CDK4/6 inhibitors are central to the clinical management of HR+HER2− breast cancer. We have recently demonstrated that immunosuppressive, IL17-secreting γδ T cells recruited to the tumor microenvironment by a CCL2-dependent mechanism upon CDK4/6 inhibition can repolarize tumor-associated macrophages toward a CX3CR1+ phenotype associated with resistance to therapy.
An immunological mechanism of resistance to CDK4/6 inhibitors in HR+ breast cancer / Galassi, Claudia; Petroni, Giulia; Knott, Simon R.V.; Galluzzi, Lorenzo. - In: ONCOIMMUNOLOGY. - ISSN 2162-402X. - ELETTRONICO. - 14:(2025), pp. 2520269.0-2520269.0. [10.1080/2162402x.2025.2520269]
An immunological mechanism of resistance to CDK4/6 inhibitors in HR+ breast cancer
Petroni, Giulia;Galluzzi, Lorenzo
2025
Abstract
CDK4/6 inhibitors are central to the clinical management of HR+HER2− breast cancer. We have recently demonstrated that immunosuppressive, IL17-secreting γδ T cells recruited to the tumor microenvironment by a CCL2-dependent mechanism upon CDK4/6 inhibition can repolarize tumor-associated macrophages toward a CX3CR1+ phenotype associated with resistance to therapy.
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