J Breast Cancer.  2016 Sep;19(3):268-274. 10.4048/jbc.2016.19.3.268.

Patients with Concordant Triple-Negative Phenotype between Primary Breast Cancers and Corresponding Metastases Have Poor Prognosis

Affiliations
  • 1Department of Surgery, Chung-Ang University Hospital, Seoul, Korea.
  • 2Department of Surgery, Seoul National University Hospital, Seoul, Korea. dynoh@snu.ac.kr
  • 3Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
  • 4Department of Pathology, Seoul National University Hospital, Seoul, Korea.

Abstract

PURPOSE
We investigated the prognostic impact of discordance between the receptor status of primary breast cancers and corresponding metastases.
METHODS
A total 144 patients with breast cancer and distant metastasis were investigated. The estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) status of primary tumor and corresponding metastases were assessed. Tumor phenotype according to receptor status was classified as triple-negative phenotype (TNP) or non-TNP. Concordance and discordance was determined by whether there was a change in receptor status or phenotype between primary and metastatic lesions.
RESULTS
The rates of discordance between primary breast cancer and metastatic lesions were 18.1%, 25.0%, and 10.3% for ER, PR, and HER2, respectively. The rates of concordant non-TNP, concordant TNP and discordant TNP were 65.9%, 20.9%, and 13.2%, respectively. Patients with concordant ER/PR-negative status had worse postrecurrence survival (PRS) than patients with concordant ER/PR-positive and discordant ER/PR status (p=0.001 and p=0.021, respectively). Patients who converted from HER2-positive to negative after distant metastasis had worst PRS (p=0.040). Multivariate analysis showed that concordant TNP was statistically significant factor for worse PRS (p<0.001).
CONCLUSION
Discordance in receptor status and tumor phenotype between primary breast cancer and corresponding metastatic lesions was observed. Patients with concordant TNP had worse long-term outcomes than patients with concordant non-TNP and discordant TNP between primary and metastatic breast cancer. Identifying the receptor status of metastatic lesions may lead to improvements in patient management and survival.

Keyword

Breast neoplasms; erbB-2; Estrogen receptor; Progesterone receptor; Survival

MeSH Terms

Breast Neoplasms
Breast*
Estrogens
Humans
Multivariate Analysis
Neoplasm Metastasis*
Phenotype*
Prognosis*
Receptor, Epidermal Growth Factor
Receptors, Progesterone
Estrogens
Receptor, Epidermal Growth Factor
Receptors, Progesterone

Figure

  • Figure 1 Postrecurrence survival based on the status of individual receptors for pair of primary and metastatic breast cancer. (A) Survival curves according to estrogen receptor (ER) change, (B) survival curves according to progesterone receptor (PR) change, and (C) survival curves according to human epidermal growth factor receptor 2 (HER2) change.

  • Figure 2 Kaplan-Meier survival curves based on breast cancer phenotype. (A) Postrecurrence survival (PRS): 5-year PRS of concordant non-triple-negative phenotype (non-TNP), 37.0%; 5-year PRS discordant TNP, 25.8%; 5-year PRS concordant TNP, 11.3%; concordant non-TNP vs. discordant, p=0.280; discordant TNP vs. concordant TNP, p=0.030; and concordant non-TNP vs. concordant TNP, p<0.001. (B) Overall survival (OS): 5-year OS concordant non-TNP, 77.4%; 5-year OS discordant TNP, 70.6%; 5-year OS concordant TNP, 23.3%; concordant non-TNP vs. discordant TNP, p=0.799; discordant TNP vs. concordant TNP, p=0.003; concordant non-TNP vs. concordant TNP, p<0.001.


Cited by  2 articles

Comment to “Patients with Concordant Triple-Negative Phenotype between Primary Breast Cancers and Corresponding Metastases Have Poor Prognosis”
Kadri Altundag
J Breast Cancer. 2016;19(4):465-465.    doi: 10.4048/jbc.2016.19.4.465.

Comment to “Patients with Concordant Triple-Negative Phenotype between Primary Breast Cancers and Corresponding Metastases Have Poor Prognosis”
Kadri Altundag
J Breast Cancer. 2016;19(4):465-465.    doi: 10.4048/jbc.2016.19.4.465.


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