ReviewPLoS biology2025
The end of the genetic paradigm of cancer.
Review in PLoS biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed.
- Measurable Residual Disease and the Unresolved Biology of Leukemic Stem Cells.Stem cell reviews and reports · 2026Review
- Network divergence analysis identifies adaptive gene modules and two orthogonal vulnerability axes in pancreatic cancer.Molecular oncology · 2026Article
- CRISPR/Cas9-mediated knockout of TopBP1 shifts the Bax/Bcl-2 balance toward apoptosis in MCF7 breast cancer cells.Molecular biology reports · 2026Article
- Role of alternative splicing in cancer progression.Irish journal of medical science · 2026Review
- Relationship Between VSELs, MUSE Cells and MSCs in Health and Disease.Stem cell reviews and reports · 2026Review
- Interpretation, extrapolation and perturbation of single cells.Nature reviews. Genetics · 2026Review
- Energy constraint on human health.Trends in endocrinology and metabolism: TEM · 2026Review
- Selection for Function in Early Life: Implications for Early-Onset Pathologies.Evolutionary applications · 2026Article
- Review
- Article
- Understanding Cancer Health Disparities.Cancers · 2026Review
- RNA-binding motif proteins as context-dependent regulators of tumor-immune crosstalk, genome stability, and therapeutic vulnerabilities in cancer.Frontiers in immunology · 2026Review
- Understanding cancer as a systemic disease through comprehension of neural stemness as the core property of cancer cell and the basic rules it dictates.Frontiers in cell and developmental biology · 2026Review
- A hybrid Ornstein-Uhlenbeck-Branching framework unifies microbial and pediatric tumor evolution.Frontiers in oncology · 2026Article
- Genomic and Transcriptomic Landscapes of MEN1-Wild-Type Low-Grade Metastatic Pancreatic NETs Uncover Key Oncogenic Drivers and Targetable Pathways.International journal of biological sciences · 2026Article
- Exploring tumorigenesis as a process of phenotypic state-space exploration and selective funneling.Evolution, medicine, and public health · 2026Article
- Cell-cycle-dependent repression of histone gene transcription by histone H4.Nature structural & molecular biology · 2026Article
- Dysfunctional, Tissue-Resident, Very Small Embryonic-Like Stem Cells (VSELs) Initiate Cancer and Result in its Progression and Metastasis, Independent of Epithelial-Mesenchymal Transition.Stem cell reviews and reports · 2026Review
- Generative epigenetic landscapes map the topology and topography of cell fates.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Redox-Adhesion-Exosome (RAX) Hub in Cancer: Lipid Peroxidation-Driven EMT Plasticity and Ferroptosis Defense with HNE/MDA Signaling and Lipidomic Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome sequencing of cancer and normal tissues, alongside single-cell transcriptomics, continues to produce findings that challenge the idea that cancer is a 'genetic disease', as posited by the somatic mutation theory (SMT). In this prevailing paradigm, tumorigenesis is caused by cancer-driving somatic mutations and clonal expansion. However, results from tumor sequencing, motivated by the genetic paradigm itself, create apparent 'paradoxes' that are not conducive to a pure SMT. But beyond genetic causation, the new results lend credence to old ideas from organismal biology. To resolve inconsistencies between the genetic paradigm of cancer and biological reality, we must complement deep sequencing with deep thinking: embrace formal theory and historicity of biological entities, and (re)consider non-genetic plasticity of cells and tissues. In this Essay, we discuss the concepts of cell state dynamics and tissue fields that emerge from the collective action of genes and of cells in their morphogenetic context, respectively, and how they help explain inconsistencies in the data in the context of SMT.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.