Potential of chimeric antigen receptor (CAR)-redirected immune cells in breast cancer therapies: Recent advances

J Cell Mol Med. 2022 Aug;26(15):4137-4156. doi: 10.1111/jcmm.17465. Epub 2022 Jun 28.

Abstract

Despite substantial developments in conventional treatments such as surgery, chemotherapy, radiotherapy, endocrine therapy, and molecular-targeted therapy, breast cancer remains the leading cause of cancer mortality in women. Currently, chimeric antigen receptor (CAR)-redirected immune cell therapy has emerged as an innovative immunotherapeutic approach to ameliorate survival rates of breast cancer patients by eliciting cytotoxic activity against cognate tumour-associated antigens expressing tumour cells. As a crucial component of adaptive immunity, T cells and NK cells, as the central innate immune cells, are two types of pivotal candidates for CAR engineering in treating solid malignancies. However, the biological distinctions between NK cells- and T cells lead to differences in cancer immunotherapy outcomes. Likewise, optimal breast cancer removal via CAR-redirected immune cells requires detecting safe target antigens, improving CAR structure for ideal immune cell functions, promoting CAR-redirected immune cells filtration to the tumour microenvironment (TME), and increasing the ability of these engineered cells to persist and retain within the immunosuppressive TME. This review provides a concise overview of breast cancer pathogenesis and its hostile TME. We focus on the CAR-T and CAR-NK cells and discuss their significant differences. Finally, we deliver a summary based on recent advancements in the therapeutic capability of CAR-T and CAR-NK cells in treating breast cancer.

Keywords: T cells; breast cancer; chimeric antigen receptor (CAR); immunotherapy; natural killer (NK) cells.

Publication types

  • Review

MeSH terms

  • Breast Neoplasms* / metabolism
  • Female
  • Humans
  • Immunotherapy, Adoptive
  • Killer Cells, Natural
  • Neoplasms* / drug therapy
  • Receptors, Chimeric Antigen* / genetics
  • Receptors, Chimeric Antigen* / metabolism
  • T-Lymphocytes
  • Tumor Microenvironment

Substances

  • Receptors, Chimeric Antigen