The prognostic value of regulatory T cells infiltration in HER2-enriched breast cancer microenvironment

Int Rev Immunol. 2018 May 4;37(3):144-150. doi: 10.1080/08830185.2017.1401620. Epub 2017 Dec 19.

Abstract

Breast cancer represents a complex and heterogeneous disease that comprises distinct disease conditions, histological features, and clinical outcome. Since many years, it has been demonstrated as an association between HER2 amplification and poor prognosis, because its overexpression is associated with an aggressive phenotype of breast tumor cells. A significant proportion of cases have developed resistance to the current therapies available. Consequently, new prognostic markers are urgently needed to identify patients who are at the highest risk for developing metastases. During the past decade, new insights provided valuable knowledge regarding mechanisms underlying the dynamic interplayed between immune cells and tumor progression. It has been shown that the presence of a lymphocytic infiltrate, particularly of regulatory T cells, in cancer tissue, is associated with clinical outcome promoting rather than inhibiting cancer development and progression. It has been also verified that the clinical value of lymphocytic infiltration in breast cancers could be subtype-dependent, including the HER2-enriched subtype. In this context, this work summarizes proposed to discuss the prognostic value of regulatory T cell infiltration in microenvironment of HER2-enriched breast cancer.

Keywords: Breast cancer; HER2 overexpression; Tregs; lymphocyte infiltration.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Biomarkers, Tumor / metabolism
  • Breast Neoplasms / diagnosis*
  • Breast Neoplasms / immunology
  • Carcinogenesis
  • Cell Movement
  • Female
  • Humans
  • Predictive Value of Tests
  • Prognosis
  • Receptor, ErbB-2 / metabolism
  • T-Lymphocytes, Regulatory / immunology*
  • Tumor Microenvironment

Substances

  • Biomarkers, Tumor
  • ERBB2 protein, human
  • Receptor, ErbB-2