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Metastasis02:30

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Related Experiment Video

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Saline Lavage for Sampling of the Canine Nasal Immune Microenvironment
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Subclonal cooperation drives metastasis by modulating local and systemic immune microenvironments.

Michalina Janiszewska1,2,3,4, Doris P Tabassum1,5, Zafira Castaño3,6

  • 1Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.

Nature Cell Biology
|July 3, 2019
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Summary

Minor breast cancer cell subclones expressing IL11 and FIGF (VEGFD) promote metastasis. These cells indirectly stimulate neutrophils, driving tumor progression and polyclonal metastases, highlighting non-cell-autonomous drivers in cancer spread.

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Area of Science:

  • Oncology
  • Cancer Biology
  • Immunology

Background:

  • Tumor heterogeneity is common in human cancers and linked to poor clinical outcomes.
  • The mechanisms driving metastatic progression in heterogeneous tumors are not fully understood.

Purpose of the Study:

  • To investigate the role of minor subclones in promoting breast cancer metastasis.
  • To elucidate the mechanisms by which cooperating subclones drive metastatic outgrowth.

Main Methods:

  • Expression profiling of epithelial and stromal cells from primary and metastatic lesions.
  • Single-cell RNA sequencing (scRNA-seq) of CD45+ immune cells.
  • In vivo experiments involving neutrophil depletion.

Main Results:

  • Minor breast cancer subclones expressing IL11 and FIGF (VEGFD) cooperate to promote metastasis.
  • This cooperation is indirect, mediated by microenvironmental interactions, particularly with neutrophils.
  • IL11 acts on mesenchymal stromal cells to induce pro-tumorigenic neutrophils, leading to polyclonal metastases.

Conclusions:

  • Minor subclones and non-cell-autonomous interactions are critical drivers of metastatic progression.
  • Targeting IL11-mediated pathways and neutrophils may offer therapeutic strategies against metastasis.