Research status of immune checkpoint inhibitors in the treatment of advanced malignant tumors with hyperprogressive diseases

Abstract

Abstract:

Immune checkpoint inhibitors have become extremely important treatments to benefit long-term survival of patients with a variety of advanced malignant tumors. However, a small number of patients will develop hyperprogressive disease (HPD), leading to a sharp decline in survival and quality of life, and there is still a lack of effective rescue treatment. Recent studies have shown that the occurrence of HPD is related to clinical factors such as advanced age, tumor recurrence and multi-focus metastasis. The possible mechanisms include inhibitory immune regulation, regulatory T cell aggregation, abnormal inflammatory response, proto-oncogene activation, tumor suppressor gene mutation and other pathways. Reasonable screening, accurate detection, close monitoring and combined treatment may reduce the risk of immunotherapy for HPD.

Key words:Neoplasms,Immunotherapy,Immune checkpoint inhibitors,Hyperprogressive disease

Zhou Shengyu. Research status of immune checkpoint inhibitors in the treatment of advanced malignant tumors with hyperprogressive diseases[J]. Journal of International Oncology, 2020, 47(2): 93-97.

References45

[1]	Ferris RL, Blumenschein G Jr, Fayette J , et al. Nivolumab for recurrent squamous-cell carcinoma of the head and neck[J]. N Engl J Med, 2016,375(19):1856-1867. DOI: 10.1056/NEJMoa 1602252. doi:10.1056/NEJMoa1602252
[2]	Borghaei H, Paz-Ares L, Horn L , et al. Nivolumab versus docetaxel in advanced nonsquamous non-small-cell lung cancer[J]. N Engl J Med, 2015,373(17):1627-1639. DOI: 10.1056/NEJMoa 1507643. doi:10.1056/NEJMoa1507643
[3]	Motzer RJ, Escudier B, McDermott DF , et al. Nivolumab versus everolimus in advanced renal-cell carcinoma[J]. N Engl J Med, 2015,373(19):1803-1813. DOI: 10.1056/NEJMoa1510665. doi:10.1056/NEJMoa1510665
[4]	Champiat S, Ferrara R, Massard C , et al. Hyperprogressive disease: recognizing a novel pattern to improve patient management[J]. Nat Rev Clin Oncol, 2018,15(12):748-762. DOI: 10.1038/s41571-018-0111-2. doi:10.1038/s41571-018-0111-2
[5]	Champiat S, Dercle L, Ammari S , et al. Hyperprogressive disease is a new pattern of progression in cancer patients treated by anti-PD-1/PD-L1[J]. Clin Cancer Res, 2017,23(8):1920-1928. DOI: 10.1158/1078-0432.CCR-16-1741.
[6]	Saâda-Bouzid E, Defaucheux C, Karabajakian A , et al. Hyperprogression during anti-PD-1/PD-L1 therapy in patients with recurrent and/or metastatic head and neck squamous cell carcinoma[J]. Ann Oncol, 2017,28(7):1605-1611. DOI: 10.1093/annonc/mdx178. doi:10.1093/annonc/mdx178
[7]	Ferrara R, Mezquita L, Texier M , et al. Hyperprogressive disease in patients with advanced non-small cell lung cancer treated with PD-1/PD-L1 inhibitors or with single-agent chemotherapy[J]. JAMA Oncol, 2018,4(11):1543-1552. DOI: 10.1001/jamaoncol.2018.3676. doi:10.1001/jamaoncol.2018.3676
[8]	Kato S, Goodman A, Walavalkar V , et al. Hyperprogressors after immunotherapy: analysis of genomic alterations associated with accelerated growth rate[J]. Clin Cancer Res, 2017,23(15):4242-4250. DOI: 10.1158/1078-0432.CCR-16-3133. doi:10.1158/1078-0432.CCR-16-3133
[9]	Sasaki A, Nakamura Y, Mishima S , et al. Predictive factors for hyperprogressive disease during nivolumab as anti-PD1 treatment in patients with advanced gastric cancer[J]. Gastric Cancer, 2019,22(4):793-802. DOI: 10.1007/s10120-018-00922-8. doi:10.1007/s10120-018-00922-8
[10]	Funazo T, Nomizo T, Kim YH . Liver metastasis is associated with poor progression-free survival in patients with non-small cell lung cancer treated with nivolumab[J]. J Thorac Oncol, 2017,12(9):e140-e141. DOI: 10.1016/j.jtho.2017.04.027. doi:10.1016/j.jtho.2017.04.027
