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Clonal Lineage Tracing Reveals Distinct Invasive Subpopulations in Triple-Negative Breast Cancer.

Carolina De Santiago¹, Andrea L Gardner¹, Patrik Parker¹

¹Department of Biomedical Engineering, The University of Texas at Austin, Austin, Texas, USA.

Tissue Engineering. Part C, Methods

|May 7, 2026

Summary

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Metastatic triple-negative breast cancer (TNBC) invasion is driven by specific, pre-existing clones with stable migratory programs. Tumor heterogeneity maintains invasion through compensatory clonal dynamics and replacement under selective pressure.

Area of Science:

Oncology
Cancer Biology
Genomics

Background:

Triple-negative breast cancer (TNBC) exhibits significant intratumoral heterogeneity.
The clonal and transcriptional drivers of TNBC metastatic dissemination are not well understood.
Existing experimental systems cannot simultaneously track clonal identity and transcriptional states of invasive cells.

Purpose of the Study:

To investigate the clonal and transcriptional programs underlying invasion in TNBC.
To develop and utilize an experimental system for simultaneous clonal and transcriptional profiling of invasive subpopulations.
To understand how tumor heterogeneity contributes to metastatic dissemination in TNBC.

Main Methods:

Application of a clonal lineage-tracing platform.

Keywords:

breast cancer cancer models invasive potential metastasis migration tumor heterogeneity

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Last Updated: May 8, 2026

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model

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Published on: March 20, 2020

Quantification of Breast Cancer Cell Invasiveness Using a Three-dimensional (3D) Model

Quantification of Breast Cancer Cell Invasiveness Using a Three-dimensional (3D) Model

Published on: June 11, 2014

Integration with single-cell RNA sequencing (scRNA-seq) for transcriptomic profiling.

Development of a TNBC model system to study invasion.

Main Results:

Invasion is driven by a subset of recurrent clones, suggesting pre-existing subpopulations primed for migration.
Two distinct, stable transcriptomic invasive cell states were identified.
Targeted suppression of dominant invasive programs led to compensatory invasion by alternative rare clones.

Conclusions:

Invasive potential in TNBC is linked to stable clonal programs.
Tumor heterogeneity sustains invasive capacity via clonal replacement and compensatory dynamics.
Clonally resolved single-cell profiling offers a framework for dissecting invasive heterogeneity and informs therapeutic strategies targeting clone-specific behaviors.