ReviewCancer science2025
The Impact of Polyploid Giant Cancer Cells: The Root of Stress Resilience.
Review in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Inflamed Yet Immune-Evasive? A Transcriptomic Meta-Analysis Identifies Conserved Inflammatory, Developmental, and Neuronal Signatures Associated with Polyploid Giant Cancer Cells.International journal of molecular sciences · 2026Pooled it
- The Sleeping Giant: Metabolism and Autophagy in the Generation and Survival of Dormant Polyploid Giant Cancer Cells.MedComm · 2026Review
- Polyploidy: A macromutational force pushing bioeconomic developments.Proceedings of the National Academy of Sciences of the United States of America · 2026Review
- Polyploid cancer cells surviving cisplatin reallocate central carbon sources to fuel antioxidant metabolism for survival.Molecular metabolism · 2026Article
- Modelling the monstrosities: experimental and computational systems for studying polyploid giant cancer cells.Expert reviews in molecular medicine · 2025Review
- Chromosomal instability is associated with paradoxical cGAS upregulation and impaired STING signaling shaping the immune microenvironment in glioblastoma.Neuro-oncology advancesArticle
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
Abstract
Polyploid giant cancer cells (PGCCs) represent a unique and distinct subset of cancer cells, characterized by either an abnormally large nucleus or the presence of multiple nuclei within a single cell. An increasing body of evidence indicates that PGCCs are closely linked to cancer progression, therapeutic resistance, and poor clinical prognosis. However, despite their distinctive morphology, no universal marker has been identified to reliably distinguish PGCCs from other cancer cell populations. This is at least partly because PGCCs arise across various cancer types in diverse contexts, displaying considerable variability in their gene expression profiles. Nevertheless, they share key features, most notably polyploidy and remarkable stress resilience. The exceptional stress resilience of PGCCs arises from various mechanisms, including genome redundancy buffering against genetic damage, dormancy induction for survival in harsh conditions, gene expression changes enhancing hypoxia resistance, and metabolic adaptations supporting growth in resource-limited environments. Collectively, these properties make PGCCs highly resilient to stress, facilitating their persistence and contributing to the progression and aggressiveness of cancer. In this review, we provide a comprehensive discussion of the mechanisms underlying PGCC stress resilience and explore its broader implications for cancer pathogenesis. Understanding these adaptive strategies may offer new insights into cancer biology and reveal potential therapeutic targets to mitigate PGCC-driven malignancy.
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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.