ReviewCancer metastasis reviews2013
Do mutator mutations fuel tumorigenesis?
Review in Cancer metastasis reviews, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 103 citations in OpenAlex.
- Integrated metabolome and transcriptome analysis reveals ferroptosis involvement in cisplatin resistance of esophageal squamous cancer cell.Computational and structural biotechnology journal · 2026Article
- Carcinogenesis trajectories.Frontiers in cell and developmental biology · 2025Article
- Signification and Application of Mutator and Antimutator Phenotype-Induced Genetic Variations in Evolutionary Adaptation and Cancer Therapeutics.Journal of microbiology (Seoul, Korea) · 2023Review
- Pairwise and higher-order epistatic effects among somatic cancer mutations across oncogenesis.Mathematical biosciences · 2023Article
- Shifts in Mutation Bias Promote Mutators by Altering the Distribution of Fitness Effects.The American naturalist · 2023Article
- Review
- APOBEC3B: Future direction of liver cancer research.Frontiers in oncology · 2022Review
- Exosomal Components and Modulators in Colorectal Cancer: Novel Diagnosis and Prognosis Biomarkers.Biomedicines · 2021Review
- Autophagy buffers Ras-induced genotoxic stress enabling malignant transformation in keratinocytes primed by human papillomavirus.Cell death & disease · 2021Article
- Comprehensive Analyses Identify APOBEC3A as a Genomic Instability-Associated Immune Prognostic Biomarker in Ovarian Cancer.Frontiers in immunology · 2021Article
- Mitigation of Iron Irradiation-Induced Genotoxicity and Genomic Instability by Postexposure Dietary Restriction in Mice.BioMed research international · 2021Article
- APOBEC: A molecular driver in cervical cancer pathogenesis.Cancer letters · 2021Review
- Mutant POLQ and POLZ/REV3L DNA polymerases may contribute to the favorable survival of patients with tumors with POLE mutations outside the exonuclease domain.BMC medical genetics · 2020Article
- Intratumor Heterogeneity: The Rosetta Stone of Therapy Resistance.Cancer cell · 2020Review
- Evidence for immortality and autonomy in animal cancer models is often not provided, which causes confusion on key issues of cancer biology.Journal of Cancer · 2020Review
- DNA damage and tissue repair: What we can learn from planaria.Seminars in cell & developmental biology · 2019Review
- Defining the impact of mutation accumulation on replicative lifespan in yeast using cancer-associated mutator phenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The variome concept: focus on CNVariome.Molecular cytogenetics · 2019Article
- Genomic Instability Promoted by Overexpression of Mismatch Repair Factors in Yeast: A Model for Understanding Cancer Progression.Genetics · 2018Article
- Evolutionary history of metastatic breast cancer reveals minimal seeding from axillary lymph nodes.The Journal of clinical investigation · 2018Article
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 at 1 institution in 1 country.
Funding
Abstract
The mutator phenotype hypothesis proposes that the mutation rate of normal cells is insufficient to account for the large number of mutations found in human cancers. Consequently, human tumors exhibit an elevated mutation rate that increases the likelihood of a tumor acquiring advantageous mutations. The hypothesis predicts that tumors are composed of cells harboring hundreds of thousands of mutations, as opposed to a small number of specific driver mutations, and that malignant cells within a tumor therefore constitute a highly heterogeneous population. As a result, drugs targeting specific mutated driver genes or even pathways of mutated driver genes will have only limited anticancer potential. In addition, because the tumor is composed of such a diverse cell population, tumor cells harboring drug-resistant mutations will exist prior to the administration of any chemotherapeutic agent. We present recent evidence in support of the mutator phenotype hypothesis, major arguments against this concept, and discuss the clinical consequences of tumor evolution fueled by an elevated mutation rate. We also consider the therapeutic possibility of altering the rate of mutation accumulation. Most significantly, we contend that there is a need to fundamentally reconsider current approaches to personalized cancer therapy. We propose that targeting cellular pathways that alter the rate of mutation accumulation in tumors will ultimately prove more effective than attempting to identify and target mutant driver genes or driver pathways.
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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 Socratic graph.