Abstract
Purpose
Cyclin-dependent kinase 4/6 inhibitors (CDK4/6i) have improved patient survival in hormone receptor-positive/human epidermal growth factor receptor 2-negative (HR+/HER2−) metastatic breast cancer (mBC) in clinical trials and real-world studies. However, investigations of survival gains in broader HR+/HER2− mBC populations using epidemiological approaches are limited.
Methods
This retrospective study used SEER registry data to assess breast cancer-specific survival (BCSS) in patients diagnosed with HR+/HER2− de novo mBC from 2010 to 2019. Kaplan–Meier and Cox proportional hazards models were used to compare BCSS in patients diagnosed before (2010‒2013 with follow-up to 2014) and after (2015‒2018 with follow-up to 2019) the 2015 guideline recommendations for CDK4/6i use. A comparison was made to patients with HR+/HER2-positive (HER2+) de novo mBC, for which no major guideline changes occurred during 2015–2018.
Results
Data from 11,467 women with HR+/HER2− mBC and 3260 women with HR+/HER2+ mBC were included. After baseline characteristic adjustment, patients with HR+/HER2− mBC diagnosed post-2015 (n = 6163), had an approximately 10% reduction in risk of BC-specific death compared with patients diagnosed pre-2015 (n = 5304; HR = 0.895, p < 0.0001). Conversely, no significant change was observed in HR+/HER2+ BCSS post-2015 (n = 1798) versus pre-2015 (n = 1462). Similar results were found in patients aged ≥ 65 years.
Conclusion
Using one of the largest US population-based longitudinal cancer databases, significant improvements in BCSS were noted in patients with HR+/HER2− mBC post-2015 versus pre-2015, potentially due to the introduction of CDK4/6i post-2015. No significant improvement in BCSS was observed in patients with HR+/HER2+ mBC post-2015 versus pre-2015, likely due to the availability of HER2-directed therapies in both time periods.
Data availability
The data that support the findings of this study are available from the National Cancer Institute and can be accessed with permission under a data use agreement.
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Funding
This work was supported by Pfizer Inc. Medical writing support was provided by Kevin Woolfrey, PhD, of Oxford PharmaGenesis Inc., (Newtown, PA, USA) and was funded by Pfizer Inc.
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AB reports consultancy fees from AstraZeneca, Pfizer, Novartis, Lilly, Genentech/Roche, Seagen, Daiichi-Sankyo, Merck, Agendia, Sanofi, and Puma, and provides research support to Agendia and AstraZeneca MLK reports ongoing collaboration on a Pfizer-funded study. SS, RS, AC, DM are employees and stockholders of Pfizer Inc. SK and RKG are full-time employees of RTI Health Solutions, an independent nonprofit research organization, which was a paid consultant to Pfizer in connection with the development of this manuscript. Their compensation is unconnected to the studies on which they work.
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