ArticleGenes2019
The Cancer Aneuploidy Paradox: In the Light of Evolution.
Article in Genes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 60 citations in OpenAlex.
- Repair and misrepair of telomeric DNA in dynamic interactions with PML nuclear bodies and lamin B1 in doxorubicin-treated cancer cells.Nucleus (Austin, Tex.) · 2026Article
- Tetraploids or polyploid giants: who is truly dangerous?Trends in cell biology · 2026Review
- Tracing Genetic Images Formed During Evolution.International journal of molecular sciences · 2026Article
- Distinct cMET inhibitors uncover pharmacological heterogeneity in SHH medulloblastoma cell lines.Discover oncology · 2026Article
- Transcriptomic response of marine dinoflagellate Prorocentrum cordatum to phosphorus deficiency.Scientific reports · 2025Article
- Aurora B inhibition induces hyper-polyploidy and loss of long-term proliferative potential in RB and p53 defective cells.Cell death & disease · 2025Article
- Diverse Genome Structures among Eukaryotes May Have Arisen in Response to Genetic Conflict.Genome biology and evolution · 2024Review
- Amitotic Cell Division, Malignancy, and Resistance to Anticancer Agents: A Tribute to Drs. Walen and Rajaraman.Cancers · 2024Article
- Morphological and Immunocytochemical Characterization of Paclitaxel-Induced Microcells in Sk-Mel-28 Melanoma Cells.Biomedicines · 2024Article
- Surviving the Storm: The Role of Poly- and Depolyploidization in Tissues and Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Drug-resilient Cancer Cell Phenotype Is Acquired via Polyploidization Associated with Early Stress Response Coupled to HIF2α Transcriptional Regulation.Cancer research communications · 2024Article
- Special Issue "Advances in Genome Regulation in Cancer".International journal of molecular sciences · 2023Article
- A mathematical investigation of polyaneuploid cancer cell memory and cross-resistance in state-structured cancer populations.Scientific reports · 2023Article
- Cisplatin-Resistant Ovarian Cancer Cells Reveal a Polyploid Phenotype with Remarkable Activation of Nuclear Processes.Advanced biomedical research · 2023Article
- The Transcriptome and Proteome Networks of Malignant Tumours Reveal Atavistic Attractors of Polyploidy-Related Asexual Reproduction.International journal of molecular sciences · 2022Article
- Polyploidy and Myc Proto-Oncogenes Promote Stress Adaptation via Epigenetic Plasticity and Gene Regulatory Network Rewiring.International journal of molecular sciences · 2022Review
- Polyploidy as an Adaptation against Loss of Heterozygosity in Cancer.International journal of molecular sciences · 2022Article
- The foundational framework of tumors: Gametogenesis, p53, and cancer.Seminars in cancer biology · 2022Review
- Life Entrapped in a Network of Atavistic Attractors: How to Find a Rescue.International journal of molecular sciences · 2022Review
- Polyploidy as a Fundamental Phenomenon in Evolution, Development, Adaptation and Diseases.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aneuploidy should compromise cellular proliferation but paradoxically favours tumour progression and poor prognosis. Here, we consider this paradox in terms of our most recent observations of chemo/radio-resistant cells undergoing reversible polyploidy. The latter perform the segregation of two parental groups of end-to-end linked dyads by pseudo-mitosis creating tetraploid cells through a dysfunctional spindle. This is followed by autokaryogamy and a homologous pairing preceding a bi-looped endo-prophase. The associated RAD51 and DMC1/γ-H2AX double-strand break repair foci are tandemly situated on the AURKB/REC8/kinetochore doublets along replicated chromosome loops, indicative of recombination events. MOS-associated REC8-positive peri-nucleolar centromere cluster organises a monopolar spindle. The process is completed by reduction divisions (bi-polar or by radial cytotomy including pedogamic exchanges) and by the release of secondary cells and/or the formation of an embryoid. Together this process preserves genomic integrity and chromosome pairing, while tolerating aneuploidy by by-passing the mitotic spindle checkpoint. Concurrently, it reduces the chromosome number and facilitates recombination that decreases the mutation load of aneuploidy and lethality in the chemo-resistant tumour cells. This cancer life-cycle has parallels both within the cycling polyploidy of the asexual life cycles of ancient unicellular protists and cleavage embryos of early multicellulars, supporting the atavistic theory of cancer.
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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.