Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Abnormal Expression Changes in AML

ABSTRACT: Acute myeloid leukemia (AML) is one of the most common and deadly forms of hematopoietic malignancies. We hypothesized that microarray studies could identify previously unrecognized expression changes that only occur only in AML blasts. We were particularly interested in those genes with increased expression in AML, believing that these genes may be potential therapeutic targets. Keywords: AML vs Normal hematopoietic cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE9476 | GEO | 2007/11/01

SECONDARY ACCESSION(S): PRJNA103247

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiling of human hematopoietic cells from 38 healthy donors and leukemic blasts from 26 AML patients

Project description:Acute myeloid leukemia (AML) is one of the most common and deadly forms of hematopoietic malignancies. We hypothesized that microarray studies could identify previously unrecognized expression changes that only occur only in AML blasts. We were particularly interested in those genes with increased expression in AML, believing that these genes may be potential therapeutic targets. Experiment Overall Design: We compared gene expression profiles between normal hematopoietic cells from 38 healthy donors and leukemic blasts from 26 AML patients. Normal hematopoietic samples included CD34+ selected cells (N = 18), unselected bone marrows (N = 10), and unselected peripheral bloods (N = 10).

2008-06-16 | E-GEOD-9476 | biostudies-arrayexpress

Aberrant expressed genes in AML

Project description:Acute myeloid leukemia (AML) is one of the most common and deadly forms of hematopoietic malignancies. We hypothesized that microarray studies could identify aberrantly expressed genes selectively expressed in AML blasts, believing that these genes may be potential therapeutic targets for adoptive T-cell strategies We compared gene expression profiles between leukemic blasts from 30 AML patients (this series and GSE9476) and prepublished samples of normal hematopoietic cells from healthy donors (N=17, GSE9476) and testis samples (N=2, GSE1133).

2012-04-16 | E-GEOD-37307 | biostudies-arrayexpress

Aberrant expressed genes in AML

Project description:Acute myeloid leukemia (AML) is one of the most common and deadly forms of hematopoietic malignancies. We hypothesized that microarray studies could identify aberrantly expressed genes selectively expressed in AML blasts, believing that these genes may be potential therapeutic targets for adoptive T-cell strategies

2012-04-17 | GSE37307 | GEO

The phosphoproteomic landscape of two FLT3+ Acute Myeloid Leukemia (AML) patient samples.

Project description:Acute myeloid leukemia (AML) is a clonal hematopoietic malignancy, characterized by expansion of immature leukemic blasts in the bone marrow. In AML, specific tyrosine kinases have been implicated in leukemogenesis, and are associated with poor treatment outcome. However, targeted therapy using kinase inhibitors (KIs) has had limited success, and may be improved by proper patient selection. We performed phosphotyrosine (pY) based, label-free phosphoproteomics to identify hyperphosphorylated, active kinases in two FLT3+ AML Pt samples.

2020-03-02 | PXD015639 | Pride

The phosphoproteomic landscape of two FLT3+ Acute Myeloid Leukemia (AML) patient samples-LYSATES.

2020-03-02 | PXD015662 | Pride

Transcriptome profiling of quiescent and cytokine induced normal human haematopoietic CD34+ HSPCs, and AML blast cells

Project description:Control group is an essential part of the research design which provide a baseline by elimating variables, bias and other factors that skew the data. Human CD34+ cells are generally used as controls to study myeloid malignancies. This study determines whether fresh or short term cytokine induced CD34+ HSPCs can provide a more appropriate normal control (compared to AML blasts) for target discovery studies. We here determine that the GEP of CD34+ cells that do not undergo ex vivo expansion best match the GEP of minimally differentiated AML blasts and would serve as a better control to identify novel targets in the AML blast population.

