p16INK4A-deficiency predicts response to combined HER2 and CDK4/6 inhibition in HER2+ breast cancer brain metastases

Jing Ni, Sheheryar Kabraji, Shaozhen Xie, Yanzhi Wang, Peichen Pan, Xiaofang He, Zongming Liu, Jose Palbo Leone, Henry W. Long, Myles A. Brown, Eric P. Winer, Deborah A. R. Dillon, Nancy U. Lin and Jean J. Zhao ()
Additional contact information
Jing Ni: Dana-Farber Cancer Institute
Sheheryar Kabraji: Dana-Farber Cancer Institute
Shaozhen Xie: Dana-Farber Cancer Institute
Yanzhi Wang: Dana-Farber Cancer Institute
Peichen Pan: Dana-Farber Cancer Institute
Xiaofang He: Dana-Farber Cancer Institute
Zongming Liu: Dana-Farber Cancer Institute
Jose Palbo Leone: Dana-Farber Cancer Institute
Henry W. Long: Dana-Farber Cancer Institute
Myles A. Brown: Dana-Farber Cancer Institute
Eric P. Winer: Dana-Farber Cancer Institute
Deborah A. R. Dillon: Brigham and Women’s Hospital
Nancy U. Lin: Dana-Farber Cancer Institute
Jean J. Zhao: Dana-Farber Cancer Institute

Nature Communications, 2022, vol. 13, issue 1, 1-8

Abstract: Abstract Approximately 50% of patients with metastatic HER2-positive (HER2+) breast cancer develop brain metastases (BCBMs). We report that the tumor suppressor p16INK4A is deficient in the majority of HER2+ BCBMs. p16INK4A-deficiency as measured by protein immunohistochemistry predicted response to combined tucatinib and abemaciclib in orthotopic patient-derived xenografts (PDXs) of HER2 + BCBMs. Our findings establish the rationale for a biomarker-driven clinical trial of combined CDK4/6- and HER2-targeted agents for patients with HER2 + BCBM.

Date: 2022
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DOI: 10.1038/s41467-022-29081-2

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