PARP inhibitors in pancreatic cancer: molecular mechanisms and clinical applications

Pancreatic cancer is a highly lethal disease with a poor prognosis, and existing therapies offer only limited effectiveness. Mutation gene sequencing has shown several gene associations that may account for its carcinogenesis, revealing a promising research direction. Poly (ADP-ribose) polymerase (P...

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Published inMolecular cancer Vol. 19; no. 1; pp. 49 - 15
Main Authors Zhu, Heng, Wei, Miaoyan, Xu, Jin, Hua, Jie, Liang, Chen, Meng, Qingcai, Zhang, Yiyin, Liu, Jiang, Zhang, Bo, Yu, Xianjun, Shi, Si
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 02.03.2020
BioMed Central
BMC
Subjects
Animals
Antineoplastic Agents - therapeutic use
Biological markers
Biotechnology
BRCA
BRCA mutations
Breast cancer
Cancer therapies
Cancer treatment
Carcinogenesis
Cell death
Chemotherapy
Chemotherapy resistance
Clinical trials
Deoxyribonucleic acid
Development and progression
Diseases
DNA
DNA damage
DNA repair
Drugs
Gene mutation
Genes
Genetic aspects
Genetic research
Genomes
Health risk assessment
Homologous recombination repair
Humans
Kinases
Medical prognosis
Metastasis
Molecular modelling
Monosaccharides
Mutation
Olaparib
Ovarian cancer
Pancreatic cancer
Pancreatic Neoplasms - drug therapy
Pancreatic Neoplasms - metabolism
Pancreatic Neoplasms - pathology
PARP inhibitor
Polo
Poly (ADP-Ribose) Polymerase-1 - antagonists & inhibitors
Poly(ADP-ribose) polymerase
Poly(ADP-ribose) Polymerase Inhibitors - therapeutic use
Prognosis
Proteins
Response rates
Review
Synthetic lethality
Talazoparib
Targeted cancer therapy
Therapeutic applications
Tumors
Homologous recombination repair
BRCA
Chemotherapy resistance
Pancreatic cancer
PARP inhibitor
Biomarkers
Synthetic lethality
Online AccessGet full text
ISSN1476-4598
1476-4598
DOI10.1186/s12943-020-01167-9

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Abstract Pancreatic cancer is a highly lethal disease with a poor prognosis, and existing therapies offer only limited effectiveness. Mutation gene sequencing has shown several gene associations that may account for its carcinogenesis, revealing a promising research direction. Poly (ADP-ribose) polymerase (PARP) inhibitors target tumor cells with a homologous recombination repair (HRR) deficiency based on the concept of synthetic lethality. The most prominent target gene is BRCA, in which mutations were first identified in breast cancer and ovarian cancer. PARP inhibitors can trap the PARP-1 protein at a single-stranded break/DNA lesion and disrupt its catalytic cycle, ultimately leading to replication fork progression and consequent double-strand breaks. For tumor cells with BRCA mutations, HRR loss would result in cell death. Pancreatic cancer has also been reported to have a strong relationship with BRCA gene mutations, which indicates that pancreatic cancer patients may benefit from PARP inhibitors. Several clinical trials are being conducted and have begun to yield results. For example, the POLO (Pancreatic Cancer Olaparib Ongoing) trial has demonstrated that the median progression-free survival was observably longer in the olaparib group than in the placebo group. However, PARP inhibitor resistance has partially precluded their use in clinical applications, and the major mechanism underlying this resistance is the restoration of HRR. Therefore, determining how to use PARP inhibitors in more clinical applications and how to avoid adverse effects, as well as prognosis and treatment response biomarkers, require additional research. This review elaborates on future prospects for the application of PARP inhibitors in pancreatic cancer.
