Similar studies for GEO DataSets (Select 200069346) - GEO DataSets

Select item 2000693461.

An immediate transcriptional signature predicts response to the histone deacetylase inhibitor Givinostat in T acute lymphoblastic leukemia xenografts

(Submitter supplied) Gene expression analysis of three sets of patient-derived T-ALL xenografted murine lines treated or not treated with Givinostat, to investigate the immediate anti-leukemic effects after 6 hours of in vivo treatment with this histone deacetylase inhibitor.

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL570
33 Samples

Download data: CEL

Series

Accession:: GSE69346

ID:: 200069346

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000654832.

Gene expression profiling of L-540 Hodgkin lymphoma cell line after in vitro and in vivo treatment with Givinostat in combination with Sorafenib

(Submitter supplied) Relapsed/refractory Hodgkin lymphoma (HL) is an unmet medical need requiring new therapeutic options. Interactions between the histone deacetylase inhibitor Givinostat and the RAF/MEK/ERK inhibitor Sorafenib were examined in HDLM-2 and L-540 HL cell lines. Exposure to Givinostat/Sorafenib induced a synergistic inhibition of cell growth (range, 70- 80%) and a dramatic increase in cell death (up to 96%) due to increased H3 and H4 acetylation and strong mitochondrial injury. more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL6947
12 Samples

Download data: TXT

Series

Accession:: GSE65483

ID:: 200065483

Select item 2000654793.

Gene expression profiling of HDLM-2 Hodgkin lymphoma cell line after in vitro and in vivo treatment with Givinostat in combination with Sorafenib

(Submitter supplied) Relapsed/refractory Hodgkin lymphoma (HL) is an unmet medical need requiring new therapeutic options. Interactions between the histone deacetylase inhibitor Givinostat and the RAF/MEK/ERK inhibitor Sorafenib were examined in HDLM-2 and L-540 HL cell lines. Exposure to Givinostat/Sorafenib induced a synergistic inhibition of cell growth (range, 70- 80%) and a dramatic increase in cell death (up to 96%) due to increased H3 and H4 acetylation and strong mitochondrial injury. more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL6947
12 Samples

Download data: TXT

Series

Accession:: GSE65479

ID:: 200065479

Select item 2000310604.

Gene expression analysis of Hodgkin lymphoma cell lines treated with the AKT inhibitor perifosine and the multikinase inhibitor sorafenib

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL6947
60 Samples

Download data

Series

Accession:: GSE31060

ID:: 200031060

Select item 2000772705.

The histone deacetylase inhibitor givinostat (ITF2357) exhibits potent anti-tumor activity against CRLF2-rearranged BCP-ALL.

(Submitter supplied) We studied the in vitro and in vivo efficacy of the HDAC inhibitor Givinostat/ITF2357 in BCP-ALL with CRLF2 rearrangements. We used BCP-ALL CRLF2- rearranged MHH-CALL4 and MUTZ5 cell lines as well as blasts from CRLF2 rearranged BCP-ALL patients and patients’ derived xenograft samples. We conclude that Givinostat may represent a novel and effective tool, in combination with current chemotherapy, to treat this subsets of ALL with poor prognosis and chemotherapy-related toxicity.

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL570
10 Samples

Download data: CEL

Series

Accession:: GSE77270

ID:: 200077270

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000419516.

Gene expression profile of the human leukemia cell line Reh after treatment with bortezomib, valproic acid or a combination of both.

(Submitter supplied) New therapy options are required for relapsed B-cell precursor ALL patients in order to improve survival and reduce adverse acute and late effects. We observed a synergistic anti-leukemic activity of concomitant treatment with bortezomib and valproic acid in BCP-ALL cells. In this experiment we aimed to identify the pathways modulated after concomitant treatment with bortezomib and valproic acid.

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL13607
4 Samples

Download data: TXT

Series

Accession:: GSE41951

ID:: 200041951

Select item 2000268077.

