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Breast Cancer Research and Treatment

, Volume 165, Issue 3, pp 743–750 | Cite as

Risk of mortality of node-negative, ER/PR/HER2 breast cancer subtypes in T1, T2, and T3 tumors

  • Carol A. PariseEmail author
  • Vincent Caggiano
Epidemiology

Abstract

Purpose

The purpose of this study was to assess differences in breast cancer-specific mortality within tumors of the same size when breast cancer was defined using the three tumor markers estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2).

Methods

We identified 104,499 cases of node-negative primary female invasive breast cancer from the California Cancer Registry. Tumor size was categorized as T1a, T1b, T1c, T2, and T3. Breast cancer was defined using ER, PR, and HER2. Kaplan–Meier Survival analysis was conducted and Cox Regression was used to compute the adjusted risk of mortality for the ER+/PR+/HER2+, ER−/PR−/HER2− (TNBC), and ER−/PR−/HER2+ (HER2-overexpressing) subtypes when compared with the ER+/PR+/HER2−. Separate models were computed for each tumor size.

Results

Unadjusted survival analysis showed that for all tumor sizes, the ER+/PR+ subtypes regardless of HER status have better breast cancer-specific survival than ER−/PR− subtypes. Subtype was not an important factor for risk of mortality for T1a tumors. The ER+/PR+/HER2+ subtype was only a risk for mortality in T1b tumors that were unadjusted for treatment. For all other tumor sizes, the ER+/PR+/HER2+ had the same mortality as the ER+/PR+/HER2− subtype regardless of adjustment for treatment. The HER2-overexpressing subtype had a higher risk of mortality than the ER+/PR+/HER2− subtype except for T1b tumors that were adjusted for treatment. For all tumor sizes, the TNBC had higher hazard ratios than all other subtypes.

Conclusions

T1a tumors have the same risk of mortality regardless of ER/PR/HER2 subtype, and ER and PR negativity plays a stronger role in survival than HER2 positivity for tumors of all size.

Keywords

Breast cancer ER/PR/HER2 subtype Tumor size 

Notes

Acknowledgements

We wish to thank Melissa Taylor and the staff at the Sutter Resource Library for their valuable assistance.

Disclaimer

The collection of cancer incidence data used in this study was supported by the California Department of Public Health as part of the statewide cancer reporting program mandated by California Health and Safety Code Section 103885; the National Cancer Institute’s Surveillance, Epidemiology and End Results Program under contract N01-PC-35136 awarded to the Northern California Cancer Center, contract N01-PC-35139 awarded to the University of Southern California, and contract N01-PC-54404 awarded to the Public Health Institute; and the Centers for Disease Control and Prevention’s National Program of Cancer Registries, under agreement 1U58DP00807-01 awarded to the Public Health Institute. The ideas and opinions expressed herein are those of the authors and endorsement by the State of California, Department of Public Health the National Cancer Institute, and the Centers for Disease Control and Prevention or their Contractors and Subcontractors is not intended nor should be inferred.

Funding

This study was funded by Grant 947110-1107555 from the Sutter Medical Center Sacramento Foundation.

Compliance and ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

Ethical approval

This research study involved analysis of existing data from the CCR without subject identifiers or intervention. Therefore, the study was categorized as exempt from institutional review board oversight.

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Copyright information

© Springer Science+Business Media, LLC 2017

Authors and Affiliations

  1. 1.Sutter Institute for Medical ResearchSacramentoUSA

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