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Related Experiment Video

Updated: Mar 16, 2026

Validated Immunochemical Assay for Comprehensive Determination of the Human Epidermal Growth Factor Receptor 2 Released from and Bound to Cells

Validated Immunochemical Assay for Comprehensive Determination of the Human Epidermal Growth Factor Receptor 2 Released from and Bound to Cells

Published on: May 9, 2025

HER2 expression identifies dynamic functional states within circulating breast cancer cells.

Nicole Vincent Jordan¹, Aditya Bardia^1,2, Ben S Wittner^1,2

¹Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, Massachusetts 02129, USA.

|August 25, 2016

Summary

Advanced breast cancer cells can develop HER2-positive traits, leading to drug resistance. Targeting both HER2 and Notch pathways shows promise in suppressing tumor growth.

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Building Up a High-throughput Screening Platform to Assess the Heterogeneity of HER2 Gene Amplification in Breast Cancers

Building Up a High-throughput Screening Platform to Assess the Heterogeneity of HER2 Gene Amplification in Breast Cancers

Published on: December 5, 2017

Area of Science:

Oncology
Molecular Biology
Genetics

Background:

Metastatic oestrogen-receptor (ER)-positive/human epidermal growth factor receptor 2 (HER2)-negative breast cancer can evolve resistance to therapy.
Acquired HER2 heterogeneity in circulating tumour cells (CTCs) during metastatic breast cancer progression is not well understood.

Purpose of the Study:

To investigate the emergence and characteristics of HER2 heterogeneity in CTCs from ER+/HER2- metastatic breast cancer patients.
To understand the interconversion dynamics and therapeutic vulnerabilities of distinct CTC subpopulations.

Main Methods:

Analysis of CTCs from 19 women with ER+/HER2- metastatic breast cancer.
In vitro culture of CTCs to study subpopulation dynamics.
Orthotopic patient-derived CTC tumor models for therapeutic testing.

Main Results:

84% of patients developed HER2-expressing CTCs, forming distinct HER2+ and HER2- subpopulations.
HER2+ CTCs were more proliferative, while HER2- CTCs showed resistance to chemotherapy but sensitivity to Notch inhibition.
CTCs spontaneously interconverted between HER2+ and HER2- phenotypes within four cell doublings.
Combined paclitaxel and Notch inhibition suppressed tumorigenesis in models.

Conclusions:

Distinct, interconverting HER2+ and HER2- phenotypes in CTCs contribute to breast cancer progression and drug resistance.
Targeting both HER2 signaling and Notch pathways offers a potential therapeutic strategy for advanced breast cancer.