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Related Experiment Video

Updated: May 31, 2026

Killer Artificial Antigen Presenting Cells (KaAPC) for Efficient In Vitro Depletion of Human Antigen-specific T Cells

Killer Artificial Antigen Presenting Cells (KaAPC) for Efficient In Vitro Depletion of Human Antigen-specific T Cells

Published on: August 11, 2014

When more target antigen expression is less.

Charles Dumontet¹

¹Université Claude Bernard Lyon 1, INSERM U-1052, CNRS 5286, Centre Léon Bérard, Hospices Civils de Lyon, Centre de Recherche en Cancérologie de Lyon, 69008 Lyon, France.

|May 28, 2026

Summary

This summary is machine-generated.

Resistance to antibody drug conjugates (ADCs) can arise from low target antigen expression. This study reveals that increased NECTIN4 expression paradoxically reduces NECTIN4-ADC internalization and increases extracellular release in resistant tumors.

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Area of Science:

Oncology
Molecular Biology
Drug Development

Background:

Antibody drug conjugates (ADCs) are crucial cancer therapeutics.
Resistance to ADCs is a significant clinical challenge.
Low target antigen expression is a known mechanism of ADC resistance.

Purpose of the Study:

To investigate the role of target antigen expression in ADC resistance.
To elucidate the mechanisms underlying resistance to NECTIN4-targeted ADCs.
To identify novel strategies for overcoming ADC resistance.

Main Methods:

Analysis of NECTIN4 expression in resistant tumor cell subpopulations.
Assessment of NECTIN4-ADC internalization and payload delivery.
Quantification of extracellular ADC release.

Main Results:

Increased NECTIN4 expression was observed in a resistant tumor cell subpopulation.
Higher NECTIN4 levels correlated with reduced NECTIN4-ADC internalization.
Enhanced extracellular release of NECTIN4-ADCs was detected in resistant cells.

Conclusions:

Contrary to expectations, elevated NECTIN4 expression can contribute to ADC resistance.
This resistance mechanism involves impaired ADC internalization and increased release.
Understanding this phenomenon is critical for optimizing ADC therapy.