[11]	Weiss GJ, Beck J, Braun DP , et al. Tumor cell-free DNA copy number instability predicts therapeutic response to immunotherapy[J]. Clin Cancer Res, 2017,23(17):5074-5081. DOI: 10.1158/1078-0432.CCR-17-0231. doi:10.1158/1078-0432.CCR-17-0231
[12]	Zaretsky JM, Garcia-Diaz A, Shin DS , et al. Mutations associated with acquired resistance to PD-1 blockade in melanoma[J]. N Engl J Med, 2016 , 375(9):819-829. DOI: 10.1056/NEJMoa1604958. doi:10.1056/NEJMoa1604958
[13]	Koyama S, Akbay EA, Li YY , et al. Adaptive resistance to therapeutic PD-1 blockade is associated with upregulation of alternative immune checkpoints[J]. Nat Commun, 2016,7:10501. DOI: 10.1038/ncomms10501. doi:10.1038/ncomms10501
[14]	Lo Russo G, Moro M, Sommariva M , et al. Antibody-Fc/FcR interaction on macrophages as a mechanism for hyperprogressive disease in non-small cell lung cancer subsequent to PD-1/PD-L1 blockade[J]. Clin Cancer Res, 2019,25(3):989-999. DOI: 10.1158/1078-0432.CCR-18-1390. doi:10.1158/1078-0432.CCR-18-1390
[15]	Adams TA, Vail PJ, Ruiz A , et al. Composite analysis of immunological and metabolic markers defines novel subtypes of triple negative breast cancer[J]. Mod Pathol, 2018,31(2):288-298. DOI: 10.1038/modpathol.2017.126. doi:10.1038/modpathol.2017.126
[16]	Kubota K, Moriyama M, Furukawa S , et al. CD163⁺CD204⁺tumor-associated macrophages contribute to T cell regulation via interleukin-10 and PD-L1 production in oral squamous cell carcinoma [J]. Sci Rep, 2017,7(1):1755. DOI: 10.1038/s41598-017-01661-z. doi:10.1038/s41598-017-01661-z
[17]	Lamichhane P, Karyampudi L, Shreeder B , et al. IL10 release upon PD-1 blockade sustains immunosuppression in ovarian cancer[J]. Cancer Res, 2017,77(23):6667-6678. DOI: 10.1158/0008-5472.CAN-17-0740. doi:10.1158/0008-5472.CAN-17-0740
[18]	Sun Z, Fourcade J, Pagliano O , et al. IL10 and PD-1 cooperate to limit the activity of tumor-specific CD8⁺T cells [J]. Cancer Res, 2015 , 75(8):1635-1644. DOI: 10.1158/0008-5472.CAN-14-3016. doi:10.1158/0008-5472.CAN-14-3016
[19]	Mantovani A, Sica A . Macrophages, innate immunity and cancer: balance, tolerance, and diversity[J]. Curr Opin Immunol, 2010,22(2):231-237. DOI: 10.1016/j.coi.2010.01.009. doi:10.1016/j.coi.2010.01.009
[20]	Spranger S, Spaapen RM, Zha Y , et al. Up-regulation of PD-L1, IDO, and T(regs) in the melanoma tumor microenvironment is driven by CD8(+) T cells Sci Transl Med, 2013, 5(200): 200ra116. DOI: 10.1126/scitranslmed.3006504.
[21]	Engblom C, Pfirschke C, Pittet MJ . The role of myeloid cells in cancer therapies[J]. Nat Rev Cancer, 2016,16(7):447-462. DOI: 10.1038/nrc.2016.54. doi:10.1038/nrc.2016.54
[22]	Gao J, Shi LZ, Zhao H , et al. Loss of IFN-γ pathway genes in tumor cells as a mechanism of resistance to anti-CTLA4 therapy[J]. Cell, 2016, 167(2):397-404. e9. DOI: 10.1016/j.cell.2016.08.069. doi:10.1016/j.cell.2016.08.069
[23]	Mandai M, Hamanishi J, Abiko K , et al. Dual faces of IFNγ in cancer progression: a role of PD-L1 induction in the determination of pro- and antitumor immunity[J]. Clin Cancer Res, 2016,22(10):2329-2334. DOI: 10.1158/1078-0432.CCR-16-0224. doi:10.1158/1078-0432.CCR-16-0224
[24]	Huang RY, Francois A, McGray AR , et al. Compensatory upregulation of PD-1, LAG-3, and CTLA-4 limits the efficacy of single-agent checkpoint blockade in metastatic ovarian cancer[J]. Oncoimmunology, 2016,6(1):e1249561. DOI: 10.1080/2162402X.2016.1249561. doi:10.1080/2162402X.2016.1249561
[25]	Kahan SM, Wherry EJ, Zajac AJ . T cell exhaustion during persistent viral infections[J]. Virology. 2015, 479-480:180-193. DOI: 10.1016/j.virol.2014.12.033. doi:10.1016/j.virol.2014.12.033
[26]	Togasaki K, Sukawa Y, Kanai T , et al. Clinical efficacy of immune checkpoint inhibitors in the treatment of unresectable advanced or recurrent gastric cancer: an evidence-based review of therapies[J]. Onco Targets Ther, 2018,11:8239-8250. DOI: 10.2147/OTT.S152514.
