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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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“In the meanwhile, based on the hypothesis that patients with mutations in BRCA1/2 or other HR components are prone to possess higher mutation burden, multiple clinical trials are ongoing to explore the efficacy of combination therapy of PARPi and immune checkpoint inhibitors [56].”
BackgroundActivating cGAS-STING pathway for the optimal effect of cancer immunotherapy
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“Therefore, immunotherapy-based combination strategy attracts extensive attention for synergistic efficacy and lower risk of resistance [20, 21].”
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“The first signal is the specific binding between T cell receptor (TCR) and antigenic peptide-major histocompatibility complex (pMHC) [59].”
BackgroundImmune activation and response to pembrolizumab in POLE-mutant endometrial cancer
Mehnert, J. M., Panda, A., Zhong, J., Hirshfield, K. M., Damare, S., Lane, K., Sokol, L. O., Stein, M. N., Rodriguez-Rodriquez, L., Kaufman, H. L., et al. (2016) · Journal of Clinical Investigation · doi:10.1172/jci84940 · Cited by 376
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“The viability of SCLC is highly dependent on hyperactive PARP, thus SCLC is prone to be sensitive to PARPi treatment [92].”
BackgroundInfluentialStructural Basis of Detection and Signaling of DNA Single-Strand Breaks by Human PARP-1
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“PARPi-mediated catastrophic DNA damage and subsequently acute inflammation could rapidly elevate the abundance of type I IFN via cGASSTING pathway [117].”
BackgroundT cell anergy and costimulation
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“In the absence of PARPi, low-level DNA damages at baseline induce the chronic inflammation which promotes the initiation and development of cancers [23].”
BackgroundPreclinical and clinical development of neoantigen vaccines
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BackgroundPARP inhibitors in ovarian cancer
Franzese, E., Centonze, S., Diana, A., Carlino, F., Guerrera, L. P., Napoli, M. D., Vita, F. D., Pignata, S., Ciardiello, F., & Orditura, M. (2018) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2018.12.002 · Cited by 220
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“PD-1 is expressed on multiple activated immune cells including T cells, B cells, natural killer (NK) cells, and dendritic cells (DCs) [63].”
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“Neoantigens are proteins exclusively expressed on cancer cells due to mutationmediated sequence alterations [4, 5].”
BackgroundKonstantinopoulos, P. A., Waggoner, S. E., Vidal, G. A., Mita, M. M., Fleming, G. F., Holloway, R. W., Le, L. V., Sachdev, J. C., Chapman‐Davis, E., Colón‐Otero, G., et al. (2018) · Journal of Clinical Oncology · doi:10.1200/jco.2018.36.15_suppl.106 · Cited by 143
Checkpoint inhibitors in hematological malignancies
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Cellular and molecular mechanisms in cancer immune escape: a comprehensive review
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BackgroundBiochemical mechanisms of chromosomal translocations resulting from DNA double-strand breaks
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The role of neoantigen in immune checkpoint blockade therapy
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DNA double-strand break repair and chromosome translocations
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“HR is an effective repair approach with high fidelity which uses the sister copy of damaged sites as the template [36].”
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“A growing body of evidence indicated that loss of cancer-specific immunodominant epitopes and T cell repertoire, downregulation of antigen processing, and presentation machinery, as well as immunosuppressive microenvironment could lead to immune tolerance to tumor antigens [9, 10].”
BackgroundInterferon-α Suppresses cAMP to Disarm Human Regulatory T Cells
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“Then, PARP is dissociated from the DNA damage site by autoPARylation [31].”
BackgroundThe promise of PD-1 inhibitors in gastro-esophageal cancers: microsatellite instability vs. PD-L1
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Clinical applications of PD-L1 bioassays for cancer immunotherapy
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“heterogeneity and dynamically evolving cancer antigen spectrum, it is hard to cure a tumor by monotherapy and tumors cells eventually acquire resistance [19].”
BackgroundDhawan, M. S., Bartelink, I. H., Aggarwal, R. R., Leng, J. X., Zhang, J. Z., Pawłowska, N., Terranova-Barberio, M., Grabowsky, J. A., Gewitz, A. D., Chien, A. J., et al. (2017) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-17-0703 · Cited by 79 · cited 1×
“It is notable that PARPi combining chemotherapy is easy to induce dose-limiting toxicity [55].”
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Immune checkpoint inhibitors: new strategies to checkmate cancer
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“CTLA-4 is constitutively expressed on Tregs and transiently upregulated on conventional T cells after activation [71].”
BackgroundEmerging therapies for breast cancer
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Poly(ADP-ribose) polymerase activity and inhibition in cancer
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“The investigations of combination therapy were mainly conducted in BRCA1/2 mutated tumors [119].”
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“The preliminary data of NCT02484404 showed that the combination therapy of Olaparib and Durvalumab effectively reduced tumor burden (measured by PSA reduction > 50%) in 8/17 unselected metastatic castrate-resistant prostate cancer [123].”
BackgroundBergs, J. W. J., Krawczyk, P. M., Borovski, T., ten Cate, R., Rodermond, H. M., Stap, J., Medema, J. P., HAVEMAN, J., Essers, J., Chris van, B. R. E. E., et al. (2012) · DNA repair · doi:10.1016/j.dnarep.2012.10.008 · Cited by 49 · cited 10×
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BackgroundImmunotherapy in genitourinary malignancies
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“Since the first ICI was approved for metastatic melanoma patients in 2011, numerous ICIs have entered clinical practice [75, 76].”
BackgroundCancer vaccine strategies: translation from mice to human clinical trials
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A Transendocytosis Perspective on the CD28/CTLA-4 Pathway
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BackgroundDissecting PARP inhibitor resistance with functional genomics
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“The anti-cancer effect of PARPi has not been completely understood yet, which is initially attributed to inhibition of catalytic effect [33].”
BackgroundUnexpected Synergy Reveals New Therapeutic Strategy in SCLC
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“The preexisting TIL is the prerequisite of tumor-killing effect of ICI, thus PARPi could synergize with ICI and decrease the risk of drug resistance [112].”
Background
Cited by
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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
Dias, M. P., Moser, S. C., Ganesan, S., & Jonkers, J. (2021) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-021-00532-x · Cited by 544
Westin, S. N., Moore, K. N., Chon, H. S., Lee, J., Pepin, J. T., Sundborg, M., Shai, A., de la Garza, J., Nishio, S., Gold, M. A., et al. (2023) · Journal of Clinical Oncology · doi:10.1200/jco.23.02132 · Cited by 389
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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