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Stochastic phenotypic interconversion in tumors can generate heterogeneity.

Giuseppina Simone1,2

  • 1Mechanical Engineering, Microsystem, Northwestern Polytechnical University, 127 West Youyi Road, Xi'an Shaanxi, 710072, People's Republic of China. giuseppina.simone@nwpu.edu.cn.

European Biophysics Journal : EBJ
|December 13, 2016
PubMed
Summary

Tumor cells exhibit phenotype variations, impacting cancer. A microfluidic assay and Markov model reveal phenotype interconversion, suggesting targeting circulating tumor cells is ineffective for preventing recurrence.

Keywords:
GalectinHeterogeneityPhenotypeStochastic Markov modelTumor

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Area of Science:

  • Oncology
  • Systems Biology
  • Biophysics

Background:

  • Phenotype variations contribute to tumor heterogeneity, a key factor in cancer progression.
  • Understanding cell subpopulation dynamics is crucial for developing effective cancer therapies.

Purpose of the Study:

  • To investigate phenotype interconversion in colon cancer cells using a microfluidic assay and Markov modeling.
  • To explore the implications of cell phenotype plasticity on tumor heterogeneity and metastasis.

Main Methods:

  • Analysis and sorting of colon cancer cells from patient blood using a galactose-active moiety-based microfluidic assay.
  • In vitro culturing of sorted cells in severe combined immunodeficiency (SCID) mice.
  • Development and application of a Markov theory-based model to explain observed phenotype equilibria.

Main Results:

  • Experimental evidence confirmed phenotype interconversion between cell subpopulations.
  • The Markov model successfully explained the equilibrium dynamics of cell phenotypes.
  • Phenotype plasticity was demonstrated to generate metastatic cells.

Conclusions:

  • Targeting circulating tumor cells (CTCs) may not be an effective strategy for preventing tumor recurrence due to phenotype interconversion.
  • Understanding cell phenotype transitions is vital for advancing the comprehension of tumor generation, growth, and metastasis.