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Combined ANA and IDA treatment is an innovative and promising therapeutic strategy for AML patients with high PDE3A expression

ABSTRACT: Combined ANA and IDA treatment is an innovative and promising therapeutic strategy for AML patients with high PDE3A expression

PROVIDER: PRJNA1119977 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29275570_1.fastq.gz	Fastqsanger.gz
	SRR29275570_2.fastq.gz	Fastqsanger.gz

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Combined ANA and IDA treatment is an innovative and promising therapeutic strategy for AML patients with high PDE3A expression

Project description:Acute myeloid leukemia (AML) is an invasive hematopoietic malignancy requiring novel treatment strategies. The PDE3A inhibitor anagrelide (ANA) profoundly suppresses the proliferation of high PDE3A-expressing AML cells while showing minimal impact on those with low PDE3A expression. Moreover, synergistic effect of ANA with other chemotherapeutic drugs in high PDE3A expression AML cells was observed. The ANA-idarubicin (IDA) combination showed the most remarkable synergistic effect among all ANA-chemotherapeutic drugs commonly used in AML cell line models. Our findings suggest that combined ANA and IDA treatment is an innovative and promising therapeutic strategy for AML patients with high PDE3A expression.

2025-06-01 | GSE269021 | GEO

Dichelostemma ida-maia

Project description:Dichelostemma ida-maia overview

| PRJNA198046 | ENA

ida-2

Project description:Chromosomal rearrangements in outcrossed ida-2 mutants

| PRJEB62448 | ENA

Dichelostemma ida-maia

Project description:Dichelostemma ida-maia Genome sequencing

| PRJNA197399 | ENA

Helicobacter pylori sabA gene is associated with iron deficiency anemia (IDA) in childhood and adolescence

Project description:Background Gastric Helicobacter pylori colonization leads to iron deficiency anemia (IDA), especially in children and adolescents. However the pathogenesis is poorly understood. Objective We sought to identify specific H. pylori genes involved in IDA development, by comparing bacterial genome-wide expression profiling in patients affected or not. Methods H. pylori were isolated from four children with IDA and four from matched controls without IDA. Based on these isolates, cDNA microarrays under iron-replete or depleted conditions were systematically performed to compare gene expression profiles at the whole genome level. Real-time reverse-transcription (RT-) PCR and protein assays were performed for further assessing the profile differentiation of the identified H. pylori IDA-associated genes. Results We identified 29 and 11 genes with significantly higher or lower expression in the IDA isolates compared to non-IDA isolates, respectively. Especially notable were higher expression of sabA gene encoding sialic acid-binding adhesin in the IDA isolates, which was confirmed by real-time RT-PCR study. Moreover, iron-depletion in vitro led to up-regulation of fecA1 and frpB1 genes and down-regulation of pfr, as predicted. Known iron-regulated genes such as fur, pfr, fecA, and feoB did not significantly differ between both groups. The IDA isolates had significantly higher expression of vacuolating cytotoxin gene vacA than non-IDA isolates, consistent with the results of VacA protein assays. There were no significant differences in bacterial growth value between IDA and non-IDA isolates. Conclusions It is likely that H. pylori carrying high expression of sabA causes IDA, especially in children and adolescents who have increased daily iron demand. In addition, it is possible that several host-interactive genes, including vacA, may play a synergistic role for sabA in IDA development.

2017-07-25 | GSE101807 | GEO

Gene Expression profiling of human PBMCs with different ANA titer

Project description:Total 48 samples with different ANA titer were analyzed for their gene expression profiles with Illumina HumanWG-6 V3 chips 10 healthy control (HC) samples with high ANA, 7 first degree relative of SLE patientw (FDR) with high ANA, 10 HCs with low ANA, 6 FDR with low ANA, 15 SLE patients (SLE) with high ANA were used for the microarray analysis.

2010-10-15 | E-GEOD-24706 | biostudies-arrayexpress

Shewanella sp. ANA-3

Project description:Shewanella sp. ANA-3

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Transcript structures in Shewanella sp ANA-3

Project description:5' RNASeq of mRNA from Shewanella sp ANA-3 grown aerobically in Luria-Bertani broth (LB) and defined lactate minimal medium

2013-03-21 | GSE45311 | GEO

Expression data from different levels of ANA in HIV+ people

Project description:Different focal adhesions, gap junction, adherens junction, and tight junction, TLR signaling pathway were seen when compared the HIV+ high ANA (anti-nuclear antibodies) group with low ANA group We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process.

2018-10-01 | GSE101589 | GEO

A T cell immune suppression signature distinguishes European American auto-antibody positive (ANA+) healthy individuals

Project description:Anti-nuclear antibody (ANA) positivity is a principal feature of individuals with an autoimmune disease, yet up to one in five healthy individuals are ANA+ and most will never develop clinical autoimmunity. Here, we show that immune profiles in ANA+ healthy individuals are altered, and differ by race. A suppressive immune signature distinguished by reduced T cell numbers and altered gene expression of HLA class I, IFN-associated, and apoptosis pathways, characterized European American (EA) ANA+ healthy individuals. In contrast, African American (AA) ANA+ healthy individuals had more elements of activation with increased CD69 gene expression on T cells and heightened pro-inflammatory cytokines. Increases in STAT4, IFNGR2 and STAT1 T cell transcripts and decreases in TGFBR1 gene expression in monocytes correlated with T cell expansion and clinical SLE. Thus, a suppressive immune signature in EA ANA+ healthy individuals may avert clinical autoimmune disease, which is associated with activation of Type I and II IFN pathways and T cell expansion.

2020-11-27 | GSE138400 | GEO

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