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BCL-2 disruption during CAR T cell production augments potency through non-apoptotic adaptive changes

GSE288296 Homo sapiens (human) Single-cell RNA-seq 12 samples Submitted 2026/03/06 Platform GPL34281
At a glance

Single-cell RNA-seq · human · 12 samples

What it is
Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart. Read from the summary: GEO's own type field only says 'expression profiling by sequencing', so confirm it in the paper.
Organism
Homo sapiens (human)
Samples
12 samples: 3 × CART19_DMSO_CD4_D vs 3 × CART19_VX800_CD4_D vs 3 × CART19_DMSO_CD8_D vs 3 × CART19_VX800_CD8_DGroups 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
Therapeutic targeting of BCL-2 during CART cell production augments potency through non-apoptotic adaptive changesSignal transduction and targeted therapy · 2026
Summary (written by the submitters)
BH3 mimetics were initially designed to induce cancer cell death through targeting key anti-apoptotic members within the BCL-2 family of proteins. Venetoclax, the only FDA-approved BCL-2-specific BH3 mimetic, has demonstrated robust clinical efficacy in killing acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL) cells attributed to its direct apoptotic tumor effect.
Read the full summary ↓
However, little is known regarding the direct effect of venetoclax on tumor infiltrating T cells. Recent studies have reported apoptosis-independent immunomodulatory activities of venetoclax that still are not fully understood. Given the vital role of BCL-2 family proteins in the dynamic processes of T cell activation, differentiation to effector or memory phenotype and contraction, it becomes imperative to dissect the direct effect of BH3 mimetics on T cell functions. We previously demonstrated that murine T cells expanded for 5 days in vitro in the presence of venetoclax acquire adaptive-like reprograming leading to cell death resistance. Further, long-term in vivo treatment with venetoclax results in transcriptional alterations of signaling pathways involved in T cell activation and exhaustion resistance. Herein, we investigate whether this venetoclax-induced T cell reprograming can be employed to improve the efficacy of adoptive T cell therapy. Using murine and human CD19-targeted chimeric antigen receptor (CAR) T cell therapy (CD19CART) as a model, we show that venetoclax treatment during expansion of CD19CARTs prepared from T cells isolated from healthy donors and patients exhibit enhanced antitumor efficacy in vitro and in vivo using pre-clinical xenograft models of lymphoma and leukemia. Mechanistically, bulk and single-cell RNA sequencing analyses reveal that venetoclax treatment during CART manufacturing transcriptionally reprograms CART cells at key T cell signaling (JAK/STAT5, PI3K/AKT, NFKB) and metabolic (PGC1α, OXPHOS, glycolysis) pathways to enhance CAR T cell fitness and durability, mechanisms dependent upon BCL-2 affinity to venetoclax. Our study highlights a possible novel therapeutic approach to induce adaptive anti-apoptotic reprograming to enhance the efficacy of CAR T cell therapy and supports the continued examination of BH3 mimetics as immune modulators.
Published in
Therapeutic targeting of BCL-2 during CART cell production augments potency through non-apoptotic adaptive changes
Aboelella NS, Park R, Tang E et al. · Signal transduction and targeted therapy 2026 · PMID 42036409 · doi:10.1038/s41392-026-02655-y
This dataset
Open GSE288296 in finder → Find more human RNA-seq datasets →
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.

Series matrix ↓
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 GSE288296_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
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.

Raw reads on ENA ↗

What the files usually look like: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1216894 and SRA study SRP560530. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42036409) ↗
Study design
3 × CART19_DMSO_CD4_D vs 3 × CART19_VX800_CD4_D vs 3 × CART19_DMSO_CD8_D vs 3 × CART19_VX800_CD8_D

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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
Datasets on a similar topic

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