TY - JOUR
T1 - Rational combination of immunotherapy for triple negative breast cancer treatment
AU - Li, Chia Wei
AU - Lim, Seung Oe
AU - Hsu, Jennifer L.
AU - Hung, Mien Chie
N1 - Publisher Copyright:
© Chinese Clinical Oncology.
PY - 2017/10/1
Y1 - 2017/10/1
N2 - Recent evidence indicates that tumor infiltrating lymphocytes (TILs), including cytotoxic T cells, are present in the tumor microenvironment of triple-negative breast cancers (TNBC). Despite the presence of cytotoxic T cells, these tumors still develop, progress, and metastasize, suggesting evasion of immune response. One mechanism of immunosuppression is the presence of the T cell inhibitory molecule, programmed death protein 1 (PD-1), on infiltrating T cells and its cognate ligand programmed death ligand 1 (PD-L1) on tumor cells, myeloid dendritic cells (DCs), and macrophages, in the tumor microenvironment. Because TNBC is immunologically insensitive, combinatorial strategies may be ideal to increase both anti-proliferation activity and cytotoxic T cells activity in TNBC. On the basis of two recently discovered regulatory mechanisms of PD-L1, we discuss the potential interactions to boost anti-tumor immunity against TNBC in this review and propose therapeutic strategies that could reduce PD-L1 expression by chemotherapeutic drugs or targeted therapies and sensitize TNBC to immunotherapies.
AB - Recent evidence indicates that tumor infiltrating lymphocytes (TILs), including cytotoxic T cells, are present in the tumor microenvironment of triple-negative breast cancers (TNBC). Despite the presence of cytotoxic T cells, these tumors still develop, progress, and metastasize, suggesting evasion of immune response. One mechanism of immunosuppression is the presence of the T cell inhibitory molecule, programmed death protein 1 (PD-1), on infiltrating T cells and its cognate ligand programmed death ligand 1 (PD-L1) on tumor cells, myeloid dendritic cells (DCs), and macrophages, in the tumor microenvironment. Because TNBC is immunologically insensitive, combinatorial strategies may be ideal to increase both anti-proliferation activity and cytotoxic T cells activity in TNBC. On the basis of two recently discovered regulatory mechanisms of PD-L1, we discuss the potential interactions to boost anti-tumor immunity against TNBC in this review and propose therapeutic strategies that could reduce PD-L1 expression by chemotherapeutic drugs or targeted therapies and sensitize TNBC to immunotherapies.
KW - Immune therapy
KW - Programmed death ligand 1 (PD-L1)
KW - Triple-negative breast cancers (TNBC)
KW - Tumor infiltrating lymphocytes (TILs)Ubiquitination
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U2 - 10.21037/cco.2017.08.04
DO - 10.21037/cco.2017.08.04
M3 - Review article
C2 - 29129094
AN - SCOPUS:85032569151
SN - 2304-3865
VL - 6
JO - Chinese clinical oncology
JF - Chinese clinical oncology
IS - 5
M1 - 54
ER -