TP53 Deficiency in B-ALL: Transcriptomic Signature and CAR-T Cell Exhaustion Data

Yu Wang's dataset on figshare, last updated 2026-05-28, contains transcriptomic and cellular assay data from an in vitro study of TP53-deficient B-cell acute lymphoblastic leukemia. The 1.8 MB DOCX file likely contains results from RNA-sequencing and co-culture assays comparing TP53-wildtype and TP53-knockout NALM-6 B-ALL cell models. The data explores the link between p53 loss, a low-adhesion gene signature, and accelerated CAR-T cell exhaustion.

Use Cases

• Analyze the low-adhesion transcriptomic signature based on the downregulation of ECM and adhesion genes like ITGB1 and LAMA5.
• Investigate correlations between TP53 status and CAR-T cell functional metrics like proliferation and cytokine secretion.
• Model the relationship between tumor-intrinsic gene expression and T-cell exhaustion markers (PD-1, TIM-3, LAG-3).
• Study the suppression of immunogenic signaling pathways, such as IL-2/STAT5, under immune pressure from CAR-T cells.

Strengths

• Data is derived from controlled isogenic cell models (TP53-wildtype vs. knockout) engineered with CRISPR/Cas9.
• Includes multi-modal in vitro assay data: cytotoxicity, proliferation, cytokine secretion, and RNA-sequencing.
• Released under a permissive CC-BY-4.0 license.

Limitations

• The dataset is small (1.8 MB) and the row count is unknown, which may limit suitability assessment.
• Column-level documentation is absent; field semantics must be inferred after download.
• Data is from a specific in vitro model (NALM-6 cells) and may not fully represent in vivo tumor microenvironments.

Provenance

Source

figshare, author Yu Wang.

Collection Method

Data generated from CRISPR/Cas9-engineered cell models, in vitro co-culture assays, and RNA-sequencing.

Freshness

Last updated 2026-05-28 05:57:48; freshness should be verified.