ReviewTrends in genetics : TIG2023
Whole-genome doubling in tissues and tumors.
Review in Trends in genetics : TIG, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 34 citations in OpenAlex.
- Heterogeneity in cancer: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Tetraploids or polyploid giants: who is truly dangerous?Trends in cell biology · 2026Review
- Article
- Growth under pressure: The pros and cons of polyploidy induced by stress.Proceedings of the National Academy of Sciences of the United States of America · 2026Review
- Profiling cell proliferation after whole-genome duplication in human cells.Biology open · 2026Article
- Spontaneous whole genome duplication renders mouse embryonic fibroblasts resistant to reprogramming.Cell & bioscience · 2026Article
- From stress to strength: mechanotransducing poly(aneu)ploidy into a community-level advantage in cancer.Cancer metastasis reviews · 2026Review
- The forbidden doubling: exploring rare spermatocyte polyploidy in mammals.Comparative cytogenetics · 2026Article
- Cell Fusion-Mediated Induction of Polyploidy, Aneuploidy, and Genomic Instability in Cancer Cells.Advances in experimental medicine and biology · 2026Review
- Genome doubling as a dynamic driver of ovarian cancer evolution: insights from single-cell sequencing.Journal of ovarian research · 2025Review
- In silico and in vitro evaluation of drug-like properties and anticancer potential of novel 5-fluorouracil derivatives.Scientific reports · 2025Article
- Energetics of whole genome doubling and genomic instability.Cancer letters · 2025Review
- The dual role of whole-genome duplication: biological mechanisms, functional consequences, and detection advances.Acta biochimica et biophysica Sinica · 2025Review
- Article
- Chromosomal Instability and Chromoanagenesis as Forces for Genomic Evolution.Methods in molecular biology (Clifton, N.J.) · 2025Review
- The Dystrophin-Dystroglycan complex ensures cytokinesis efficiency in Drosophila epithelia.EMBO reports · 2025Article
- Integrating the Study of Polyploidy Across Organisms, Tissues, and Disease.Annual review of genetics · 2024Review
- Polyploidy mitigates the impact of DNA damage while simultaneously bearing its burden.Cell death discovery · 2024Article
- Review
- Cell-cell fusion in cancer: The next cancer hallmark?The international journal of biochemistry & cell biology · 2024Review
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 3 institutions in 1 country.
Funding
Abstract
The overwhelming majority of proliferating somatic human cells are diploid, and this genomic state is typically maintained across successive cell divisions. However, failures in cell division can induce a whole-genome doubling (WGD) event, in which diploid cells transition to a tetraploid state. While some WGDs are developmentally programmed to produce nonproliferative tetraploid cells with specific cellular functions, unscheduled WGDs can be catastrophic: erroneously arising tetraploid cells are ill-equipped to cope with their doubled cellular and chromosomal content and quickly become genomically unstable and tumorigenic. Deciphering the genetics that underlie the genesis, physiology, and evolution of whole-genome doubled (WGD
Indexed as
Identifiers
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.