ArticleHistochemistry and cell biology2016
Disentangling the aneuploidy and senescence paradoxes: a study of triploid breast cancers non-responsive to neoadjuvant therapy.
Article in Histochemistry and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers, 2 of them syntheses that pooled it.
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Who cites it
31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 50 citations in OpenAlex.
- Pooled it
- DNA aneuploidy and breast cancer: a meta-analysis of 141,163 cases.Oncotarget · 2016Pooled it
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- Unscheduled polyploidy synergizes with oncogenic mutations to enhance genome instability and tumorigenesis.Cancer letters · 2025Article
- Article
- High-Throughput Empirical and Virtual Screening To Discover Novel Inhibitors of Polyploid Giant Cancer Cells in Breast Cancer.Analytical chemistry · 2025Article
- Establishment and genomic profiling of cholangiocarcinoma cells with functional characterization.Scientific reports · 2025Article
- High-Throughput Empirical and Virtual Screening to Discover Novel Inhibitors of Polyploid Giant Cancer Cells in Breast Cancer.bioRxiv : the preprint server for biology · 2024Article
- Single-cell morphological and transcriptome analysis unveil inhibitors of polyploid giant breast cancer cells in vitro.Communications biology · 2023Article
- Metronomic and single high-dose paclitaxel treatments produce distinct heterogenous chemoresistant cancer cell populations.Scientific reports · 2023Article
- Intratumor Heterogeneity and Treatment Resistance of Solid Tumors with a Focus on Polyploid/Senescent Giant Cancer Cells (PGCCs).International journal of molecular sciences · 2023Review
- Review
- Presence of cells in the polyaneuploid cancer cell (PACC) state predicts the risk of recurrence in prostate cancer.The Prostate · 2023Article
- The Transcriptome and Proteome Networks of Malignant Tumours Reveal Atavistic Attractors of Polyploidy-Related Asexual Reproduction.International journal of molecular sciences · 2022Article
- High Hemin Concentration Induces Escape from Senescence of Normoxic and Hypoxic Colon Cancer Cells.Cancers · 2022Article
- Polyploidy as an Adaptation against Loss of Heterozygosity in Cancer.International journal of molecular sciences · 2022Article
- Revisiting Epithelial Carcinogenesis.International journal of molecular sciences · 2022Article
- Polyploid giant cancer cell characterization: New frontiers in predicting response to chemotherapy in breast cancer.Seminars in cancer biology · 2022Review
- Review
- The integrative bioinformatic analysis deciphers the predicted molecular target gene and pathway from curcumin derivative CCA-1.1 against triple-negative breast cancer (TNBC).Journal of the Egyptian National Cancer Institute · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aneuploid cells should have a reduced proliferation rate due to difficulty in proceeding through mitosis. However, contrary to this, high aneuploidy is associated with aggressive tumour growth and poor survival prognosis, in particular in triploid breast cancer. A further paradox revolves around the observation that, while cell senescence should inhibit proliferation, the senescence marker p16INK4a correlates with poor treatment outcome in patients with a very aggressive triple-negative breast carcinoma (TNBC). In this study, we aim to pour light on the possible relationship of these conundrums with polyploidy of tumour cells. We performed detailed analysis of DNA histogram profiles in diagnostic core biopsies of 30 cases of operable breast cancer and found that near triploidy in TNBC and other forms correlated with weak or no response to neoadjuvant chemotherapy (NAC) as scored by Miller-Payne index. Polyploid cells in operation samples from tumours that were non-responsive to NAC treatment were Ki67 and CD44 positive. In addition, polyploid cells were positive for markers of embryonic stemness (OCT4, SOX2, NANOG) and senescence (p16INK4a). The relationship patterns between p16INK4a and NANOG were heterogeneous, with predominantly mutually exclusive expression but also synergistic and intermediate variants in the same samples. We conclude that the aneuploidy and senescence paradoxes can be explained by the mutual platform of polyploidy, conferring genomic and epigenetic instability as a survival advantage. Such cells are able to bypass aneuploidy restrictions of conventional mitosis and overcome the barrier of senescence by a shift to self-renewal, resulting in progression of cancer.
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Registered trials
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