The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Homo sapiens

Type:: Expression profiling by array; Methylation profiling by array; Expression profiling by SNP array; SNP genotyping by SNP array

Platforms:: GPL3720 GPL8490 GPL6244
36 Samples

Download data: CEL

Series

Accession:: GSE26807

ID:: 200026807

Select item 2000267928.

The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (SNP)

(Submitter supplied) Histone deacetylases (HDACs) have been identified as therapeutic targets due to regulatory function in DNA structure and organization. We have analyzed the role of the LBH589, a novel pan inhibitor of class I and II HDACs, in Acute Lymphoblastic Leukemia. In vitro, LBH589 was shown to induce a dose dependent antiproliferative and apoptotic effect which was associated with an increase in the acetylation of H3 and H4 histone acetylation which was uniformly in every genetic subgroup of ALL. more...

Organism:: Homo sapiens

Type:: Expression profiling by SNP array; SNP genotyping by SNP array

Platform:: GPL3720
6 Samples

Download data: CEL

Series

Accession:: GSE26792

ID:: 200026792

PubMed Similar studies

Select item 2000267919.

The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (Illumina)

(Submitter supplied) Histone deacetylases (HDACs) have been identified as therapeutic targets due to regulatory function in DNA structure and organization. We have analyzed the role of the LBH589, a novel pan inhibitor of class I and II HDACs, in Acute Lymphoblastic Leukemia. In vitro, LBH589 was shown to induce a dose dependent antiproliferative and apoptotic effect which was associated with an increase in the acetylation of H3 and H4 histone acetylation which was uniformly in every genetic subgroup of ALL. more...

Organism:: Homo sapiens

Type:: Methylation profiling by array

Platform:: GPL8490
12 Samples

Download data: TXT

Series

Accession:: GSE26791

ID:: 200026791

Select item 20002679010.

The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (TOM-1 and MOLT-4)

(Submitter supplied) Histone deacetylases (HDACs) have been identified as therapeutic targets due to regulatory function in DNA structure and organization. We have analyzed the role of the LBH589, a novel pan inhibitor of class I and II HDACs, in Acute Lymphoblastic Leukemia. In vitro, LBH589 was shown to induce a dose dependent antiproliferative and apoptotic effect which was associated with an increase in the acetylation of H3 and H4 histone acetylation which was uniformly in every genetic subgroup of ALL. more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL6244
12 Samples

Download data: CEL

Series

Accession:: GSE26790

ID:: 200026790

Select item 20002678911.

The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (ALL-B and ALL-T)

(Submitter supplied) Histone deacetylases (HDACs) have been identified as therapeutic targets due to regulatory function in DNA structure and organization. We have analyzed the role of the LBH589, a novel pan inhibitor of class I and II HDACs, in Acute Lymphoblastic Leukemia. In vitro, LBH589 was shown to induce a dose dependent antiproliferative and apoptotic effect which was associated with an increase in the acetylation of H3 and H4 histone acetylation which was uniformly in every genetic subgroup of ALL. more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL6244
6 Samples

Download data: CEL

Series

Accession:: GSE26789

ID:: 200026789

Select item 20006246012.

Preclinical antitumor activity of ST7612AA1: a novel second generation oral histone deacetylase (HDAC) inhibitor

(Submitter supplied) assess the efficacy of ST7612AA1 oral pan-histone deacetylase inhibitor (HDACi), with respect to various solid and haematological tumors, and to characterize its mechanism of action

Organism:: Homo sapiens

Type:: Expression profiling by array

Dataset:: GDS5615
Platform:: GPL10558
12 Samples

Download data: TXT

Series

Accession:: GSE62460

ID:: 200062460

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 561513.

Oral histone deacetylase inhibitor ST7612AA1 effect on diffuse large B-cell lymphoma in vitro models

Analysis of lymphoma cell lines DOHH2 (derived from GCB-DLBCL) and TMD8 (derived from ABC-DLBCL) exposed to ST7612AA1 (300nM) for 8 hrs. ST7612AA1 is an oral thiol-based histone deacetylase inhibitor (HDACi). Results provide insight into the molecular mechanisms underlying ST7612AA1 action in DLBCL.

