Early and Locally Advanced Metaplastic Breast Cancer: Presentation and Survival by Receptor Status in Surveillance, Epidemiology, and End Results (SEER) 2010-2014.

dc.contributor.author

Schroeder, Mary C

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Rastogi, Priya

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Geyer, Charles E

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Miller, Lance D

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Thomas, Alexandra

dc.date.accessioned

2024-02-01T14:27:56Z

dc.date.available

2024-02-01T14:27:56Z

dc.date.issued

2018-04

dc.description.abstract

Background

Metaplastic breast cancer (MBC) is a rare disease subtype characterized by an aggressive clinical course. MBC is commonly triple negative (TN), although hormone receptor (HR) positive and human epidermal growth receptor 2 (HER2) positive cases do occur. Previous studies have reported similar outcomes for MBC with regard to HR status. Less is known about outcomes for HER2 positive MBC.

Materials and methods

Surveillance, Epidemiology, and End Results Program data were used to identify women diagnosed 2010-2014 with MBC or invasive ductal carcinoma (IDC). Kaplan-Meier curves estimated overall survival (OS) and multivariate Cox models were fitted. For survival analyses, only first cancers were included, and 2014 diagnoses were excluded to allow for sufficient follow-up.

Results

Our MBC sample included 1,516 women. Relative to women with IDC, women with MBC were more likely to be older (63 vs. 61 years), black (16.0% vs. 11.1%), and present with stage III disease (15.6% vs. 10.8%). HER2 positive and HER2 negative/HR positive MBC tumors represented 5.2% and 23.0% of cases. For MBC overall, 3-year OS was greatest for women with HER2 positive MBC (91.8%), relative to women with TN (75.4%) and HER2 negative/HR positive MBC (77.1%). This difference was more pronounced for stage III MBC, for which 3-year OS was 92.9%, 47.1%, and 42.2% for women with HER2 positive, TN, and HER2 negative/HR positive MBC, respectively. A multivariate Cox model of MBC demonstrated that HER2 positive tumors (relative to TN) were associated with improved survival (hazard ratio = 0.32, 95% confidence interval [CI] 0.13-0.79). In a second Cox model of exclusively HER2 positive tumors, OS did not differ between MBC and IDC disease subtypes (hazard ratio = 1.16, 95% CI 0.48-2.81).

Conclusion

In this contemporary, population-based study of women with MBC, HER2 but not HR status was associated with improved survival. Survival was similar between HER2 positive MBC and HER2 positive IDC. This suggests HER2 positive MBC is responsive to HER2-directed therapy, a finding that may offer insights for additional therapeutic approaches to MBC.

Implications for practice

This population-based study reports recent outcomes, by receptor status, for women with metaplastic breast cancer. Survival in metaplastic breast cancer is not impacted by hormone receptor status. To the authors' knowledge, this is the first report indicating that women with human epidermal growth receptor 2 (HER2) positive metaplastic breast cancer have survival superior to women with HER2 negative metaplastic breast cancer and survival similar to women with HER2 positive invasive ductal carcinoma. This information can be used for counseling patients diagnosed with metaplastic breast cancer. Further understanding of HER2 positive metaplastic breast cancer could offer insights for the development of therapeutic approaches to metaplastic breast cancer more broadly.
dc.identifier

theoncologist.2017-0398

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1083-7159

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1549-490X

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https://hdl.handle.net/10161/29971

dc.language

eng

dc.publisher

Oxford University Press (OUP)

dc.relation.ispartof

The oncologist

dc.relation.isversionof

10.1634/theoncologist.2017-0398

dc.rights.uri

https://creativecommons.org/licenses/by-nc/4.0

dc.subject

Humans

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Carcinoma, Ductal, Breast

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Breast Neoplasms

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Metaplasia

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Receptor, erbB-2

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Receptors, Estrogen

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Receptors, Progesterone

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Neoplasm Staging

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SEER Program

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Survival Analysis

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Aged

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Middle Aged

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Female

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Neoplasm Grading

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Biomarkers, Tumor

dc.title

Early and Locally Advanced Metaplastic Breast Cancer: Presentation and Survival by Receptor Status in Surveillance, Epidemiology, and End Results (SEER) 2010-2014.

dc.type

Journal article

duke.contributor.orcid

Thomas, Alexandra|0000-0001-9022-2229

pubs.begin-page

481

pubs.end-page

488

pubs.issue

4

pubs.organisational-group

Duke

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School of Medicine

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Clinical Science Departments

pubs.organisational-group

Medicine

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Medicine, Medical Oncology

pubs.publication-status

Published

pubs.volume

23

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