ArticleNature communications2025
DiffInvex identifies evolutionary shifts in driver gene repertoires during tumorigenesis and chemotherapy.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- An organoid-guided platform for ovarian cancer: enabling prediction of patients' chemotherapy response.Journal of ovarian research · 2026Article
- MAP3K1: A Multifunctional Kinase at the Crossroads of Cancer Progression and Tumor Suppression.Cells · 2026Review
- Deciphering double-negative prostate cancer: from aggressive subtype to novel therapeutic paradigms.Cell communication and signaling : CCS · 2026Review
- Green Nanodrugs: Research Progress and Challenges of Plant-Derived Nanovesicles in Tumor Treatment.Pharmaceutics · 2026Review
- Targeting the epigenome and tumor heterogeneity: advances in immunotherapy for chemoresistant metastatic colorectal cancer.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Somatic cells can transform into tumors due to mutations, and the tumors further evolve towards increased aggressiveness and therapy resistance. We develop DiffInvex, a framework for identifying changes in selection acting on individual genes in somatic genomes, drawing on an empirical mutation rate baseline derived from non-coding DNA that accounts for shifts in neutral mutagenesis during cancer evolution. We apply DiffInvex to >11,000 somatic whole-genome sequences from ~30 cancer types or healthy tissues, identifying genes where point mutations are under conditional positive or negative selection during exposure to specific chemotherapeutics, suggesting drug resistance mechanisms occurring via point mutation. DiffInvex identifies 11 genes exhibiting treatment-associated selection for different classes of chemotherapies, linking selected mutations in PIK3CA, APC, MAP2K4, SMAD4, STK11 and MAP3K1 with drug exposure. Various gene-chemotherapy associations are further supported by differential functional impact of mutations pre- versus post-therapy, and are also replicated in independent studies. In addition to nominating drug resistance genes, we contrast the genomes of healthy versus cancerous cells of matched human tissues. We identify noncancerous expansion-specific drivers, including NOTCH1 and ARID1A. DiffInvex can also be applied to diverse analyses in cancer evolution to identify changes in driver gene repertoires across time or space.
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Registered trials
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