AbstractList Pancreatic cancer is a highly lethal disease with a poor prognosis, and existing therapies offer only limited effectiveness. Mutation gene sequencing has shown several gene associations that may account for its carcinogenesis, revealing a promising research direction. Poly (ADP-ribose) polymerase (PARP) inhibitors target tumor cells with a homologous recombination repair (HRR) deficiency based on the concept of synthetic lethality. The most prominent target gene is BRCA, in which mutations were first identified in breast cancer and ovarian cancer. PARP inhibitors can trap the PARP-1 protein at a single-stranded break/DNA lesion and disrupt its catalytic cycle, ultimately leading to replication fork progression and consequent double-strand breaks. For tumor cells with BRCA mutations, HRR loss would result in cell death. Pancreatic cancer has also been reported to have a strong relationship with BRCA gene mutations, which indicates that pancreatic cancer patients may benefit from PARP inhibitors. Several clinical trials are being conducted and have begun to yield results. For example, the POLO (Pancreatic Cancer Olaparib Ongoing) trial has demonstrated that the median progression-free survival was observably longer in the olaparib group than in the placebo group. However, PARP inhibitor resistance has partially precluded their use in clinical applications, and the major mechanism underlying this resistance is the restoration of HRR. Therefore, determining how to use PARP inhibitors in more clinical applications and how to avoid adverse effects, as well as prognosis and treatment response biomarkers, require additional research. This review elaborates on future prospects for the application of PARP inhibitors in pancreatic cancer. Keywords: PARP inhibitor, Pancreatic cancer, BRCA, Synthetic lethality, Homologous recombination repair, Chemotherapy resistance, Biomarkers
Pancreatic cancer is a highly lethal disease with a poor prognosis, and existing therapies offer only limited effectiveness. Mutation gene sequencing has shown several gene associations that may account for its carcinogenesis, revealing a promising research direction. Poly (ADP-ribose) polymerase (PARP) inhibitors target tumor cells with a homologous recombination repair (HRR) deficiency based on the concept of synthetic lethality. The most prominent target gene is BRCA, in which mutations were first identified in breast cancer and ovarian cancer. PARP inhibitors can trap the PARP-1 protein at a single-stranded break/DNA lesion and disrupt its catalytic cycle, ultimately leading to replication fork progression and consequent double-strand breaks. For tumor cells with BRCA mutations, HRR loss would result in cell death. Pancreatic cancer has also been reported to have a strong relationship with BRCA gene mutations, which indicates that pancreatic cancer patients may benefit from PARP inhibitors. Several clinical trials are being conducted and have begun to yield results. For example, the POLO (Pancreatic Cancer Olaparib Ongoing) trial has demonstrated that the median progression-free survival was observably longer in the olaparib group than in the placebo group. However, PARP inhibitor resistance has partially precluded their use in clinical applications, and the major mechanism underlying this resistance is the restoration of HRR. Therefore, determining how to use PARP inhibitors in more clinical applications and how to avoid adverse effects, as well as prognosis and treatment response biomarkers, require additional research. This review elaborates on future prospects for the application of PARP inhibitors in pancreatic cancer.
Abstract Pancreatic cancer is a highly lethal disease with a poor prognosis, and existing therapies offer only limited effectiveness. Mutation gene sequencing has shown several gene associations that may account for its carcinogenesis, revealing a promising research direction. Poly (ADP-ribose) polymerase (PARP) inhibitors target tumor cells with a homologous recombination repair (HRR) deficiency based on the concept of synthetic lethality. The most prominent target gene is BRCA, in which mutations were first identified in breast cancer and ovarian cancer. PARP inhibitors can trap the PARP-1 protein at a single-stranded break/DNA lesion and disrupt its catalytic cycle, ultimately leading to replication fork progression and consequent double-strand breaks. For tumor cells with BRCA mutations, HRR loss would result in cell death. Pancreatic cancer has also been reported to have a strong relationship with BRCA gene mutations, which indicates that pancreatic cancer patients may benefit from PARP inhibitors. Several clinical trials are being conducted and have begun to yield results. For example, the POLO (Pancreatic Cancer Olaparib Ongoing) trial has demonstrated that the median progression-free survival was observably longer in the olaparib group than in the placebo group. However, PARP inhibitor resistance has partially precluded their use in clinical applications, and the major mechanism underlying this resistance is the restoration of HRR. Therefore, determining how to use PARP inhibitors in more clinical applications and how to avoid adverse effects, as well as prognosis and treatment response biomarkers, require additional research. This review elaborates on future prospects for the application of PARP inhibitors in pancreatic cancer.
Pancreatic cancer is a highly lethal disease with a poor prognosis, and existing therapies offer only limited effectiveness. Mutation gene sequencing has shown several gene associations that may account for its carcinogenesis, revealing a promising research direction. Poly (ADP-ribose) polymerase (PARP) inhibitors target tumor cells with a homologous recombination repair (HRR) deficiency based on the concept of synthetic lethality. The most prominent target gene is BRCA, in which mutations were first identified in breast cancer and ovarian cancer. PARP inhibitors can trap the PARP-1 protein at a single-stranded break/DNA lesion and disrupt its catalytic cycle, ultimately leading to replication fork progression and consequent double-strand breaks. For tumor cells with BRCA mutations, HRR loss would result in cell death. Pancreatic cancer has also been reported to have a strong relationship with BRCA gene mutations, which indicates that pancreatic cancer patients may benefit from PARP inhibitors. Several clinical trials are being conducted and have begun to yield results. For example, the POLO (Pancreatic Cancer Olaparib Ongoing) trial has demonstrated that the median progression-free survival was observably longer in the olaparib group than in the placebo group. However, PARP inhibitor resistance has partially precluded their use in clinical applications, and the major mechanism underlying this resistance is the restoration of HRR. Therefore, determining how to use PARP inhibitors in more clinical applications and how to avoid adverse effects, as well as prognosis and treatment response biomarkers, require additional research. This review elaborates on future prospects for the application of PARP inhibitors in pancreatic cancer.Pancreatic cancer is a highly lethal disease with a poor prognosis, and existing therapies offer only limited effectiveness. Mutation gene sequencing has shown several gene associations that may account for its carcinogenesis, revealing a promising research direction. Poly (ADP-ribose) polymerase (PARP) inhibitors target tumor cells with a homologous recombination repair (HRR) deficiency based on the concept of synthetic lethality. The most prominent target gene is BRCA, in which mutations were first identified in breast cancer and ovarian cancer. PARP inhibitors can trap the PARP-1 protein at a single-stranded break/DNA lesion and disrupt its catalytic cycle, ultimately leading to replication fork progression and consequent double-strand breaks. For tumor cells with BRCA mutations, HRR loss would result in cell death. Pancreatic cancer has also been reported to have a strong relationship with BRCA gene mutations, which indicates that pancreatic cancer patients may benefit from PARP inhibitors. Several clinical trials are being conducted and have begun to yield results. For example, the POLO (Pancreatic Cancer Olaparib Ongoing) trial has demonstrated that the median progression-free survival was observably longer in the olaparib group than in the placebo group. However, PARP inhibitor resistance has partially precluded their use in clinical applications, and the major mechanism underlying this resistance is the restoration of HRR. Therefore, determining how to use PARP inhibitors in more clinical applications and how to avoid adverse effects, as well as prognosis and treatment response biomarkers, require additional research. This review elaborates on future prospects for the application of PARP inhibitors in pancreatic cancer.
