GEO series

Gene expression of AML patient samples

GSE97393 Homo sapiens (human) Expression microarray 21 samples Submitted 2017/06/25 Platform GPL16686

At a glance

Expression microarray · human · 21 samples

What it is: Expression microarrayGene activity read on a chip (the older technology that RNA-seq replaced).
Organism: Homo sapiens (human)
Samples: 21 samples
Data you can get: A processed expression table (series matrix) and the array files, from NCBI.

Summary (written by the submitters)

It has been hypothesized that chemotherapy resistant human acute myeloid leukemia (AML) cells are enriched in an immature phenotype, cellular quiescence and leukemic initiating cells (LICs). However, these hypotheses have never been validated completely in vivo. We have developed a physiologically relevant chemotherapeutic approach with cytosine arabinoside AraC using patient-derived xenograft (PDX) models.

Read the full summary ↓

AraC-treated AML cells are not consistently enriched for either immature cells or quiescent cells. AraC treatment does not enrich for LICs as measured by limiting dilution in secondary transplantations. Rather chemotherapy resistant cells in vivo have high levels of reactive oxygen species (ROS) and a gene signature consistent with oxidative phosphorylation (OXPHOS). Treatment of human HIGH OXPHOS but not LOW OXPHOS AML cell lines showed chemotherapy resistance in vivo, showing that essential mitochondrial functions make significant contributions to AraC resistance in AML. Accordingly, targeting mitochondrial OXPHOS metabolism through the inhibition of mitochondrial protein synthesis, the electron transfer chain or fatty acid oxidation induced an energetic shift towards LOW OXPHOS and strongly enhanced anti-leukemic effects of AraC in AML cells. These results demonstrate that chemotherapy resistance in AML is not necessarily associated with stemness but is highly dependent on a distinct oxidative metabolism, and that the HIGH OXPHOS gene signature is a robust hallmark of the AraC response in PDX and a promising therapeutic avenue to treat AML residual disease.

This dataset

Open GSE97393 in finder → Find more human microarray datasets →

Download · which file do I need?

Direct links to NCBI, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need.

All supplementary files ↗

3 · The original raw files

Whole study · RAW.tar

Everything the authors deposited as one archive (GSE97393_RAW.tar), including the raw array or instrument files. Can be large; the picker in step 2 takes just the samples you need.

Whole study · RAW.tar ↓

What the files usually look like: For arrays the series matrix is normally the normalised expression table you want; the raw array files (CEL and similar) are in the RAW.tar.

Also filed as BioProject PRJNA381625. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 28416471) ↗

Samples in this study

The sample list for this study is not cached yet. Press Load samples and it will be fetched from NCBI.

+ 21 more — browse all 21 samples with per-sample file links →

Datasets on a similar topic

GSE270621 Gene epression analyses on pre- and post-treatment samples obtained from AML patients who respond or failed to respond to Venetoclax/Decitabine treatment 26 samples shares aml
GSE232130 Leucegene: AML sequencing (GRCh38 reference) 691 samples shares aml
GSE232129 Leucegene: AML sequencing (part 1-6, GRCh38 reference) 452 samples shares aml
GSE293201 Ectopic MYC Expression Reprograms Epigenetic Landscapes and Transcription Factor Networks to Drive Differentiation Block and Malignant Transformation in AML [ATAC-seq] 35 samples shares aml
GSE297413 Genomic and transcriptomic determinants of clinical outcomes in patients with AML and DNMT3A mutations 264 samples shares aml
GSE221578 CRISPR-based genetic screens to interrogate therapeutic targets on tumor maintenance and heterogeneity in AML patient cells 31 samples shares aml
GSE256353 Upregulated cholesterol biosynthesis facilitates the survival of methylation-retaining AML cells following decitabine treatment [single_colony_TEM-Seq] 1728 samples shares aml
GSE247095 Preclinical efficacy of targeting epigenetic mechanisms in AML with 3q26 lesions and EVI1 overexpression 28 samples shares aml

Search all human microarray datasets in GEO →

Share this dataset

Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.