ArticleMolecular therapy. Oncology2025
Functional characterization of tumor-specific CRISPR-directed gene editing as a combinatorial therapy for the treatment of solid tumors.
Article in Molecular therapy. Oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Genotypic and Phenotypic Diversity as a Function of CRISPR-Directed Gene Knock-Out ofBiomolecules · 2026Article
- Target choice and exon skipping regulate CRISPR-directed gene editing of NRF2 in head/neck and esophageal cancer cells.Molecular therapy. Oncology · 2026Article
- Wise as a Serpent and Gentle as a Dove: Pharmacological Targeting of NRF2/KEAP1 Pathway from Treasure Trove of Mother Nature.Drug design, development and therapy · 2026Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
As we pursue clinical applications for CRISPR-directed gene editing in overcoming resistance to anticancer drugs, we have focused on genetic disruption of the transcription factor, NRF2, a master regulator of cellular stress and detoxification. The level of NRF2 in tumor cells is often a clear determinant of the effectiveness of standard of care. We began to craft a therapeutic approach using tumor-specific CRISPR editing, building upon our previous work elucidating the effect of NRF2 knockout. We selected a prevalent mutation, R34G, that occurs in the Neh2 domain of NRF2, which has been shown to disrupt KEAP1-mediated degradation, thus impacting the NRF2-KEAP1 pathway. Here, we take a global approach by assessing the genomic, transcriptomic, proteomic, and phenotypic profile of a CRISPR-targeted population of cells, both
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