Evidence map›Paper›PMID 40181035›Full record

ArticleScientific reports2025

The depth of tumor hierarchy and its impact on hypertumor susceptibility.

Jibeom Choi, Suhyeon Kim, Sunmi Lee, Junpyo Park

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Fraternal cooperation of hierarchical cancer parallels metazoan multicellularity and eusociality.Biological reviews of the Cambridge Philosophical Society · 2026
    Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Jibeom ChoiDepartment of Applied Mathematics, College of Applied Sciences, Kyung Hee University, Yongin, 17104, Republic of Korea. snu10@snu.ac.kr.
Suhyeon KimDepartment of Applied Mathematics, College of Applied Sciences, Kyung Hee University, Yongin, 17104, Republic of Korea.
Sunmi LeeDepartment of Applied Mathematics, College of Applied Sciences, Kyung Hee University, Yongin, 17104, Republic of Korea.
Junpyo ParkDepartment of Applied Mathematics, College of Applied Sciences, Kyung Hee University, Yongin, 17104, Republic of Korea. junpyopark@khu.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells, despite their shared origin, could be heterogeneous with respect to their stemness, plasticity, self-renewal, and oncogenicity. Recent findings indicate that a small proportion of the cancer cells oligopolize the capacity to produce diverse cancer subtypes and metastasize to other sites. Analogous to the apical hierarchy observed in adult stem cells, such versatile cancer cells were termed cancer stem cells. Meanwhile, hypertumors that exploit the cooperation of other cancer cells may disrupt the integrity of the tumor, prompting tumor regression. The biology of cancer stem cells and hypertumors has substantial clinical potential, but no study up to date has investigated the effect of cancer hierarchy on hypertumor progression. In this study, we developed biologically relevant models that elucidate the dynamics of hypertumor progression under different hierarchical structures. Our models align with previously observed data from human breast cancer subpopulations capable of state transitions. We tested and compared the progression dynamics of cancer clusters with different characteristics. Considering the trade-off between proliferation and mutation risk, our computational results suggest that existence of the cancer stem cells with high self-renewal and replication could be the prerequisite for attaining larger cancer size. In contrast, if a small cancer size is sufficient to induce lethality, a tumor composed of homogeneous cells would take less time to reach such a threshold size. Consequently, the hierarchical structure of cancer that reaches a lethal size may vary across species, representing a relevant mechanism of Peto's paradox. The formulations presented in this study link the less attended aspects of cancer which would provide integrative insights for therapeutic strategies.

Indexed as

Breast NeoplasmsNeoplasmsNeoplastic Stem CellsCell ProliferationDisease ProgressionDisease SusceptibilityFemaleHumansModels, BiologicalMutation

Identifiers

PMID40181035
PMCPMC11968861

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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.