ArticleNumber 49
Audience Academic
Author Hua, Jie
Liang, Chen
Yu, Xianjun
Wei, Miaoyan
Liu, Jiang
Zhang, Bo
Shi, Si
Meng, Qingcai
Zhang, Yiyin
Xu, Jin
Zhu, Heng
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  givenname: Heng
  surname: Zhu
  fullname: Zhu, Heng
– sequence: 2
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  fullname: Wei, Miaoyan
– sequence: 3
  givenname: Jin
  surname: Xu
  fullname: Xu, Jin
– sequence: 4
  givenname: Jie
  surname: Hua
  fullname: Hua, Jie
– sequence: 5
  givenname: Chen
  surname: Liang
  fullname: Liang, Chen
– sequence: 6
  givenname: Qingcai
  surname: Meng
  fullname: Meng, Qingcai
– sequence: 7
  givenname: Yiyin
  surname: Zhang
  fullname: Zhang, Yiyin
– sequence: 8
  givenname: Jiang
  surname: Liu
  fullname: Liu, Jiang
– sequence: 9
  givenname: Bo
  surname: Zhang
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  givenname: Xianjun
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  fullname: Yu, Xianjun
– sequence: 11
  givenname: Si
  orcidid: 0000-0002-6652-0629
  surname: Shi
  fullname: Shi, Si
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32122376$$D View this record in MEDLINE/PubMed
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Issue 1
Keywords Homologous recombination repair
BRCA
Chemotherapy resistance
Pancreatic cancer
PARP inhibitor
Biomarkers
Synthetic lethality
Language English
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Snippet Pancreatic cancer is a highly lethal disease with a poor prognosis, and existing therapies offer only limited effectiveness. Mutation gene sequencing has shown...
Abstract Pancreatic cancer is a highly lethal disease with a poor prognosis, and existing therapies offer only limited effectiveness. Mutation gene sequencing...
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SubjectTerms Animals
Antineoplastic Agents - therapeutic use
Biological markers
Biotechnology
BRCA
BRCA mutations
Breast cancer
Cancer therapies
Cancer treatment
Carcinogenesis
Cell death
Chemotherapy
Chemotherapy resistance
Clinical trials
Deoxyribonucleic acid
Development and progression
Diseases
DNA
DNA damage
DNA repair
Drugs
Gene mutation
Genes
Genetic aspects
Genetic research
Genomes
Health risk assessment
Homologous recombination repair
Humans
Kinases
Medical prognosis
Metastasis
Molecular modelling
Monosaccharides
Mutation
Olaparib
Ovarian cancer
Pancreatic cancer
Pancreatic Neoplasms - drug therapy
Pancreatic Neoplasms - metabolism
Pancreatic Neoplasms - pathology
PARP inhibitor
Polo
Poly (ADP-Ribose) Polymerase-1 - antagonists & inhibitors
Poly(ADP-ribose) polymerase
Poly(ADP-ribose) Polymerase Inhibitors - therapeutic use
Prognosis
Proteins
Response rates
Review
Synthetic lethality
Talazoparib
Targeted cancer therapy
Therapeutic applications
Tumors
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Title PARP inhibitors in pancreatic cancer: molecular mechanisms and clinical applications
URI https://www.ncbi.nlm.nih.gov/pubmed/32122376
https://www.proquest.com/docview/2379153373
https://www.proquest.com/docview/2370496030
https://pubmed.ncbi.nlm.nih.gov/PMC7053129
https://doaj.org/article/a36f2a674c4c420e9fbf056ab660d4ba
Volume 19
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