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Transcriptomic Hallmarks of Tumor Plasticity and Stromal Interactions in Brain Metastasis

Emily Wingrove1, Zongzhi Z Liu1, Kiran D Patel1

  • 1Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.

Cell Reports
|April 25, 2019
PubMed

Insights

This study deciphers brain metastasis mechanisms by analyzing gene expression in the brain tumor microenvironment (TME). It reveals how cancer cells adapt and the brain responds, identifying key molecular hallmarks.

Area of Science:

  • Oncology
  • Neuroscience
  • Molecular Biology

Background:

  • Brain metastasis is a frequent cause of cancer relapse.
  • The brain tumor microenvironment (TME) complexity hinders understanding of metastasis mechanisms.

Purpose of the Study:

  • To define the molecular landscape of brain metastasis in vivo.
  • To investigate tumor cell adaptation and the brain's neuroinflammatory response within the TME.

Main Methods:

  • Utilized RNA-sequencing on xenografts to analyze transcriptomes.
  • Differentiated tumor cell and stromal gene expression with high sensitivity and accuracy.

Main Results:

  • Identified shifts in epithelial and neuronal-like lineage programs in malignant cells adapting to the brain TME.
  • Revealed a reciprocal neuroinflammatory response from the brain stroma.
  • Discovered transcriptional hallmarks of metastasis specific to brain regions, tumor types, and confirmed in patient biopsies.

Conclusions:

  • The study provides a molecular resource for understanding TME co-adaptation in brain metastasis.
  • Findings offer insights into regional and cross-tumor type similarities in metastatic adaptation.
Keywords:
brain metastasislineage plasticityneuroinflammationtranscriptomic analysis in vivo

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