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Review
. 2023 Jun 28;9(1):56.
doi: 10.1038/s41523-023-00560-z.

Incorporating clinicopathological and molecular risk prediction tools to improve outcomes in early HR+/HER2- breast cancer

Affiliations
Review

Incorporating clinicopathological and molecular risk prediction tools to improve outcomes in early HR+/HER2- breast cancer

Giuseppe Curigliano et al. NPJ Breast Cancer. .

Abstract

Stratification of recurrence risk is a cornerstone of early breast cancer diagnosis that informs a patient's optimal treatment pathway. Several tools exist that combine clinicopathological and molecular information, including multigene assays, which can estimate risk of recurrence and quantify the potential benefit of different adjuvant treatment modalities. While the tools endorsed by treatment guidelines are supported by level I and II evidence and provide similar prognostic accuracy at the population level, they can yield discordant risk prediction at the individual patient level. This review examines the evidence for these tools in clinical practice and offers a perspective of potential future risk stratification strategies. Experience from clinical trials with cyclin D kinase 4/6 (CDK4/6) inhibitors in the setting of hormone receptor-positive (HR+)/human epidermal growth factor receptor 2-negative (HER2-) early breast cancer is provided as an illustrative example of risk stratification.

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Conflict of interest statement

G.C. declares no Competing Non-Financial Interests but the following Competing Financial Interests: The author has received institutional financial support and served as an advisor for clinical trials from Bristol-Myers Squibb, Roche, Novartis, Eli Lilly, Pfizer, Daiichi Sankyo, Celcuity, Veracyte, Seagen, AstraZeneca, and Ellipses Pharma. R.D. declares no Competing Non-Financial Interests but the following Competing Financial Interests: The author has served as an advisory consultant for AstraZeneca, Eisai, Merck Sharp & Dohme, Novartis, Pfizer, and Roche; has received fees for expenses from Eisai, Merck Sharp & Dohme, Pfizer, and Roche. A.L-C. declares no Competing Non-Financial Interests but the following Competing Financial Interests: The author has patents and intellectual property with MEDSIR and owns stock in MEDSIR; has served in a leadership role for Eisai, Celgene-BMS, Eli Lilly, Pfizer, Roche, Novartis, Merck Sharp & Dohme, and TESARO-GSK; has been a consultant/advisory board member for Eli Lilly, Roche, Pfizer, Novartis, Pierre Fabre, Genomic Health, and TESARO-GSK; has received speakers bureau honoraria from Eli Lilly, AstraZeneca, Merck Sharp & Dohme, Pfizer, and Roche; has received institutional research funding from Roche, Foundation Medicine, Pierre Fabre, and Agendia; has received fees for expenses, travel, and accommodations (paid or reimbursed) by Roche, Eli Lilly, Novartis, Pfizer, and AstraZeneca. M.P. declares no Competing Non-Financial Interests but the following Competing Financial Interests: The author has received consultation fees from Roche/Genentech, Pfizer, Seagen, and Eli Lilly. L.P. declares no Competing Non-Financial Interests but the following Competing Financial Interests: The author has received consultation fees and honoraria from Seagen, Pfizer, AstraZeneca, Merck, Novartis, Bristol-Myers Squibb, Genentech, Eisai, Pieris Pharmaceuticals, Immunomedics, Clovis Oncology, Syndax, H3 Biomedicine, Radius Health, Personalis, Daiichi Sankyo, Natera; has received institutional research funding from Seagen, AstraZeneca, Merck, Pfizer, and Bristol-Myers Squibb. N.T. declares no Competing Non-Financial Interests but the following Competing Financial Interests: The author has received advisory board honoraria from AstraZeneca, Bristol-Myers Squibb, Eli Lilly, Merck Sharp & Dohme, Novartis, Pfizer, Roche/Genentech, GlaxoSmithKline, Zentalis Pharmaceuticals, Repare Therapeutics, Arvinas; has received research funding from AstraZeneca, BioRad, Pfizer, Roche/Genentech, Merck Sharp & Dohme, Guardant Health, Invitae, Inivata, Personalis, and Natera. G.V. declares no Competing Non-Financial Interests but the following Competing Financial Interests: The author has received consultation fees from Dako/Agilent, Roche, MSD Oncology, AstraZeneca, Daiichi Sankyo, Pfizer, and Eli Lilly.

Figures

Fig. 1
Fig. 1. Impact of Ki-67 expression on iDFS following CDK4/6 inhibition.
Two-sided analysis. Error bars are representative of 95% CI. CDK4/6 Cyclin D kinase 4/6, HR Hazard ratio, iDFS Invasive disease-free survival.

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