The Impact of Polyploid Giant Cancer Cells: The Root of Stress Resilience

Ogawa, Yuta; Fisher, Lydia; Matsumoto, Tomonori

Cancer Science, 2025

Number of Access:185（2026-05-25 01:17 Counts）

Identifier to cite or link to this item: https://hdl.handle.net/11094/102943

Link to primary information 

File Format Terms of use Size Views Date.Available Description information
CancerSci_70191 pdf None 1.86 MB 170 2025.10.31  
Creative Commons : Attribution - NonCommercial

Item Information

Output File Export EndNote Basic Export Mendeley

Title
The Impact of Polyploid Giant Cancer Cells: The Root of Stress Resilience
Creator
CreatorName
Ogawa, Yuta
CreatorName
Fisher, Lydia
NRID
1000040886610 1000040886610
ORCID
0000-0003-4483-2178 0000-0003-4483-2178
researchmap permalink
tomo_matsumoto tomo_matsumoto
Scopus Author ID
55628587431 55628587431
CreatorName
Matsumoto, Tomonori
Subject
adaptation
dormancy
genome redundancy
polyploid giant cancer cell
stress resilience
Description
Ogawa Y., Fisher L., Matsumoto T.. The Impact of Polyploid Giant Cancer Cells: The Root of Stress Resilience. Cancer Science (2025); https://doi.org/10.1111/cas.70191.
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.
Publisher
John Wiley and Sons Inc
Source Title
Cancer Science
Date of Issued
2025-09-08
Language
English
Handle URL
https://hdl.handle.net/11094/102943
PISSN
13479032
eISSN
13497006
Relation.isIdenticalTo
DOI (Publisher Version)
https://doi.org/10.1111/cas.70191
Access Rights
open access
CopyRight
This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
© 2025 The Author(s). Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
oaire:version
Version of Record
Category
学術雑誌論文 Journal Article