Author Correction: Breast-cancer-specific mortality in patients treated based on the 21-gene assay: a SEER population-based study

e13034 Background: Patients successfully treated for hormone receptor (HR)-positive early breast cancer remain at risk of recurrence and metastatic disease even after extended periods of disease-free years. Whether prolonged metastatic-free intervals ultimately confer a benefit to breast cancer-specific survival is not well understood. This study aimed to investigate metastatic-free intervals and risk of breast cancer-specific mortality among patients with HR-positive breast cancer after adjuvant therapy. Methods: We conducted a retrospective cohort study of women aged 18 years and older diagnosed with recurrent metastatic HR-positive breast cancer between 1990 and 2016 in the Surveillance, Epidemiology, and End Results registries. Patients with longitudinal information on primary stage I-III HR-positive breast cancer through the occurrence of metastatic disease and survival were included. Risks of breast cancer-specific mortality associated with metastatic-free intervals (defined as time from primary breast cancer diagnosis to metastasis) of ≥5 years compared to < 5 years were estimated. Fine and Gray competing risks regression models were used to calculate subdistribution hazard ratios (SHR) and 95% confidence intervals (CI). Results: Among 1,057 women with HR-positive breast cancer with a median age of 54 years at primary breast cancer diagnosis and 62 years at metastatic progression, 65% of women had a metastatic-free disease interval ≥5 years, whereas 35% had an interval of < 5 years. Overall, patients with metastatic-free intervals < 5 years had a five-year breast cancer-specific survival rate of 31% compared to 52% in women with intervals of ≥5 years. In multivariable analyses adjusted for age, race, diagnosis year, grade, treatment and sites of metastasis, patients with intervals of ≥5 years had decreased risk of breast cancer-specific mortality (SHR = 0.72, 95% CI 0.58-0.89, P = 0.002) compared to women with metastatic-free intervals of < 5 years. Conclusions: In this population-based study, rates of cancer-specific mortality among patients who experienced metastatic recurrence of HR-positive breast cancer were lower in women with metastatic-free intervals of 5 years or more. The results of this study may inform patient-clinician discussions surrounding prognosis and treatment selection among HR-positive patients.

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Beta Blockers and Breast Cancer Mortality: A Population- Based Study

Journal of Clinical Oncology ◽

10.1200/jco.2010.33.5422 ◽

2011 ◽

Vol 29 (19) ◽

pp. 2635-2644 ◽

Cited By ~ 305

Author(s):

Thomas I. Barron ◽

Roisin M. Connolly ◽

Linda Sharp ◽

Kathleen Bennett ◽

Kala Visvanathan

Keyword(s):

Breast Cancer ◽

Beta Blocker ◽

Breast Tumor ◽

Breast Cancer Mortality ◽

Population Based ◽

Cumulative Probability ◽

Adrenergic Signaling ◽

Breast Cancer Specific Mortality ◽

Specific Mortality ◽

Cancer Specific Mortality

Purpose Preclinical studies have demonstrated that antagonism of β2-adrenergic signaling inhibits several pathways necessary for breast tumor progression and metastasis. A series of population-based observational studies were conducted to examine associations between beta blocker use and breast tumor characteristics at diagnosis or breast cancer–specific mortality. Patients and Methods Linked national cancer registry and prescription dispensing data were used to identify women with a diagnosis of stage I to IV invasive breast cancer between January 1, 2001, and December 31, 2006. Women taking propranolol (β1/β2 antagonist; n = 70) or atenolol (β1 antagonist; n = 525), in the year before breast cancer diagnosis were matched (1:2) to women not taking a beta blocker (n = 4,738). Associations between use of propranolol or atenolol and risk of local tumor invasion at diagnosis (T4 tumor), nodal or metastatic involvement at diagnosis (N2/N3/M1 tumor), and time to breast cancer–specific mortality were assessed. Results Propranolol users were significantly less likely to present with a T4 (odds ratio [OR], 0.24, 95% CI, 0.07 to 0.85) or N2/N3/M1 (OR, 0.20; 95% CI, 0.04 to 0.88) tumor compared with matched nonusers. The cumulative probability of breast cancer–specific mortality was significantly lower for propranolol users compared with matched nonusers (hazard ratio, 0.19; 95% CI, 0.06 to 0.60). There was no difference in T4 or N2/N3/M1 tumor incidence or breast cancer–specific mortality between atenolol users and matched nonusers. Conclusion The results provide evidence in humans to support preclinical observations suggesting that inhibiting the β2-adrenergic signaling pathway can reduce breast cancer progression and mortality.

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