Role of PARP in TNBC: Mechanism of Inhibition, Clinical Applications, and Resistance

Triple-negative breast cancer is a combative cancer type with a highly inflated histological grade that leads to poor theragnostic value. Gene, protein, and receptor-specific targets have shown effective clinical outcomes in patients with TNBC. Cells are frequently exposed to DNA-damaging agents. DN...

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Autores principales:	Desh Deepak Singh, Amna Parveen, Dharmendra Kumar Yadav
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	breast cancer PARP (poly(ADP-ribose) polymerase) TNBC therapeutic target DNA damage repair signaling pathway Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/108999712fb24e77aa9273b0efcdafe2
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spelling	oai:doaj.org-article:108999712fb24e77aa9273b0efcdafe22021-11-25T16:48:25ZRole of PARP in TNBC: Mechanism of Inhibition, Clinical Applications, and Resistance10.3390/biomedicines91115122227-9059https://doaj.org/article/108999712fb24e77aa9273b0efcdafe22021-10-01T00:00:00Zhttps://www.mdpi.com/2227-9059/9/11/1512https://doaj.org/toc/2227-9059Triple-negative breast cancer is a combative cancer type with a highly inflated histological grade that leads to poor theragnostic value. Gene, protein, and receptor-specific targets have shown effective clinical outcomes in patients with TNBC. Cells are frequently exposed to DNA-damaging agents. DNA damage is repaired by multiple pathways; accumulations of mutations occur due to damage to one or more pathways and lead to alterations in normal cellular mechanisms, which lead to development of tumors. Advances in target-specific cancer therapies have shown significant momentum; most treatment options cause off-target toxicity and side effects on healthy tissues. PARP (poly(ADP-ribose) polymerase) is a major protein and is involved in DNA repair pathways, base excision repair (BER) mechanisms, homologous recombination (HR), and nonhomologous end-joining (NEJ) deficiency-based repair mechanisms. DNA damage repair deficits cause an increased risk of tumor formation. Inhibitors of PARP favorably kill cancer cells in <i>BRCA</i>-mutations. For a few years, PARPi has shown promising activity as a chemotherapeutic agent in <i>BRCA1</i>- or <i>BRCA2</i>-associated breast cancers, and in combination with chemotherapy in triple-negative breast cancer. This review covers the current results of clinical trials testing and future directions for the field of PARP inhibitor development.Desh Deepak SinghAmna ParveenDharmendra Kumar YadavMDPI AGarticlebreast cancerPARP (poly(ADP-ribose) polymerase)TNBCtherapeutic targetDNA damage repairsignaling pathwayBiology (General)QH301-705.5ENBiomedicines, Vol 9, Iss 1512, p 1512 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	breast cancer PARP (poly(ADP-ribose) polymerase) TNBC therapeutic target DNA damage repair signaling pathway Biology (General) QH301-705.5
spellingShingle	breast cancer PARP (poly(ADP-ribose) polymerase) TNBC therapeutic target DNA damage repair signaling pathway Biology (General) QH301-705.5 Desh Deepak Singh Amna Parveen Dharmendra Kumar Yadav Role of PARP in TNBC: Mechanism of Inhibition, Clinical Applications, and Resistance
description	Triple-negative breast cancer is a combative cancer type with a highly inflated histological grade that leads to poor theragnostic value. Gene, protein, and receptor-specific targets have shown effective clinical outcomes in patients with TNBC. Cells are frequently exposed to DNA-damaging agents. DNA damage is repaired by multiple pathways; accumulations of mutations occur due to damage to one or more pathways and lead to alterations in normal cellular mechanisms, which lead to development of tumors. Advances in target-specific cancer therapies have shown significant momentum; most treatment options cause off-target toxicity and side effects on healthy tissues. PARP (poly(ADP-ribose) polymerase) is a major protein and is involved in DNA repair pathways, base excision repair (BER) mechanisms, homologous recombination (HR), and nonhomologous end-joining (NEJ) deficiency-based repair mechanisms. DNA damage repair deficits cause an increased risk of tumor formation. Inhibitors of PARP favorably kill cancer cells in <i>BRCA</i>-mutations. For a few years, PARPi has shown promising activity as a chemotherapeutic agent in <i>BRCA1</i>- or <i>BRCA2</i>-associated breast cancers, and in combination with chemotherapy in triple-negative breast cancer. This review covers the current results of clinical trials testing and future directions for the field of PARP inhibitor development.
format	article
author	Desh Deepak Singh Amna Parveen Dharmendra Kumar Yadav
author_facet	Desh Deepak Singh Amna Parveen Dharmendra Kumar Yadav
author_sort	Desh Deepak Singh
title	Role of PARP in TNBC: Mechanism of Inhibition, Clinical Applications, and Resistance
title_short	Role of PARP in TNBC: Mechanism of Inhibition, Clinical Applications, and Resistance
title_full	Role of PARP in TNBC: Mechanism of Inhibition, Clinical Applications, and Resistance
title_fullStr	Role of PARP in TNBC: Mechanism of Inhibition, Clinical Applications, and Resistance
title_full_unstemmed	Role of PARP in TNBC: Mechanism of Inhibition, Clinical Applications, and Resistance
title_sort	role of parp in tnbc: mechanism of inhibition, clinical applications, and resistance
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/108999712fb24e77aa9273b0efcdafe2
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Role of PARP in TNBC: Mechanism of Inhibition, Clinical Applications, and Resistance

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