Alterations of Signaling Pathways Related to the Immune System in Breast Cancer: New Perspectives in Patient Management

Int J Mol Sci. 2018 Sep 12;19(9):2733. doi: 10.3390/ijms19092733.

Abstract

In recent years, immune manipulation for cancer treatment, including breast cancer, has been increasingly gaining consent, and many attempts have been made, mainly by either strengthening the immune response (IR) or by inhibiting immune evasion. Therefore, elucidating the related mechanisms is of importance due to the potential to improve the management of cancer patients by immunotherapy. This review article summarized some recent experimental studies, which have discovered novel alterations of signaling pathways related to the immune system in breast cancer. These altered signaling pathways have been grouped according to the general biological mechanism involved: tumor-initiating cells (TICs), cancer stem cells (CSCs), immune evasion, tumor growth and progression, prediction of clinical outcome and prediction of response, or resistance to chemotherapy. These altered pathways related to the immune system open clinical opportunities for the prognosis or treatment of patients. Many of these pathways are related to the origin of breast cancer and immune evasion. We recommended development of new drugs which act on these molecular pathways, and the designing of clinical trials to be carried out mainly in breast cancer patients who required adjuvant treatment.

Keywords: CD47 upregulation; NF-κB; STAT-1; STAT-3; TNF; breast cancer; cancer stem cells; immune response; signaling pathways; tumor initiating cells.

Publication types

  • Review

MeSH terms

  • Breast Neoplasms / immunology*
  • Breast Neoplasms / metabolism*
  • Female
  • Humans
  • NF-kappa B / metabolism
  • Neoplastic Stem Cells / metabolism*
  • STAT1 Transcription Factor / metabolism
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction / physiology
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • NF-kappa B
  • STAT1 Transcription Factor
  • STAT3 Transcription Factor
  • Tumor Necrosis Factor-alpha