Organism:: Homo sapiens

Type:: Expression profiling by array, transformed count, 2 agent, 2 cell line sets

Platform:: GPL10558
Series:: GSE62460
12 Samples

Download data

DataSet

Accession:: GDS5615

ID:: 5615

PubMed Full text in PMC Similar studies GEO Profiles Analyze DataSet

Select item 20006680014.

Gene expression profiling of histone deacetylase inhibition in epithelioid sarcoma

(Submitter supplied) Epithelioid Sarcoma (ES) is a rare neoplasm uniquely comprised of cells exhibiting both mesenchymal and epithelial features. Having propensity for local and distant recurrence, it can pose a diagnostic dilemma secondary to pathologic complexity. Patients have dismal prognosis due to lack of effective therapy. HDAC inhibitors exhibit marked anti-tumor effects in various malignancies. Our studies demonstrate that pan-HDAC inhibitors constitute potentially novel therapeutics versus ES. more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL10904
12 Samples

Download data: TXT

Series

Accession:: GSE66800

ID:: 200066800

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20005100115.

PI3K inhibition synergizes with glucocorticoids but antagonizes with methotrexate in T-cell acute lymphoblastic leukemia.

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Homo sapiens

Type:: Expression profiling by array

Platforms:: GPL570 GPL6244
87 Samples

Download data: CEL

Series

Accession:: GSE51001

ID:: 200051001

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20005100016.

Gene expression signature of primary T-ALL cells treated with the PI3K inhibitor AS605240

(Submitter supplied) The PI3K pathway is frequently hyperactivated in primary T-cell acute lymphoblastic leukemia (T-ALL) cells. Activation of the PI3K pathway has been suggested as one mechanism of glucocorticoid resistance in T-ALL, and patients harboring mutations in the PI3K negative regulator PTEN may be at increased risk of induction failure and relapse. In this study, we identified Myc as an important downstream integrator of PI3K pathway activity in T-ALL and we provide data supportive of an association of higher PI3K activity with glucocorticoid resistance and worse clinical outcome. more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL6244
30 Samples

Download data: CEL

Series

Accession:: GSE51000

ID:: 200051000

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20005099917.

Gene expression data of diagnostic childhood T-ALL samples

(Submitter supplied) The PI3K pathway is frequently hyperactivated in primary T-cell acute lymphoblastic leukemia (T-ALL) cells. Activation of the PI3K pathway has been suggested as one mechanism of glucocorticoid resistance in T-ALL, and patients harboring mutations in the PI3K negative regulator PTEN may be at increased risk of induction failure and relapse. In this study, we identified Myc as an important downstream integrator of PI3K pathway activity in T-ALL and we provide data supportive of an association of higher PI3K activity with glucocorticoid resistance and worse clinical outcome. more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL6244
43 Samples

Download data: CEL

Series

Accession:: GSE50999

ID:: 200050999

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20005099818.

Gene expression signature of T-ALL cell lines treated with the PI3K inhibitor AS605240

(Submitter supplied) The PI3K pathway is frequently hyperactivated in primary T-cell acute lymphoblastic leukemia (T-ALL) cells. Activation of the PI3K pathway has been suggested as one mechanism of glucocorticoid resistance in T-ALL, and patients harboring mutations in the PI3K negative regulator PTEN may be at increased risk of induction failure and relapse. In this study, we identified Myc as an important downstream integrator of PI3K pathway activity in T-ALL and we provide data supportive of an association of higher PI3K activity with glucocorticoid resistance and worse clinical outcome. more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL570
14 Samples

Download data: CEL

Series

Accession:: GSE50998

ID:: 200050998

PubMed Full text in PMC Similar studies Analyze with GEO2R

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