Co-targeting CDK2 and CDK4/6 overcomes resistance to aromatase and CDK4/6 inhibitors in ER+ breast cancer

Co-targeting CDK2 and CDK4/6 overcomes resistance to aromatase and CDK4/6 inhibitors in ER+ breast cancer

Resistance to aromatase inhibitor (AI) treatment and combined CDK4/6 inhibitor (CDK4/6i) and endocrine therapy (ET) are crucial clinical challenges in treating estrogen receptor-positive (ER+) breast cancer. Understanding the resistance mechanisms and identifying reliable predictive biomarkers and n...

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Published in:NPJ precision oncology Vol. 6; no. 1; p. 68
Main Authors: Al-Qasem, Abeer J., Alves, Carla L., Ehmsen, Sidse, Tuttolomondo, Martina, Terp, Mikkel G., Johansen, Lene E., Vever, Henriette, Hoeg, Luna V. A., Elias, Daniel, Bak, Martin, Ditzel, Henrik J.
Format: Journal Article
Language:English
Published: London Nature Publishing Group UK 24-09-2022
Nature Publishing Group
Nature Portfolio
Subjects:
631/67/1059/602
692/53/2423
Biomarkers
Breast cancer
Cancer Research
Cell cycle
Drug resistance
Gene Therapy
Human Genetics
Internal Medicine
Medicine
Medicine & Public Health
Oncology
Targeted cancer therapy
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Abstract Resistance to aromatase inhibitor (AI) treatment and combined CDK4/6 inhibitor (CDK4/6i) and endocrine therapy (ET) are crucial clinical challenges in treating estrogen receptor-positive (ER+) breast cancer. Understanding the resistance mechanisms and identifying reliable predictive biomarkers and novel treatment combinations to overcome resistance are urgently needed. Herein, we show that upregulation of CDK6, p-CDK2, and/or cyclin E1 is associated with adaptation and resistance to AI-monotherapy and combined CDK4/6i and ET in ER+ advanced breast cancer. Importantly, co-targeting CDK2 and CDK4/6 with ET synergistically impairs cellular growth, induces cell cycle arrest and apoptosis, and delays progression in AI-resistant and combined CDK4/6i and fulvestrant-resistant cell models and in an AI-resistant autocrine breast tumor in a postmenopausal xenograft model. Analysis of CDK6, p-CDK2, and/or cyclin E1 expression as a combined biomarker in metastatic lesions of ER+ advanced breast cancer patients treated with AI-monotherapy or combined CDK4/6i and ET revealed a correlation between high biomarker expression and shorter progression-free survival (PFS), and the biomarker combination was an independent prognostic factor in both patients cohorts. Our study supports the clinical development of therapeutic strategies co-targeting ER, CDK4/6 and CDK2 following progression on AI-monotherapy or combined CDK4/6i and ET to improve survival of patients exhibiting high tumor levels of CDK6, p-CDK2, and/or cyclin E1.
AbstractList Resistance to aromatase inhibitor (AI) treatment and combined CDK4/6 inhibitor (CDK4/6i) and endocrine therapy (ET) are crucial clinical challenges in treating estrogen receptor-positive (ER+) breast cancer. Understanding the resistance mechanisms and identifying reliable predictive biomarkers and novel treatment combinations to overcome resistance are urgently needed. Herein, we show that upregulation of CDK6, p-CDK2, and/or cyclin E1 is associated with adaptation and resistance to AI-monotherapy and combined CDK4/6i and ET in ER+ advanced breast cancer. Importantly, co-targeting CDK2 and CDK4/6 with ET synergistically impairs cellular growth, induces cell cycle arrest and apoptosis, and delays progression in AI-resistant and combined CDK4/6i and fulvestrant-resistant cell models and in an AI-resistant autocrine breast tumor in a postmenopausal xenograft model. Analysis of CDK6, p-CDK2, and/or cyclin E1 expression as a combined biomarker in metastatic lesions of ER+ advanced breast cancer patients treated with AI-monotherapy or combined CDK4/6i and ET revealed a correlation between high biomarker expression and shorter progression-free survival (PFS), and the biomarker combination was an independent prognostic factor in both patients cohorts. Our study supports the clinical development of therapeutic strategies co-targeting ER, CDK4/6 and CDK2 following progression on AI-monotherapy or combined CDK4/6i and ET to improve survival of patients exhibiting high tumor levels of CDK6, p-CDK2, and/or cyclin E1.
