PD-1/PD-L1 Blockade: A New Promising Therapy for the Treatment of Pancreatic Cancer?
DOI:
https://doi.org/10.17140/POJ-2-e007Keywords:
monocytes, B-cells, den-dritic cells, and tumor-infiltrating lymphocytesAbstract
Programmed cell death protein 1 (PD-1), a member of the CD28 family, is an immune-checkpoint receptor expressed on a variety of immune cells, such as T-cells, monocytes, B-cells, den-dritic cells, and tumor-infiltrating lymphocytes (TILs).1 PD-1 ma-jor role is to limit the activity of T-cells in peripheral tissues at the time of an inflammatory response to constrain autoimmunity and tissue damage.1,2 Engagement of PD-1 by one of its two known ligands (PD-L1 and PD-L2) inhibits kinases involved in immune cell activation.2 Interestingly, PD-1 has an opposite function in Treglymphocytes.
References
Keir ME, Butte MJ, Freeman GJ, Sharpe AH. PD-1 and its li-gands in tolerance and immunity. Annu Rev Immunol. 2008; 26: 677- 704. doi: 10.1146/annurev.immunol.26.021607.090331 e6 Gagliano N
Pardoll DM. The blockade of immune checkpoints in cancer immunotherapy. Nat Rev Cancer. 2012; 12: 252-264. doi: 10.1038/ nrc3239
Francisco LM, Salinas VH, Brown KE, et al. PD-L1 regulates the development, maintenance, and function of induced regulatory T cells. J Exp Med. 2009; 206: 3015-3029. doi: 10.1084/jem.20090847
Chen J, Jiang CC, Jin L, Zhang XD. Regulation of PD-L1: A novel role of pro-survival signalling in cancer. Ann Oncol. 2016; 27: 409-416. doi: 10.1093/annonc/mdv615
Zou W, Wolchok JD, Chen L. PD-L1 (B7-H1) and PD-1 pathway blockade for cancer therapy: Mechanisms, response biomarkers, and combinations. Sci Transl Med. 2016; 8: 328rv4. doi: 10.1126/ scitranslmed.aad7118
Gibbons Johnson RM, Dong H. Functional expression of pro-grammed death-ligand 1 (B7-H1) by immune cells and tumor cells. Front Immunol. 2017; 8: 961. doi: 10.3389/fimmu.2017.00961
Gong J, Chehrazi-Raffle A, Reddi S, Salgia R. Development of PD-1 and PD-L1 inhibitors as a form of cancer immunotherapy: A comprehensive review of registration trials and future consid-erations. J Immunother Cancer. 2018; 6: 8. doi: 10.1186/s40425-018- 0316-z
Hamanishi J, Mandai M, Matsumura N, Abiko K, Baba T, Koni-shi I. PD-1/PD-L1 blockade in cancer treatment: perspectives and issues. Int J Clin Oncol. 2016; 21: 462-473. doi: 10.1007/s10147- 016-0959-z
Yang Y, Pang Z, Ding N, et al. The efficacy and potential pre-dictive factors of PD-1/PD-L1 blockades in epithelial carcinoma patients: A systematic review and meta analysis. Oncotarget. 2016; 7: 74350-74361. doi: 10.18632/oncotarget.11291
Kamisawa T, Wood LD, Itoi T, Takaori K. Pancreatic cancer. Lancet. 2016; 388: 73-85. doi: 10.1016/S0140-6736(16)00141-0
Chiaravalli M, Reni M, O’Reilly EM. Pancreatic ductal adeno-carcinoma: State-of-the-art 2017 and new therapeutic strategies. Cancer Treat Rev. 2017; 60: 32-43. doi: 10.1016/j.ctrv.2017.08.007
Amrutkar M, Gladhaug IP. Pancreatic cancer chemoresistance to gemcitabine. Cancers (Basel). 2017; 9. pii: E157. doi: 10.3390/ cancers9110157
