Combinatorial Epigenetic and Immunotherapy in Breast Cancer Management: A Literature Review

被引:10
作者
Lee, Yu-Ting [1 ,2 ,3 ,4 ]
Chuang, Yu-Ming [1 ,2 ,3 ]
Chan, Michael W. Y. [1 ,2 ,3 ]
机构
[1] Natl Chung Cheng Univ, Dept Biomed Sci, Chiayi 621, Taiwan
[2] Natl Chung Cheng Univ, Epigenom & Human Dis Res Ctr, Chiayi 621, Taiwan
[3] Natl Chung Cheng Univ, Ctr Innovat Res Aging Soc CIRAS, Chiayi 621, Taiwan
[4] Ditmanson Med Fdn Chiayi Christian Hosp, Div Hematol & Oncol, Dept Med, Chiayi 621, Taiwan
关键词
immune checkpoint inhibitors; epi-drug; combination therapy; breast cancer; HISTONE DEACETYLASE INHIBITOR; PHASE-I TRIAL; HOMOLOGOUS RECOMBINATION DEFICIENCY; GENE-EXPRESSION; SOLID TUMORS; BROMODOMAIN INHIBITION; THERAPY; ESTROGEN; CELLS; CHEMOTHERAPY;
D O I
10.3390/epigenomes4040027
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
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.
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页数:15
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共 96 条
[91]  
Wilcken NRC, 1997, CLIN CANCER RES, V3, P849
[92]   T cells lacking HDAC11 have increased effector functions and mediate enhanced alloreactivity in a murine model [J].
Woods, David M. ;
Woan, Karrune V. ;
Cheng, Fengdong ;
Sodre, Andressa L. ;
Wang, Dapeng ;
Wu, Yongxia ;
Wang, Zi ;
Chen, Jie ;
Powers, John ;
Pinilla-Ibarz, Javier ;
Yu, Yu ;
Zhang, Ya ;
Wu, Xuefeng ;
Zheng, Xiaoyan ;
Weber, Jeffrey ;
Hancock, Wayne W. ;
Seto, Edward ;
Villagra, Alejandro ;
Yu, Xue-Zhong ;
Sotomayor, Eduardo M. .
BLOOD, 2017, 130 (02) :146-155
[93]   TET-mediated active DNA demethylation: mechanism, function and beyond [J].
Wu, Xiaoji ;
Zhang, Yi .
NATURE REVIEWS GENETICS, 2017, 18 (09) :517-534
[94]   Histone Deacetylase 9 Deficiency Protects against Effector T Cell-mediated Systemic Autoimmunity [J].
Yan, Kailin ;
Cao, Qiang ;
Reilly, Christopher M. ;
Young, Nicolas L. ;
Garcia, Benjamin A. ;
Mishra, Nilamadhab .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2011, 286 (33) :28833-28843
[95]   Randomized Phase II, Double-Blind, Placebo-Controlled Study of Exemestane With or Without Entinostat in Postmenopausal Women With Locally Recurrent or Metastatic Estrogen Receptor-Positive Breast Cancer Progressing on Treatment With a Nonsteroidal Aromatase Inhibitor [J].
Yardley, Denise A. ;
Ismail-Khan, Roohi R. ;
Melichar, Bohuslav ;
Lichinitser, Mikhail ;
Munster, Pamela N. ;
Klein, Pamela M. ;
Cruickshank, Scott ;
Miller, Kathy D. ;
Lee, Min J. ;
Trepel, Jane B. .
JOURNAL OF CLINICAL ONCOLOGY, 2013, 31 (17) :2128-+
[96]   Histone deacetylase inhibitor LBH589 reactivates silenced estrogen receptor alpha (ER) gene expression without loss of DNA hypermethylation [J].
Zhou, Qun ;
Atadja, Peter ;
Davidson, Nancy E. .
CANCER BIOLOGY & THERAPY, 2007, 6 (01) :64-69