Association between p53 Expression and Amount of Tumor-Infiltrating Lymphocytes in Triple-Negative Breast Cancer
- Author:
Miseon LEE
1
;
In Ah PARK
;
Sun Hee HEO
;
Young Ae KIM
;
Gyungyub GONG
;
Hee Jin LEE
Author Information
- Publication Type:Original Article
- Keywords: p53; Breast neoplasms; Lymphocytes, Tumor-infiltrating
- MeSH: Breast Neoplasms; Endoplasmic Reticulum; Endoplasmic Reticulum Stress; Humans; Lymphocytes, Tumor-Infiltrating; Mutation, Missense; Survival Rate; Triple Negative Breast Neoplasms
- From:Journal of Pathology and Translational Medicine 2019;53(3):180-187
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND: Most triple-negative breast cancers (TNBCs) have a high histologic grade, are associated with high endoplasmic stress, and possess a high frequency of TP53 mutations. TP53 missense mutations lead to the production of mutant p53 protein and usually show high levels of p53 protein expression. Tumor-infiltrating lymphocytes (TILs) accumulate as part of the anti-tumor immune response and have a strong prognostic and predictive significance in TNBC. We aimed to elucidate the association between p53 expression and the amount of TILs in TNBC. METHODS: In 678 TNBC patients, we evaluated TIL levels and expression of endoplasmic stress molecules. Immunohistochemical examination of p53 protein expression was categorized into three groups: no, low, and high expression. RESULTS: No, low, and high p53 expression was identified in 44.1% (n = 299), 20.1% (n = 136), and 35.8% (n = 243) of patients, respectively. Patients with high p53 expression showed high histologic grade (p < .001), high TIL levels (p = .009), and high expression of endoplasmic reticulum stress-associated molecules (p-eIF2a, p = .013; XBP1, p = .007), compared to patients with low p53 expression. There was no significant difference in disease-free (p = .406) or overall survival rates (p = .444) among the three p53 expression groups. CONCLUSIONS: High p53 expression is associated with increased expression of endoplasmic reticulum stress molecules and TIL influx.
