The DOI matches its Crossref record; 130 of the 130 references it cites were found in a registry or an index.
Prospects for combining immune checkpoint blockade with PARP inhibition
Open accessAbstract
The immunogenicity of a cancer cell is derived from accumulated somatic mutations. However, on the contrary to increased immunogenicity, anti-cancer immune response tends to be feeble. This impaired anti-cancer immunity could be attributed to multiple factors including loss of immunodominant epitopes, downregulation of major histocompatibility complex, and immunosuppressive microenvironment, as well as aberrant negative co-stimulatory signals. Immune checkpoint inhibitors block negative co-stimulatory signals such as programmed cell death-1 and cytotoxic T-lymphocyte-associated protein 4, ultimately reactivating anti-cancer immunity. Immune checkpoint inhibitors elicit potent anti-cancer effect and have been approved for multiple cancers. Nevertheless, there still are significant potential improvements for the applications of checkpoint inhibitor, especially considering frequent resistance. Recent studies demonstrated that additional PARP inhibition could alleviate resistance and enhance efficacy of immune checkpoint blockade therapy via promoting cross-presentation and modifying immune microenvironment. We proposed that PARP inhibitors could enhance the priming and tumor-killing activities of T cell, boost the whole cancer-immunity cycle, and thereby improve the response to immune checkpoint blockade. In this review, we focused the latest understanding of the effect of PARP inhibitors on anti-cancer immunity and PARP inhibitors combining immune checkpoint blockade therapy. Moreover, we summarized the preclinical and clinical evidence and discussed the feasibility of this combination therapy in future clinical practice.
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“However, some HR-deficient (e.g. BRCA1/2 mutant) cancer cells only repair DSB by nonhomologous end joining, which is a low fidelity repair pathway [219].”
From Combination strategies with PD-1/PD-L1 blockade: current advances and future directions (2022) · cites this paper as [219]
In the citing paper
“Normal cells preferentially repair double strand break (DSB) via homologous recombination (HR).”
From Combination strategies with PD-1/PD-L1 blockade: current advances and future directions (2022) · cites this paper as [219]
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Cites
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Cited by
Sorted by citations
Combination strategies with PD-1/PD-L1 blockade: current advances and future directions
Yi, M., Zheng, X., Niu, M., Zhu, S., Ge, H., & Wu, K. (2022) · Molecular Cancer · doi:10.1186/s12943-021-01489-2 · Cited by 1,445
“Inspired by the results of preclinical studies, numerous clinical studies are ongoing to evaluate the efficacy of PARPi combined with α-PD-1/PD-L1 [219].”
BackgroundSelf-citationUnderstanding and overcoming resistance to PARP inhibitors in cancer therapy
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Tumor Immune Microenvironment during Epithelial–Mesenchymal Transition
Taki, M., Abiko, K., Ukita, M., Murakami, R., Yamanoi, K., Yamaguchi, K. D., Hamanishi, J., Baba, T., Matsumura, N., & Mandai, M. (2021) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-20-4459 · Cited by 368
“The FDA has approved several monoclonal antibodies targeting PD-1 (pembrolizumab, nivolumab, and cemiplimab) and PD-L1 (atezolizumab, avelumab, and durvalumab), which have been used as monotherapy or in combination with chemotherapies or other ICIs in several cancer types (27).”
BackgroundInfluentialHorvath, L., Thienpont, B., Zhao, L., Wolf, D. G. F., & Pircher, A. (2020) · Molecular Cancer · doi:10.1186/s12943-020-01260-z · Cited by 288
“As observed preclinically, PARPi induces genetic instability, increases TMB and neoantigen burden via DDR deficiency and may be involved in PD-L1 upregulation by cancer cells [97, 98].”
Background
Metadata
- Authors
- Li, A., Yi, M., Qin, S., Chu, Q., Luo, S., & Wu, K.
- Affiliations
- Zhengzhou University (CN)
- Tongji Hospital (CN)
- Corresponding author
- Luo, Suxia
- Wu, Kongming
- Venue
- Journal of Hematology & Oncology
- Published
- 2019-09-14
- Volume
- 12
- Issue
- 1
- Pages
- 98-98
- ISSN
- 1756-8722 (ISSN-L)
- PMC
- PMC6744711
- OpenAlex
- W2972535107
- Cited by
- 143
- References
- 130
- Citations by year
- 2026: 10 · 2025: 14 · 2024: 14 · 2023: 16 · 2022: 21 · 2021: 36 · 2020: 30 · 2019: 2
- FWCI
- 2.17
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Hematology & Oncology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81874120, 81572608, 81672984)
- Wuhan Municipal Science and Technology Bureau (2017060201010170)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- immune checkpoint blockade, PARP inhibitors, combination therapy, cancer immunotherapy, tumor immune microenvironment, PD-1, CTLA-4, immunosuppression, tumor immunogenicity, T cell priming, cross-presentation, drug resistance, cancer-immunity cycle
- MeSH terms
- Poly(ADP-ribose) Polymerase Inhibitors, Antineoplastic Agents, Humans, Immunotherapy, Poly(ADP-ribose) Polymerases
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