- Open Access
Is immune checkpoint modulation a potential therapeutic option in triple negative breast cancer?
© Klinke; licensee BioMed Central Ltd. 2014
- Published: 7 November 2014
- Breast Cancer
- Epidermal Growth Factor Receptor
- Natural Killer Cell
- Programme Cell Death
The emergence of molecular targeted therapies has revolutionized the clinical treatment of breast cancer. To guide treatment, patient samples are screened for expression of hormone receptors for estrogen and progesterone and the epidermal growth factor receptor HER2. Patients with tumors that do not express any of these three receptors (that is, triple-negative breast cancer) exhibit a worse outcome . Sequencing of cancer genomes suggests that over-expressing an oncogene or eliminating a tumor suppressor gene is also associated with passenger mutations. The presence of these passenger mutations may provide a collective signature that distinguishes malignant from normal cells. Conceptually, the adaptive immune system recognizes cells that present a different antigenic signature and provides a mechanism to control for malignant transformation. One approach to enhance anti-tumor immunity is to increase the number of T cells, either systemically, through inhibiting the action of CTLA-4, or locally, through inhibiting the programmed cell death 1 pathway. Therapeutic inhibition of these pathways is called immune checkpoint modulation . The clinical benefit received by a subset of patients with metastatic melanoma demonstrates proof-of-principle for this therapeutic approach .
DJK conceived the study, performed the bioinformatic analysis, analyzed the experimental data, and wrote the manuscript.
This work was supported by grants from the National Science Foundation (CAREER 1053490) and the National Cancer Institute (NCI) R15CA123123. The content is solely the responsibility of the author and does not necessarily represent the official views of the NCI, the National Institutes of Health, or the National Science Foundation.
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