DNA Repair Deficiency in Breast Cancer: Opportunities for Immunotherapy

Historically the development of anticancer treatments has been focused on their effect on tumor cells alone. However, newer treatments have shifted attention to targets on immune cells, resulting in dramatic responses. The effect of DNA repair deficiency on the microenvironment remains an area of ke...

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Main Authors: Elaine Gilmore, Nuala McCabe, Richard D. Kennedy, Eileen E. Parkes
Format: Article
Language:English
Published: Hindawi Limited 2019-01-01
Series:Journal of Oncology
Online Access:http://dx.doi.org/10.1155/2019/4325105
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spelling doaj-4c45cc05834f4140865701d7fc7d2f6c2020-11-25T00:20:06ZengHindawi LimitedJournal of Oncology1687-84501687-84692019-01-01201910.1155/2019/43251054325105DNA Repair Deficiency in Breast Cancer: Opportunities for ImmunotherapyElaine Gilmore0Nuala McCabe1Richard D. Kennedy2Eileen E. Parkes3Queen’s University Belfast, Centre for Cancer Research and Cell Biology, 97 Lisburn Road, Belfast BT9 7AE, UKQueen’s University Belfast, Centre for Cancer Research and Cell Biology, 97 Lisburn Road, Belfast BT9 7AE, UKQueen’s University Belfast, Centre for Cancer Research and Cell Biology, 97 Lisburn Road, Belfast BT9 7AE, UKQueen’s University Belfast, Centre for Cancer Research and Cell Biology, 97 Lisburn Road, Belfast BT9 7AE, UKHistorically the development of anticancer treatments has been focused on their effect on tumor cells alone. However, newer treatments have shifted attention to targets on immune cells, resulting in dramatic responses. The effect of DNA repair deficiency on the microenvironment remains an area of key interest. Moreover, established therapies such as DNA damaging treatments such as chemotherapy and PARP inhibitors further modify the tumor microenvironment. Here we describe DNA repair pathways in breast cancer and activation of innate immune pathways in DNA repair deficiency, in particular, the STING (STimulator of INterferon Genes) pathway. Breast tumors with DNA repair deficiency are associated with upregulation of immune checkpoints including PD-L1 (Programmed Death Ligand-1) and may represent a target population for single agent or combination immunotherapy treatment.http://dx.doi.org/10.1155/2019/4325105
collection DOAJ
language English
format Article
sources DOAJ
author Elaine Gilmore
Nuala McCabe
Richard D. Kennedy
Eileen E. Parkes
spellingShingle Elaine Gilmore
Nuala McCabe
Richard D. Kennedy
Eileen E. Parkes
DNA Repair Deficiency in Breast Cancer: Opportunities for Immunotherapy
Journal of Oncology
author_facet Elaine Gilmore
Nuala McCabe
Richard D. Kennedy
Eileen E. Parkes
author_sort Elaine Gilmore
title DNA Repair Deficiency in Breast Cancer: Opportunities for Immunotherapy
title_short DNA Repair Deficiency in Breast Cancer: Opportunities for Immunotherapy
title_full DNA Repair Deficiency in Breast Cancer: Opportunities for Immunotherapy
title_fullStr DNA Repair Deficiency in Breast Cancer: Opportunities for Immunotherapy
title_full_unstemmed DNA Repair Deficiency in Breast Cancer: Opportunities for Immunotherapy
title_sort dna repair deficiency in breast cancer: opportunities for immunotherapy
publisher Hindawi Limited
series Journal of Oncology
issn 1687-8450
1687-8469
publishDate 2019-01-01
description Historically the development of anticancer treatments has been focused on their effect on tumor cells alone. However, newer treatments have shifted attention to targets on immune cells, resulting in dramatic responses. The effect of DNA repair deficiency on the microenvironment remains an area of key interest. Moreover, established therapies such as DNA damaging treatments such as chemotherapy and PARP inhibitors further modify the tumor microenvironment. Here we describe DNA repair pathways in breast cancer and activation of innate immune pathways in DNA repair deficiency, in particular, the STING (STimulator of INterferon Genes) pathway. Breast tumors with DNA repair deficiency are associated with upregulation of immune checkpoints including PD-L1 (Programmed Death Ligand-1) and may represent a target population for single agent or combination immunotherapy treatment.
url http://dx.doi.org/10.1155/2019/4325105
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AT richarddkennedy dnarepairdeficiencyinbreastcanceropportunitiesforimmunotherapy
AT eileeneparkes dnarepairdeficiencyinbreastcanceropportunitiesforimmunotherapy
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