Giants and monsters: Unexpected characters in the story of cancer recurrence
Open accessAbstract
Polyploid giant cancer cells (PGCC) constitute a dangerous subpopulation of cancer cells and are a driving force in cancer recurrence. These unique cells arise from diploid tumor cells in response to stress encountered in the tumor microenvironment or during cancer therapy. PGCC are greatly dedifferentiated, acquire pluripotency, and are able to replicate through a form of asymmetric division called neosis, which results in new populations that are themselves able to differentiate into new cell types or to re-establish tumors. Progeny tend to be more genetically unstable than the founding population due to the dysregulation required to transition through a PGCC state. Therefore, cancers that escape stressors through this mechanism tend to re-emerge with a more aggressive phenotype that is therapy resistant. This review focuses on the clinical significance of PGCC, the need for standardized nomenclature and molecular markers, as well as possible avenues to develop therapies aimed at PGCC and the process of neosis. The biology underlying the development of PGCC including cell cycle checkpoint dysregulation, stress responses, dedifferentiation, stemness and epithelial-mesenchymal transition is discussed.
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The results on the histological class pairs associated with pCR and RD are in line with previously published studies.
“These results are in line with previously published studies [58–66].”
From Digital image analysis and machine learning-assisted prediction of neoadjuvant chemotherapy response in triple-negative breast cancer (2024) · cites this paper as [65]
The Clinical significance of PGCC and neosis > Colorectal cancer section discusses tumor differentiation and changes after neoadjuvant chemoradiation, but does not compare histological class pairs associated with pathological complete response (pCR) and residual disease (RD). Searches for those terms and their expanded forms found no passage in our copy addressing the claimed agreement with previous studies. No page number was provided for the passages. (LLM, conf=0.73)
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Docetaxel plus Prednisone or Mitoxantrone plus Prednisone for Advanced Prostate Cancer
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Cited by
Sorted by citations
Fisher, T. B., Saini, G., Rekha, T. S., Krishnamurthy, J., Bhattarai, S., Callagy, G., Webber, M., Janssen, E. A. M., Kong, J., & Aneja, R. (2024) · Breast Cancer Research · doi:10.1186/s13058-023-01752-y · Cited by 42 · see citing works
- Authors
- White‐Gilbertson, S. J., & Voelkel‐Johnson, C.
- Affiliations
- Medical University of South Carolina (US)
- Corresponding author
- Christina Voelkel‐Johnson
- Venue
- Advances in Cancer Research
- Publisher
- Elsevier
- Published
- 2020
- Volume
- 148
- Pages
- 201-232
- ISSN
- 0065-230X (ISSN-L)
- PMC
- PMC7731118
- OpenAlex
- W3023373003
- Cited by
- 78
- References
- 1
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 18 · 2023: 15 · 2022: 8 · 2021: 19 · 2020: 5
- FWCI
- 22.61
- Type
- book chapter
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Advances in cancer research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (P01 CA203628)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- polyploid giant cancer cells, tumor recurrence, asymmetric cell division, dedifferentiation, pluripotency, treatment resistance, genomic instability, stress response, cancer stemness, epithelial-mesenchymal transition, molecular markers, nomenclature
- MeSH terms
- Animals, Humans, Neoplasm Recurrence, Local, Neoplasms, Polyploidy, Neoplastic Stem Cells, Epithelial-Mesenchymal Transition, Tumor Microenvironment, Cell Cycle Checkpoints
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