Abstract Resistance to aromatase inhibitor (AI) treatment and combined CDK4/6 inhibitor (CDK4/6i) and endocrine therapy (ET) are crucial clinical challenges in treating estrogen receptor-positive (ER+) breast cancer. Understanding the resistance mechanisms and identifying reliable predictive biomarkers and novel treatment combinations to overcome resistance are urgently needed. Herein, we show that upregulation of CDK6, p-CDK2, and/or cyclin E1 is associated with adaptation and resistance to AI-monotherapy and combined CDK4/6i and ET in ER+ advanced breast cancer. Importantly, co-targeting CDK2 and CDK4/6 with ET synergistically impairs cellular growth, induces cell cycle arrest and apoptosis, and delays progression in AI-resistant and combined CDK4/6i and fulvestrant-resistant cell models and in an AI-resistant autocrine breast tumor in a postmenopausal xenograft model. Analysis of CDK6, p-CDK2, and/or cyclin E1 expression as a combined biomarker in metastatic lesions of ER+ advanced breast cancer patients treated with AI-monotherapy or combined CDK4/6i and ET revealed a correlation between high biomarker expression and shorter progression-free survival (PFS), and the biomarker combination was an independent prognostic factor in both patients cohorts. Our study supports the clinical development of therapeutic strategies co-targeting ER, CDK4/6 and CDK2 following progression on AI-monotherapy or combined CDK4/6i and ET to improve survival of patients exhibiting high tumor levels of CDK6, p-CDK2, and/or cyclin E1.
ArticleNumber 68
Author Hoeg, Luna V. A.
Ehmsen, Sidse
Terp, Mikkel G.
Elias, Daniel
Alves, Carla L.
Johansen, Lene E.
Al-Qasem, Abeer J.
Vever, Henriette
Bak, Martin
Tuttolomondo, Martina
Ditzel, Henrik J.
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  organization: Department of Cancer and Inflammation Research, Institute of Molecular Medicine, University of Southern Denmark
– sequence: 2
  givenname: Carla L.
  surname: Alves
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  organization: Department of Cancer and Inflammation Research, Institute of Molecular Medicine, University of Southern Denmark
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  organization: Department of Oncology, Odense University Hospital, Institute of Clinical Research, University of Southern Denmark
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  surname: Tuttolomondo
  fullname: Tuttolomondo, Martina
  organization: Department of Cancer and Inflammation Research, Institute of Molecular Medicine, University of Southern Denmark
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  fullname: Terp, Mikkel G.
  organization: Department of Cancer and Inflammation Research, Institute of Molecular Medicine, University of Southern Denmark
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  surname: Johansen
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  organization: Department of Cancer and Inflammation Research, Institute of Molecular Medicine, University of Southern Denmark
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  givenname: Luna V. A.
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  fullname: Hoeg, Luna V. A.
  organization: Department of Cancer and Inflammation Research, Institute of Molecular Medicine, University of Southern Denmark
– sequence: 9
  givenname: Daniel
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  organization: Department of Pathology, Sydvestjysk Sygehus
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  givenname: Henrik J.
  orcidid: 0000-0003-3927-5135
  surname: Ditzel
  fullname: Ditzel, Henrik J.
  email: hditzel@health.sdu.dk
  organization: Department of Cancer and Inflammation Research, Institute of Molecular Medicine, University of Southern Denmark, Department of Oncology, Odense University Hospital, Institute of Clinical Research, University of Southern Denmark, Academy of Geriatric Cancer Research (AgeCare), Odense University Hospital
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Snippet Resistance to aromatase inhibitor (AI) treatment and combined CDK4/6 inhibitor (CDK4/6i) and endocrine therapy (ET) are crucial clinical challenges in treating...
Abstract Resistance to aromatase inhibitor (AI) treatment and combined CDK4/6 inhibitor (CDK4/6i) and endocrine therapy (ET) are crucial clinical challenges in...
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SubjectTerms 631/67/1059/602
692/53/2423
Biomarkers
Breast cancer
Cancer Research
Cell cycle
Drug resistance
Gene Therapy
Human Genetics
Internal Medicine
Medicine
Medicine & Public Health
Oncology
Targeted cancer therapy
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Title Co-targeting CDK2 and CDK4/6 overcomes resistance to aromatase and CDK4/6 inhibitors in ER+ breast cancer
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