BCR) and p185(BCR/AB)L in hematopoietic stem cells. Co-expression of p96(ABL/BCR) abolished the capacity of p185(BCR/ABL) to induce a CML-like disease and led to the induction of ALL. Taken together our here presented data reveal an important role of p96(ABL/BCR) for the pathogenesis of Ph(+) ALL.

| S-EPMC4412790 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data