2015-12-09 | E-MTAB-3328 | biostudies-arrayexpress

Acquired TET2 mutation-linked clonal hematopoiesis in FPD/AML patient led to the development of pre-leukemic clone resulting independently in T2-ALL and AML-M0

Project description:Germline RUNX1 mutations are found in familial platelet disorders with predisposition to acute myelogenous leukemia (FPD/AML). This very rare disease is characterized by thrombocytopenia, platelet dysfunction and a 35% lifetime risk of developing MDS/AML and in rare cases also T-ALL. Here, we focus on a case of a man with a familial history of RUNX1 R174Q mutation who developed at the age of 42 years an EGIL T2-ALL and, two years after remission, an AML-M0. To investigate whether initial and relapsed leukemic blasts originated from the same clone, we performed CGH array and WES on both blasts populations. In both T2-ALL and AML-M0 samples, CGH array revealed loss of 1p36.32-23 and 17q11.2 and nine other small deletions. Both AML-M0 and T2-ALL blasts demonstrated clonal rearrangements of both TCRÎ³ (VÎ³9-JÎ³1-1) and TCRÎ´ (DÎ´2-JÎ´1 and DÎ´2-JÎ´3). 18 genes were found by WES to be mutated in both blasts at a frequency of more than 40%. Additional variants were identified only in T2-ALL or in AML-M0 evoking the existence of a common original clone, which gave rise to subclonal populations. MiSeq technology performed on peripheral blood-derived CD34+ cells five years prior T2-ALL development revealed only missense TET2 P1962T mutation at a frequency of 1% (which reaches a frequency of 50 % in fully transformed leukemic clone) suggesting that this mutation in association with germline RUNX1 R174Q mutation led to amplification of a hematopoietic clone susceptible to acquire other transforming alterations. Identification of clonal hematopoiesis with acquired mutations at low frequency in hematopoietic progenitors before leukemia development could clearly serve as a marker of pre-leukemic state and be helpful in patient care.

2017-06-29 | E-MTAB-4623 | biostudies-arrayexpress

DNR pulse treatment of primary AML

Project description:Primary human AML bone marrow sample (newly diagnosed, prior to treatment initation) was obtained from donor after consent and AML blasts were isolated by standard Ficoll centrifugation. AML blasts were pulse-treated with daunorubicine (100 nM, 200 nM, 400 nM) or DMSO control for 1 hour, followed by wash-out and short-term cell culture to allow cellular responses to develop. 20,000 cells were analysed by LC-MS3, and 5,000 cells were subjected to flow cytometry apoptosis assay.

2022-10-15 | PXD030280 | Pride

Phosphoproteomics of primary human FLT3-ITD+ AML cells treated with gilteritinib

Project description:Primary human AML cells (newly diagnosed, prior to treatment initation) were obtained from donor after consent and AML blasts were isolated by standard Ficoll centrifugation. AML blasts were treated with FLT3 inhibitor gilteritinib (or DMSO vehicle control) at 10 nM concentration for 6 h, followed by harvest for LC/MS.

2022-08-25 | PXD034080 | Pride

Human AML secretome and correlation with Anti-Apoptotic Index, part 1

Project description:Expression of proteins regulating apoptosis (BCL-2, MCL-1, BCL-X and BAX) in acute myeloid leukemia (AML) blasts at diagnosis have been shown to be associated with disease-free survival. We previously found that the initially high apoptosis-resistance of AML cells decreased after therapy, while regaining high levels at relapse. This suggested a dynamic regulation of apoptosis. Herein, we further explored this aspect of apoptosis in AML. Firstly, the intra-individual ex vivo apoptosis-related profiles of normal lymphocytes and AML blasts showed a strong correlation, with expression values far beyond control lymphocytes. Secondly, we demonstrated that apoptosis-resistant primary AML blasts, as opposed to apoptosis-sensitive cells, were able to up-regulate BCL-2 expression in sensitive AML blasts in contact cultures (p=0.0067 and p=1.0 respectively). Using proteomics we further set out to identify novel proteins possibly engaged in apoptosis regulation. Proteomics analysis revealed that major functional protein clusters upregulated in secretomes of apoptosis-resistant AML, were presumably engaged in global gene regulation including mRNA splicing, protein translation and chromatin remodeling.

2016-02-03 | PXD001476 | Pride

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