The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Combination therapy strategies for improving PD‐1 blockade efficacy: a new era in cancer immunotherapy
Open accessAbstract
Programmed death 1 (PD‐1) is an immune checkpoint molecule that negatively regulates T‐cell immune function through the interaction with its ligand PD‐L1. Blockage of this interaction unleashes the immune system to fight cancer. Immunotherapy using PD‐1 blockade has led to a paradigm shift in the field of cancer drug discovery, owing to its durable effect against a wide variety of cancers with limited adverse effects. A brief history and development of PD‐1 blockade, from the initial discovery of PD‐1 to the recent clinical output of this therapy, have been summarized here. Despite its tremendous clinical success rate over other cancer treatments, PD‐1 blockade has its own pitfall; a significant fraction of patients remains unresponsive to this therapy. The key to improve the PD‐1 blockade therapy is the development of combination therapies. As this approach has garnered worldwide interest, here, we have summarized the recent trends in the development of PD‐1 blockade‐based combination therapies and the ongoing clinical trials. These include combinations with checkpoint inhibitors, radiation therapy, chemotherapy and several other existing cancer treatments. Importantly, FDA has approved PD‐1 blockade agent to be used in combination with either CTLA‐4 blockade or chemotherapy. Responsiveness to the PD‐1 blockade therapy is affected by tumour and immune system‐related factors. The role of the immune system, especially T cells, in determining the responsiveness has been poorly studied compared with those factors related to the tumour side. Energy metabolism has emerged as one of the important regulatory mechanisms for the function and differentiation of T cells. We have documented here the recent results regarding the augmentation of PD‐1 blockade efficacy by augmenting mitochondrial energy metabolism of T cell.
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Cites
Nivolumab versus Docetaxel in Advanced Squamous-Cell Non–Small-Cell Lung Cancer
Brahmer, J., Reckamp, K. L., Baas, P., Crinò, L., Eberhardt, W. E. E., Poddubskaya, E., Antonia, S., Pluzanski, A., Vokes, E. E., Holgado, E., et al. (2015) · New England Journal of Medicine · doi:10.1056/nejmoa1504627 · Cited by 8,447
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PD-1 blockade induces responses by inhibiting adaptive immune resistance
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PD-1 and Its Ligands in Tolerance and Immunity
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Elements of cancer immunity and the cancer–immune set point
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Tumor-associated B7-H1 promotes T-cell apoptosis: A potential mechanism of immune evasion
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Nivolumab plus Ipilimumab in Advanced Melanoma
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PD-L2 is a second ligand for PD-1 and inhibits T cell activation
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Self-citationAn immunogenic personal neoantigen vaccine for patients with melanoma
Ott, P. A., Hu, Z., Keskin, D. B., Shukla, S. A., Sun, J., Bozym, D. J., Zhang, W., Luoma, A., Giobbie-Hurder, A., Peter, L., et al. (2017) · Nature · doi:10.1038/nature22991 · Cited by 2,936
Cited by
IL-6 in inflammation, autoimmunity and cancer
Hirano, T. (2021) · International Immunology · doi:10.1093/intimm/dxaa078 · Cited by 1,453
“Inhibitors of immune checkpoints, such as inhibitors of CTLA-4 and PD-1 and their ligands, have been shown to be effective to treat several cancers such as melanoma (25, 220).”
BackgroundRegulatory mechanisms of PD-1/PD-L1 in cancers
Lin, X., Kang, K., Chen, P., Zeng, Z., Li, G., Xiong, W., Yi, M., & Xiang, B. (2024) · Molecular Cancer · doi:10.1186/s12943-024-02023-w · Cited by 784
Chowdhury, P. S., Chamoto, K., Kumar, A., & Honjo, T. (2018) · Cancer Immunology Research · doi:10.1158/2326-6066.cir-18-0095 · Cited by 353
Self-citationA snapshot of the PD-1/PD-L1 pathway
Ghosh, C., Luong, G., & Sun, Y. (2021) · Journal of Cancer · doi:10.7150/jca.57334 · Cited by 292
Obesity and Breast Cancer: Role of Leptin
Sánchez-Jiménez, F., Pérez-Pérez, A., de la Cruz-Merino, L., & Sánchez-Margalet, V. (2019) · Frontiers in Oncology · doi:10.3389/fonc.2019.00596 · Cited by 268
Metadata
- Authors
- Chowdhury, P. S., Chamoto, K., & Honjo, T.
- Venue
- Journal of Internal Medicine
- Publisher
- Wiley
- Published
- 2017-11-16
- Volume
- 283
- Issue
- 2
- Pages
- 110-120
- ISSN
- 0954-6820 (ISSN-L)
- 1365-2796
- OpenAlex
- W2765943070
- Cited by
- 191
- References
- 31
- FWCI
- 7.97
- Type
- journal article
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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