CD16+ Fibroblasts Foster a Trastuzumab-Refractory Microenvironment that Is Reversed by VAV2 Inhibition

An abundance of CD16+ fibroblasts in HER2+ breast cancer patients was associated with poor prognosis and response to trastuzumab. Functionally, upon trastuzumab stimulation, CD16+ fibroblasts reduced drug delivery by enhancing extracellular matrix stiffness.
[Cancer Cell]
AbstractGraphical Abstract

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