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Comparison of gene expression pattern of THP-1 cell treated with ATRA and RAD001

ABSTRACT: To explore the mechanism related to the induction of monocytic differentiation in AML combination of ATRA and RAD001, gene expression patterns of THP-1 cells were analyzed using the Agilent Whole Human Genome Expression Array.

ORGANISM(S): Homo sapiens

PROVIDER: GSE28818 | GEO | 2011/04/25

SECONDARY ACCESSION(S): PRJNA138771

REPOSITORIES: GEO

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Comparison of gene expression pattern of THP-1 cell treated with ATRA and RAD001

Project description:To explore the mechanism related to the induction of monocytic differentiation in AML combination of ATRA and RAD001, gene expression patterns of THP-1 cells were analyzed using the Agilent Whole Human Genome Expression Array. Gene expression patterns of THP-1 cell cultured under four different conditions were analyzed. The conditions were as follows; 1, untreated. 2, treated with ATRA (1mM) and RAD001 (2.5nM). Total RNA was extracted at 5 days after starting treatment.

2011-04-25 | E-GEOD-28818 | biostudies-arrayexpress

OCI/AML2 ATRA AND VPA GENE EXPRESSION

Project description:Purpose: Treatment of acute promyelocytic leukemia (APL) with the retinoid, all trans retinoic acid (ATRA), along with standard chemotherapy has significantly improved survival compared to chemotherapy alone1. ATRA mediates its benefit in APL by overcoming the transcriptional block mediated by PML-RAR-alpha fusion oncoprotein, thereby, restoring expression of retinoid response genes2. The therapeutic benefits observed with ATRA treatment in APL have not been achieved in the other more common sub-types of acute myeloblastic leukemia (AML)3. This likely reflects the recruitment of histone deacetylase complexes by other recurrent chromosomal translocations in AML cells4. In this experiment, we evaluated if treatment of the AML cell line, OCI/AML-2, with the histone deacetylase inhibitor, valproic acid (VPA), would alter the expression of sub-sets of genes by itself or in conjunction with ATRA that have been shown to be modulated by ATRA in APL2. Keywords: other

2005-05-17 | GSE2668 | GEO

THP-1 cells treated with CXCL14

Project description:Monocytic leukemia cell line, THP-1 cells are known to respond to CXCL14. To identfy transcriptional regulation of CXCL14 signalling, we analyse gene expression changed with CXCL14 treatment. THP-1 treated with CXCL14 or PBS treated sample were used.

2013-12-17 | E-GEOD-44550 | biostudies-arrayexpress

Expression profiling of myeloid leukemia cell treated with vibsanine A, PMA and ATRA

Project description:All-trans retinoic acid (ATRA)-based differentiation therapy has achieved success with the treatment of acute promyelocytic leukemia (APL), a unique subtype of acute myeloid leukemia (AML). However, other subtypes of AML display resistance to ATRA-based treatment. Here, we demonstrate that a novel natural vibsane-type diterpenoid vibsanine A promotes the differentiation of myeloid leukemia cell lines and primary AML blasts. To reveal how vibsanine A function on promoting myeloid leukemia cell differentiation, we analyzed and compared the gene expression profiles in myeloid leukemia HL-60 cells treated with vibsanine A, PMA, and ATRA. HL-60 cells were treated with vibsanine A, PMA and ATRA for 6 hours or longer up to 24 hours. Gene expression profiling was conducted

2016-02-28 | E-GEOD-78734 | biostudies-arrayexpress

THP-1 cells treated with CXCL14

2013-12-17 | GSE44550 | GEO

Expression profiling of myeloid leukemia cell treated with vibsanin A, PMA and ATRA

Project description:All-trans retinoic acid (ATRA)-based differentiation therapy has achieved success with the treatment of acute promyelocytic leukemia (APL), a unique subtype of acute myeloid leukemia (AML). However, other subtypes of AML display resistance to ATRA-based treatment. Here, we demonstrate that a novel natural vibsane-type diterpenoid vibsanin A promotes the differentiation of myeloid leukemia cell lines and primary AML blasts. To reveal how vibsanin A function on promoting myeloid leukemia cell differentiation, we analyzed and compared the gene expression profiles in myeloid leukemia HL-60 cells treated with vibsanin A, PMA, and ATRA.

2016-02-28 | GSE78734 | GEO

Bortezomib resistance in THP-1 cell line

Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the THP-1 monocytic/macrophage cell line. On these subclones expression arrays were performed. We performed expression array three different bortezomib resistant subclones of the THP-1 cell line. The resistant subclones were spotted against the parental THP-1 wildtype cell line.

2008-06-14 | E-GEOD-11771 | biostudies-arrayexpress

Pre and post ATRA/VP treatment proteomic and phophoproteomic profiling of AML responders and non-responders

Project description:Proteome and phosphoproteome raw files from AML patient samples obtained before and after 3 and 8 days of ATRA/valproic acid treatment

2021-09-10 | PXD024197 | Pride

Phase I Dose Escalation Study of ATRA Combined with the LSD1 inhibitor Tranylcypromine in AML and MDS

Project description:Preclinical studies have shown that combining the LSD1 inhibitor tranylcypromine (TCP) with all-trans retinoic acid (ATRA) induces differentiation and impairs survival in non-APL acute myeloid leukemia (AML). We conducted a Phase 1 clinical trial (NCT02273102) to evaluate the safety and preliminary activity of ATRA in combination with TCP in patients with relapsed/refractory AML and myelodysplasia (MDS). Seventeen patients (11 AML and 6 MDS) received ATRA-TCP therapy with ATRA (45 mg/m2 daily in divided doses) and TCP (3 dose levels: 10 mg twice-daily [BID], 20 mg BID, and 30 mg BID). ATRA-TCP had an acceptable safety profile. The maximum tolerated dose of TCP was 20 mg BID. There were 3 DLTs: dizziness (20 mg BID), asthenia (30 mg BID), and nausea/vomiting (30 mg BID). Best evaluable responses included 1 morphologic leukemia-free state (MLFS), 1 marrow complete remission (CR) with hematologic improvement, 2 stable disease with hematologic improvement, and 2 stable disease. In 13 response-evaluable patients, the overall response rate was 30.8% and clinical benefit rate 46.2%. Gene expression profiling of patient blasts showed that responding patients had a more dormant phenotype compared to non-responders at baseline. In human AML cell lines, we showed that treatment with ATRA-TCP increases differentiation capacity and/or cell death, and that ATRA-TCP regulates the in vitro expression of genes that segregate primary patients by their clinical response. These data indicate that LSD1 inhibition sensitizes AML cells to ATRA-induced differentiation and cell death and may restore clinical responsiveness in subsets of MDS and AML patients.

2021-06-21 | GSE151594 | GEO

Fulica atra

Project description:Fulica atra

| PRJNA815160 | ENA