Ansari D, Carvajo M, Bauden M, Andersson R. Pancreatic can-cer stroma: Controversies and current insights. Scand J Gastroenterol. 2017; 52: 641-646. doi: 10.1080/00365521.2017.1293726
Sun XJ, Jiang TH, Zhang XP, Mao AW. Role of the tumor mi-croenvironment in pancreatic adenocarcinoma. Front Biosci (Land-mark Ed). 2016; 21: 31-41. doi: 10.2741/4374
Wang S, Huang S, Sun YL. Epithelial-mesenchymal transition , et al Editorial | Volume 2 | Number 1| Pancreas Open J. 2018; 2(1): e5-e7. doi: 10.17140/POJ-2-e007 in pancreatic cancer: A review. Biomed Res Int. 2017; 2017: 2646148. doi: 10.1155/2017/2646148
Feng M, Xiong G, Cao Z, et al. PD-1/PD-L1 and immuno-therapy for pancreatic cancer. Cancer Lett. 2017; 407: 57-65. doi: 10.1016/j.canlet.2017.08.006
Foley K, Kim V, Jaffee E, Zheng L. Current progress in im-munotherapy for pancreatic cancer. Cancer Lett. 2016; 381: 244-251. doi: 10.1016/j.canlet.2015.12.020
Martinez-Bosch N, Vinaixa J, Navarro P. Immune evasion in pancreatic cancer: From mechanisms to therapy. Cancers (Basel). 2018; 10. pii: E6. doi: 10.3390/cancers10010006
Melstrom LG, Salazar MD, Diamond DJ. The pancreatic cancer microenvironment: A true double agent. J Surg Oncol. 2017; 116: 7-15. doi: 10.1002/jso.24643
Pergamo M, Miller G. Myeloid-derived suppressor cells and their role in pancreatic cancer. Cancer Gene Ther. 2017; 24: 100-105. doi: 10.1038/cgt.2016.65
Seo YD, Pillarisetty VG. T-cell programming in pancreatic ad-enocarcinoma: A review. Cancer Gene Ther. 2017; 24: 106-113. doi: 10.1038/cgt.2016.66
Habtezion A, Edderkaoui M, Pandol SJ. Macrophages and pan-creatic ductal adenocarcinoma. Cancer Lett. 2016; 381: 211-216. doi: 10.1016/j.canlet.2015.11.049 Submit your article to this journal | https://openventio.org/submit-manuscript/ Editorial | Volume 2 | Number 1| Gagliano N
Skelton RA, Javed A, Zheng L, He J. Overcoming the resistance of pancreatic cancer to immune checkpoint inhibitors. J Surg Oncol. 2017; 116: 55-62. doi: 10.1002/jso.24642
Jamieson NB, Maker AV. Gene-expression profiling to predict responsiveness to immunotherapy. Cancer Gene Ther. 2017; 24: 134- 140. doi: 10.1038/cgt.2016.63
Balachandran VP, Łuksza M, Zhao JN, et al. Identification of unique neoantigen qualities in long-term survivors of pancreatic cancer. Nature. 2017; 551: 512-516. doi: 10.1038/nature24462
Humphris JL, Patch AM, Nones K, et al. Hypermutation In Pancreatic Cancer. Gastroenterology. 2017; 152: 68-74.e2. doi: 10.1053/j.gastro.2016.09.060
Pandha H, Rigg A, John J, Lemoine N. Loss of expression of antigen-presenting molecules in human pancreatic cancer and pan-creatic cancer cell lines. Clin Exp Immunol. 2007; 148: 127-135. doi: 10.1111/j.1365-2249.2006.03289.x
Spranger S. Mechanisms of tumor escape in the context of the T-cell-inflamed and the non-T-cell-inflamed tumor microen-vironment. Int Immunol. 2016; 28: 383-391. doi: 10.1093/intimm/ dxw014
Pitt JM, Vétizou M, Daillère R, et al. Resistance mechanisms to immune-checkpoint blockade in cancer: Tumor-intrinsic and -extrinsic factors. Immunity. 2016; 44: 1255-1269. doi: 10.1016/j. immuni.2016.06.001. , et al e7
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