Abstract
Breast cancer is one of the leading causes of death among cancer patients worldwide. To date, there are several drugs that have been developed for breast cancer therapy. In the 21st century, immunotherapy is considered a pioneering method for improving the management of malignancies; however, breast cancer is an exception. According to the immunoediting model, many immunosuppressive cells contribute to immunological quiescence. Therefore, there is an urgent need to enhance the therapeutic efficacy of breast cancer treatments. In the last few years, numerous combinatorial therapies involving immune checkpoint blockade have been demonstrated that effectively improve clinical outcomes in breast cancer and combining these with methods of targeting epigenetic regulators is also an innovative strategy. Nevertheless, few studies have discussed the benefits of epi-drugs in non-cancerous cells. In this review, we give a brief overview of ongoing clinical trials involving combinatorial immunotherapy with epi-drugs in breast cancer and discuss the role of epi-drugs in the tumor microenvironment, including the results of recent research.
Highlights
Breast cancer, a malignancy of mammalian cells, is the most commonly diagnosed cancer in females and one of the leading causes of cancer death worldwide [1]
The programmed cell death 1 (PD-1) receptor on the surface of immune cells interacts with its ligand, programmed cell death ligand 1 (PD-L1), which can be produced by tumor cells or immunosuppressive cells, and suppresses the cytotoxic function of T-cells
We review ongoing and completed clinical trials involving epi-drugs combined with other therapies, including immunotherapy, in breast cancer (Table 2), and discuss the potential mechanism by which epi-drugs target the microenvironment of breast cancer
Summary
A malignancy of mammalian cells, is the most commonly diagnosed cancer in females and one of the leading causes of cancer death worldwide [1]. A phase III study (BOLERO-2) demonstrated that the mTOR inhibitor everolimus, combined with exemestane, can overcome endocrine resistance [9]. Combined therapy of alpelisib and fulvestrant improved PFS among patients with PIK3CA-mutated, HR-positive, HER2-negative breast cancer who had received endocrine therapy previously [10]. A CDK4/6 inhibitor combined with fulvestrant or aromatase inhibitor was shown to markedly increase PFS and overall survival (OS), and will become an upfront therapy for hormone receptor (HR)-positive breast cancer [13,14,15,16]. In 2018, the IMpassion130 study demonstrated that atezolizumab, an anti-PD-L1 monoclonal ab, plus chemotherapy, improves survival among patients with TNBC whose tumors express PD-L1 [20]. ER: estrogen receptor; PR: progesterone receptor; HER2: human epidermal growth factor receptor 2; AI: aromatase inhibitor; SERM: selective estrogen receptors modulator; SERD: selective ER down-regulator
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