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Establishment of Cancer Stem Cell Cultures from Human Conventional Osteosarcoma
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How cancer arises: Genetics releases, plasticity creates, genetics stabilizes.

Steven A Frank1

  • 1Department of Ecology and Evolutionary Biology, University of California, Irvine, CA 92697-2525.

Proceedings of the National Academy of Sciences of the United States of America
|July 31, 2025
PubMed
Summary

Cancer arises when genetic mutations unleash developmental plasticity, enabling cells to form novel tissues. Subsequent genetic changes then stabilize these cancer traits, creating complex tumors.

Keywords:
cancer evolutioncell statedevelopmental plasticitysingle-cell technology

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Area of Science:

  • Oncology
  • Developmental Biology
  • Genetics

Background:

  • Cancer is characterized by novel tissue formation, resource acquisition, immune evasion, and uncontrolled growth.
  • Tumorigenesis is traditionally linked to (epi)genetic mutations (e.g., KRAS, TP53) and hijacking developmental plasticity.
  • Reconciling genetic drivers with the complex tissue-level changes in cancer remains a challenge.

Purpose of the Study:

  • To propose a new model for cancer origin and progression.
  • To explain how genetic mutations and developmental plasticity interact in carcinogenesis.
  • To re-evaluate the primary roles of key cancer genes like KRAS and TP53.

Main Methods:

  • This is a perspective piece, not an experimental study.
  • It synthesizes existing evidence from cancer genetics and developmental biology.
  • It proposes a conceptual framework for understanding cancer as a developmental process.

Main Results:

  • A new model posits that (epi)genetic mutations initially release developmental plasticity.
  • This released plasticity drives the creation of novel cellular interactions and complex tumor tissues.
  • Subsequent genetic events are necessary to stabilize these acquired traits and ensure heritability.

Conclusions:

  • Cancer origin involves a dynamic interplay between genetic alterations and developmental plasticity.
  • Key mutations (e.g., KRAS, TP53) may function primarily as releasers of plasticity in early cancer.
  • The model suggests genetics initiates, plasticity creates, and genetics stabilizes cancerous phenotypes.