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Differential gene expression profile of newly diagnosed versus relapse acute promyelocytic leukemia

ABSTRACT: The aim of this study was to gain insight into the potential mechanism of resistance to arsenic trioxide and to identify genes that are modulated in the malignant promyelocytes at the time of relapse in APL patients. We analyzed the gene expression profile by the whole genome microarray of primary promyelocytes obtained from 8 newly diagnosed and 8 at relapse patients.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42030 | GEO | 2013/08/02

SECONDARY ACCESSION(S): PRJNA178949

REPOSITORIES: GEO

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Differential gene expression profile of newly diagnosed versus relapse acute promyelocytic leukemia

Project description:The aim of this study was to gain insight into the potential mechanism of resistance to arsenic trioxide and to identify genes that are modulated in the malignant promyelocytes at the time of relapse in APL patients. We analyzed the gene expression profile by the whole genome microarray of primary promyelocytes obtained from 8 newly diagnosed and 8 at relapse patients. Agilent one-color experiment,Organism: Human ,Agilent Whole Genome Human 4x44k (AMADID: 014850) , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442) newly diagnosed versus relapse acute promyelocytic leukemia

2013-08-02 | E-GEOD-42030 | biostudies-arrayexpress

Comparison of gene expression profile of naive versus arsenic trioxide resistant acute promyelocytic leukemia cell line NB4

Project description:The aim of this study was to gain insight into the potential mechanism of resistance to arsenic trioxide (ATO). The gene expression profile of naive (NB4) (Acute promyelocytic leukemia (APL) cell line and one of its in house generated ATO resistant sub clone (NB4-VM-AsR1) was done using whole genome microarray and compared to generate the differential expression profile which will give insight into the mechanisms of ATO resistance in APL. Agilent one-color experiment,Organism: Human ,Agilent Whole Genome Human 4x44k (AMADID: 014850) , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442) naive versus arsenic trioxide resistant acute promyelocytic leukemia cell line NB4

2013-08-02 | E-GEOD-42031 | biostudies-arrayexpress

Torque Teno Mini Virus as a cause of childhood acute promyelocytic leukemia lacking PML/RARA fusion

Project description:We describe a case of a child affected by a relapsed PML/RARA-negative acute promyelocytic leukemia (APL) rescued by a combination of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) and subsequent HSCT. We provide evidence of the presence of a chimeric viral transcript generated through genomic integration of a Torque Teno Mini Virus sequence into RARA intron 2, the recurrent breakpoint of all chimeric RARA fusions found in APL. This generates an in-frame TTMV/RARA chimeric fusion that is highly expressed at disease diagnosis and relapse and fully cleared at remission achievement.

2021-12-01 | GSE169521 | GEO

Comprehensive mutational analysis of primary and relapse acute promyelocytic leukemia

Project description:Acute promyelocytic leukemia (APL) is a subtype of myeloid leukemia characterized by differentiation block at the promyelocyte stage. Besides the presence of chromosomal rearrangement t(15;17) leading to formation of PML-RARA fusion, other genetic alterations have also been implicated in APL. Here, we performed comprehensive mutational analysis of primary and relapse APL to identify somatic alterations which cooperate with PML-RARA in the pathogenesis of APL. We explored the mutational landscape using whole-exome (n=12) and subsequent targeted sequencing of 398 genes in 153 primary and 69 relapse APL. Both primary and relapse APL harbored an average of eight non-silent somatic mutations per exome. We observed recurrent alterations of FLT3, WT1, NRAS and KRAS in the newly diagnosed APL, while mutations in other genes commonly mutated in myeloid leukemia were rarely detected. The molecular signature of APL relapse was characterized by emergence of frequent mutations in PML and RARA genes. Our sequencing data also demonstrates incidence of loss-of-function mutations in previously unidentified genes, ARID1B and ARID1A, both of which encode for key components of the SWI/SNF complex. We show that knockdown of ARID1B in APL cell line, NB4, results in large scale activation of gene expression and reduced in vitro differentiation potential.

2016-02-17 | GSE77946 | GEO

Comprehensive mutational analysis of primary and relapse acute promyelocytic leukemia

2016-02-17 | E-GEOD-77946 | biostudies-arrayexpress

Comparison of gene expression profile of naive versus arsenic trioxide resistant acute promyelocytic leukemia cell line NB4

2013-08-02 | GSE42031 | GEO

Genome-wide expression profiling of acute promyelocytic leukemia NB4 cells treated with all-trans-retinoic acid

Project description:Acute promyelocytic leukemia (APL) is a hematological disease characterized by a balanced reciprocal translocation that leads to the synthesis of the oncogenic fusion protein PML-RARα. APL is mainly managed by a differentiation therapy based on the administration of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). However, therapy resistance, differentiation syndrome, and relapses require the development of new low-toxicity therapies based on the induction of blasts differentiation. Here, we performed a high-throughput gene expression profile of the maturation inducible APL cell line NB4 untreated or exposed to ATRA.

2020-11-05 | GSE155779 | GEO

FLT3-ITD impedes retinoic acid, but not arsenic, responses in murine acute promyelocytic leukemias

Project description:Combined all trans retinoic acid (ATRA) / arsenic regimen cures virtually all acute promyelocytic leukemi (APL) patients. However, APL is often associated with activating FLT3-internal tandem duplication (ITD) mutation and the molecular bases for this effect remain unknown. Using mouse APL models, we demonstrate the FLT3-ITD severely blunts ATRA response.

2019-03-18 | E-MTAB-7566 | biostudies-arrayexpress

Bone marrow microenvironment mediated drug resistance in Acute promyelocytic leukemia

2020-01-10 | GSE124987 | GEO

Bone marrow micro-environment mediated drug resistance in Acute promyelocytic leukemia

Project description:About 5-10% newly diagnosed and about 20-30% of relapsed acute promyelocytic leukemia (APL) patients will have disease recurrence after receiving currently accepted standards of care. While there are reports of micro-environment mediated drug resistance (EM-DR) in AML, there is no data on the effect of malignant promyelocyte and stromal interaction on Arsenic trioxide (ATO) induced apoptosis. We undertook a preliminary study to evaluate the role of EM-DR to ATO in APL. In direct co-culture (contact dependent system) of malignant promyelocyte with stromal cells, the stromal cells gave a significant protective effect against ATO at different concentrations used (1 to 8 Î¼mol; NB4 (APL cell line) In a gene expression profiling comparing NB4 cells in co-culture with NB4 cells alone, 1846 genes were differentially regulated. On a preliminary analysis, we observed an up-regulation of various pathways such as adhesion (ITGB1, ITGB2, ITGB7, etc.), Cytokines (IL-6, IL-8, IL-18, CCL2, CCL10, etc.) Wnt signalling (Wnt5a, Wnt11, NFATC4, etc,) NF-kB pathway (ICAM1, BIRC2, BIRC3, XIAP1, etc.) in the leukemic cells. The NF-kB pathway has been validated using real time PCR which correlated with the genes being differentially regulated in NB4 cells co-cultured in stroma. Agilent one-color experiment,Organism: Homo sapiens ,Custom Agilent 8x60k Human Whole Genome Microarray Gene expression (AMADID: 039494) , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)

2016-09-01 | E-GEOD-73157 | biostudies-arrayexpress

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