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Generating and Imaging Mouse and Human Epithelial Organoids from Normal and Tumor Mammary Tissue Without Passaging
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Linking changes in epithelial morphogenesis to cancer mutations using computational modeling.

Katarzyna A Rejniak1, Shizhen E Wang, Nicole S Bryce

  • 1Integrated Mathematical Oncology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, Florida, United States of America. Kasia.Rejniak@moffitt.org

Plos Computational Biology
|September 25, 2010
PubMed
Summary
This summary is machine-generated.

This study uses the IBCell computational model to link cancer cell morphology changes to underlying molecular defects. It reveals how mutations in mammary cells affect their structure and behavior, aiding in understanding tumor progression.

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Area of Science:

  • Biophysics
  • Cell Biology
  • Computational Biology

Background:

  • Tumorigenesis often involves epithelial architecture disruption, with increased proliferation and loss of cell polarization being key phenotypic changes.
  • Three-dimensional (3D) cultures of tumor cells exhibit aberrant morphologies compared to normal epithelial acini.
  • Understanding the link between molecular alterations and morphological changes is crucial for cancer research.

Purpose of the Study:

  • To apply the bio-mechanical IBCell model to quantitatively analyze phenotypic changes in mammary epithelial cells.
  • To investigate how modifications in cell proliferation, apoptosis, and cell-ECM adhesion influence epithelial morphogenesis.
  • To establish a computational/experimental platform for linking histopathology to molecular defects in neoplastic lesions.

Main Methods:

  • Quantitative matching of the IBCell model to experimental data from MCF10A cells.
  • High-throughput simulation to assess the impact of parameter variations on simulated architecture.
  • Mapping experimental morphologies of oncogenic mutant cell lines onto the IBCell model parameter space.

Main Results:

  • Identified specific changes in cellular processes (proliferation, apoptosis, ECM adhesion) underlying structural modifications in mutant cell lines.
  • Quantitatively assessed alterations in cell doubling time, apoptotic rate, and ECM sensitivity for HER2-YVMA mutant MCF10A cells.
  • Demonstrated the ability to link in vitro mutant morphologies to in silico models, bridging morphological and molecular scales.

Conclusions:

  • The IBCell model, combined with 3D acini cultures, provides a powerful platform for studying cancer cell morphogenesis.
  • This approach facilitates the correlation of observed histopathological features with underlying molecular defects.
  • The study offers a novel method for understanding the biophysical basis of tumor development and progression.