[27]	Barnaba V, Schinzari V . Induction, control, and plasticity of Treg cells: the immune regulatory network revised?[J]. Eur J Immunol, 2013,43(2):318-322. DOI: 10.1002/eji.201243265.
[28]	Lowther DE, Goods BA, Lucca LE , et al. PD-1 marks dysfunctional regulatory T cells in malignant gliomas[J]. JCI Insight, 2016, 1(5). pii: e85935. DOI: 10.1172/jci.insight.85935.
[29]	Ellestad KK, Thangavelu G, Ewen CL , et al. PD-1 is not required for natural or peripherally induced regulatory T cells: severe autoimmunity despite normal production of regulatory T cells[J]. Eur J Immunol, 2014 , 44(12):3560-3572. DOI: 10.1002/eji.201444688.
[30]	Moorman JP, Wang JM, Zhang Y , et al. Tim-3 pathway controls regulatory and effector T cell balance during hepatitis C virus infection[J]. J Immunol, 2012,189(2):755-766. DOI: 10.4049/jimmunol.1200162.
[31]	Nakamura K, Smyth MJ . Targeting cancer-related inflammation in the era of immunotherapy[J]. Immunol Cell Biol, 2017,95(4):325-332. DOI: 10.1038/icb.2016.126.
[32]	Dulos J, Carven GJ, van Boxtel SJ , et al. PD-1 blockade augments Th1 and Th17 and suppresses Th2 responses in peripheral blood from patients with prostate and advanced melanoma cancer[J]. J Immunother, 2012,35(2):169-178. DOI: 10.1097/CJI.0b013e318247a4e7.
[33]	Koenen HJ, Smeets RL, Vink PM , et al. Human CD25highFoxp3pos regulatory T cells differentiate into IL-17-producing cells[J]. Blood, 2008,112(6):2340-2352. DOI: 10.1182/blood-2008-01-133967.
[34]	Kargl J, Busch SE, Yang GH , et al. Neutrophils dominate the immune cell composition in non-small cell lung cancer[J]. Nat Commun, 2017,8:14381. DOI: 10.1038/ncomms14381.
[35]	Fabre J, Giustiniani J, Garbar C , et al. Targeting the tumor microenvironment: the protumor effects of IL-17 related to cancer type[J]. Int J Mol Sci, 2016, 17(9). pii: E1433. DOI: 10.3390/ijms17091433.
[36]	Dong Y, Sun Q, Zhang X . PD-1 and its ligands are important immune checkpoints in cancer[J]. Oncotarget, 2017,8(2):2171-2186. DOI: 10.18632/oncotarget.13895.
[37]	龙丽, 段赵宁, 蔡海贝 , 等. NFATc1对裸鼠上皮性卵巢癌移植瘤脉管生成的影响[J]. 中国病理生理杂志, 2016,32(2):193-200. DOI: 10.3969/j.issn.1000-4718.2016.02.001.
[38]	Ratner L, Waldmann TA, Janakiram M , et al. Rapid progression of adult T-cell leukemia-lymphoma after PD-1 inhibitor therapy[J]. N Engl J Med, 2018,378(20):1947-1948. DOI: 10.1056/NEJMc1803181.
[39]	Du S, McCall N, Park K , et al. Blockade of tumor-expressed PD-1 promotes lung cancer growth[J]. Oncoimmunology, 2018,7(4):e1408747. DOI: 10.1080/2162402X.2017.1408747.
[40]	Dong ZY, Zhong WZ, Zhang XC , et al. Potential predictive value of TP53 and KRAS mutation status for response to PD-1 blockade immunotherapy in lung adenocarcinoma[J]. Clin Cancer Res, 2017,23(12):3012-3024. DOI: 10.1158/1078-0432.
[41]	Mariathasan S, Turley SJ, Nickles D , et al. TGFβ attenuates tumour response to PD-L1 blockade by contributing to exclusion of T cells[J]. Nature, 2018,554(7693):544-548. DOI: 10.1038/nature25501.
[42]	Xiong D, Wang Y, Singavi AK , et al. Immunogenomic landscape contributes to hyperprogressive disease after anti-PD-1 immunotherapy for cancer[J]. iScience, 2018,9:258-277. DOI: 10.1016/j.isci.2018.10.021.
[43]	Niknafs N, Kim D, Kim R , et al. MuPIT interactive: webserver for mapping variant positions to annotated, interactive 3D structures[J]. Hum Genet, 2013,132(11):1235-1243. DOI: 10.1007/s00439-013-1325-0.
[44]	Gossage L, Eisen T, Maher ER . VHL, the story of a tumour suppressor gene[J]. Nat Rev Cancer, 2015,15(1):55-64. DOI: 10.1038/nrc3844. doi:10.1038/nrc3844
[45]	Kammerer-Jacquet SF, Crouzet L, Brunot A , et al. Independent association of PD-L1 expression with noninactivated VHL clear cell renal cell carcinoma-A finding with therapeutic potential[J]. Int J Cancer, 2017,140(1):142-148. DOI: 10.1002/ijc.30429.