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NK cell cytotoxicity shapes the clonal evolution of B cell leukemia [RNA-seq]

GSE278006 Homo sapiens (human) RNA-seq (gene expression) 241 samples Submitted 2024/11/26 Platform GPL21103Platform GPL24247Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 241 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 lymphoblastic leukemiaThis series is part of our curated briefing on it.
Samples
241 samples: 78 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.
Paper
Natural Killer Cell-Mediated Cytotoxicity Shapes the Clonal Evolution of B-cell LeukemiaCancer immunology research · 2025
Summary (written by the submitters)
The term cancer immunoediting describes the dual role by which the immune system can suppress and promote tumour growth and is divided into three phases: elimination, equilibrium and escape. The role of NK cells has mainly been attributed to the elimination phase. Here we show that NK cells play a role in all three phases of cancer immunoediting.
Read the full summary ↓
Extended co-culturing of DNA barcoded mouse BCR/ABLp185+ B acute lymphoblastic leukaemia cells with NK cells allowed for a quantitative measure of NK cell-mediated immunoediting. Whereas most tumour cell clones were efficiently eliminated by NK cells, a certain fraction of tumour cells harboured an intrinsic primary resistance. Furthermore, DNA barcoding revealed tumour cell clones with secondary resistance, which stochastically acquired resistance to NK cells. NK cell cytotoxicity put a selective pressure on B-ALL cells inducing primary and secondary resistance, while resistant tumour cells were characterised by a full-blown IFN-g signature. Besides well-known regulators of immune evasion, our analysis of NK resistant tumour cells revealed the upregulation of novel genes, including Ly6a, which we found to drive NK cell resistance in leukaemic cells. We further translated our findings to the human system and showed that high LY6E expression on tumour cells impaired the physical interaction with NK cells and led to worse prognosis in leukaemia. Our results demonstrate that tumour cells are actively edited by NK cells during the equilibrium phase and use different avenues to escape NK cell-mediated eradication.
Published in
Natural Killer Cell-Mediated Cytotoxicity Shapes the Clonal Evolution of B-cell Leukemia
Buri MC, Shoeb MR, Bykov A et al. · Cancer immunology research 2025 · PMID 39642167 · doi:10.1158/2326-6066.CIR-24-0189
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 GSE278006_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 PRJNA1165216 and SRA study SRP534716. Searching any of these in the dataset finder brings you back here.

Study design
78 conditions, mostly in triplicate
Tumor_only, Cell_line_C, timepoint_1, EXP_9.4, ×3 Tumor_only, Cell_line_D, timepoint_1, EXP_9.4, ×3 Tumor_plus_NK, Cell_line_C, timepoint_2, EXP_… ×3 Tumor_plus_NK, Cell_line_D, timepoint_2, EXP_… ×3 Tumor_plus_NK, Cell_line_C, timepoint_1, EXP_… ×3 Tumor_plus_NK, Cell_line_D, timepoint_1, EXP_… ×3 Tumor_only, Cell_line_A, timepoint_1, EXP_9.5, ×3 Tumor_only, Cell_line_B, timepoint_1, EXP_9.5, ×3 +81 more

Supports a case/control comparison: 193 samples read as cases, 18 as controls.

How we read this: 78 replicated groups read from 241 sample titles; they account for 230 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

+ 201 more — browse all 241 samples with per-sample file links →

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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.