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Targeting polyamine metabolism and eIF5A hypusination in pediatric acute myeloid leukemia

GSE342172 Homo sapiens (human) RNA-seq (gene expression) 18 samples Submitted 2026/08/02 Platform GPL29480Platform GPL34284
At a glance

RNA-seq (gene expression) · human · 18 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Topic
Acute myeloid leukemiaThis series is part of our curated briefing on it.
Samples
18 samples: 6 conditions, mostly in triplicateGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Summary (written by the submitters)
Pediatric acute myeloid leukemia (AML) is a devasting disease with 5-year survival outcomes of approximately 60%. Therefore, there is an urgent need to develop novel therapies for pediatric AML patients. Numerous studies have demonstrated that cellular metabolism is a key vulnerability in adult AML; however, we understand very little about metabolism in pediatric AML.
Read the full summary ↓
Using pediatric AML patient derived xenograft models, we demonstrate that polyamine metabolism is a pharmacologically targetable vulnerability of pediatric AML cells. Further, depletion of polyamines sensitizes pediatric AML cells to chemotherapy in vitro and in vivo. Mechanistically, polyamine depletion causes reduced protein synthesis through decreased hypusination of translational elongation factor eIF5A. Pharmacologic polyamine depletion and inhibition of eIF5A hypusination result in reduced protein synthesis and decreased expression of cell cycle regulatory proteins resulting in a G1 cell cycle arrest and eventual cell death through apoptosis. In summary, this study reveals polyamine metabolism and hypusination of eIF5A as a vulnerability in pediatric AML that can be targeted using clinically trackable approaches.
This dataset
Download · which file do I need?

Direct links to NCBI and ENA, 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.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE342172_RAW.tar (it can run to tens of gigabytes).

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1505732 and SRA study SRP723310. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in triplicate
Ribo AML vehicle ×3 Ribo AML DENSpm ×3 Ribo AML GC7 ×3 RNA AML vehicle ×3 RNA AML DENSpm ×3 RNA AML GC7 ×3

Supports a between-group comparison across 18 samples.

How we read this: 6 replicated groups read from 18 sample titles; they account for 18 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
More Acute myeloid leukemia datasets

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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.