Tumor microenvironment and immune evasion in head and neck squamous cell carcinoma

Areeg Elmusrati , Justin Wang , Cun-Yu Wang

International Journal of Oral Science ›› 2021, Vol. 13 ›› Issue (1) : 24

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International Journal of Oral Science ›› 2021, Vol. 13 ›› Issue (1) : 24 DOI: 10.1038/s41368-021-00131-7
Review Article

Tumor microenvironment and immune evasion in head and neck squamous cell carcinoma

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Abstract

Head and neck squamous cell carcinoma (HNSCC), an aggressive malignancy, is characterized by high morbidity and low survival rates with limited therapeutic options outside of regional surgery, conventional cytotoxic chemotherapy, and irradiation. Increasing studies have supported the synergistic role of the tumor microenvironment (TME) in cancer advancement. The immune system, in particular, plays a key role in surveillance against the initiation, development, and progression of HNSCC. The understanding of how neoplastic cells evolve and evade the immune system whether through self-immunogenicity manipulation, or expression of immunosuppressive mediators, provides the foundation for the development of advanced therapies. Furthermore, the crosstalk between cancer cells and the host immune system have a detrimental effect on the TME promoting angiogenesis, proliferation, and metastasis. This review provides a recent insight into the role of the key inflammatory cells infiltrating the TME, with a focus on reviewing immunological principles related to HNSCC, as cancer immunosurveillance and immune escape, including a brief overview of current immunotherapeutic strategies and ongoing clinical trials.

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Areeg Elmusrati, Justin Wang, Cun-Yu Wang. Tumor microenvironment and immune evasion in head and neck squamous cell carcinoma. International Journal of Oral Science, 2021, 13(1): 24 DOI:10.1038/s41368-021-00131-7

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References

[1]

Bray F, . Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA: Cancer J. Clin., 2018, 68: 394-424.

[2]

Siegel R, Miller K, Jemal A. Cancer statistics, 2020. CA Cancer J. Clin., 2020, 70: 7-30.

[3]

Cleary C, . Biological features of human papillomavirus-related head and neck cancers contributing to improved response. Clin. Oncol., 2016, 28: 467-474.

[4]

Warnakulasuriya S. Living with oral cancer: epidemiology with particular reference to prevalence and life-style changes that influence survival. Oral. Oncol., 2010, 46: 407-410.

[5]

Fakhry C, D’Souza G. Discussing the diagnosis of HPV-OSCC: common questions and answers. Oral. Oncol., 2013, 49: 863-871.

[6]

DeFilippis R, Goodwin E, Wu L, DiMaio D. Endogenous human papillomavirus E6 and E7 proteins differentially regulate proliferation, senescence, and apoptosis in HeLa cervical carcinoma cells. J. Virol., 2003, 77: 1551-1563.

[7]

Saada-Bouzid E, Peyrade F, Guigay J. Molecular genetics of head and neck squamous cell carcinoma. Curr. Opin. Oncol., 2019, 31: 131-137.

[8]

Cancer Genome Atlas Network. Comprehensive genomic characterization of head and neck squamous cell carcinomas. Nature, 2015, 517: 576-582.

[9]

Zhang Y, . Subtypes of HPV-positive head and neck cancers are associated with HPV characteristics, copy number alterations, PIK3CA mutation, and pathway signatures. Clin. Cancer Res., 2016, 22: 4735-4745.

[10]

Rieckmann T, . HNSCC cell lines positive for HPV and p16 possess higher cellular radiosensitivity due to an impaired DSB repair capacity. Radiother. Oncol., 2013, 107: 242-246.

[11]

Zanoni D, Patel S, Shah J. Changes in the 8th edition of the American Joint Committee on Cancer (AJCC) staging of head and neck cancer: rationale and implications. Curr. Oncol. Rep., 2019, 21: 52-59.

[12]

Jiang X, Ye J, Dong Z, Hu S, Xiao M. Novel genetic alterations and their impact on target therapy response in head and neck squamous cell carcinoma. Cancer Manag. Res., 2019, 11: 1321-1336.

[13]

Li H, . Genomic analysis of head and neck squamous cell carcinoma cell lines and human tumors: a rational approach to preclinical model selection. Mol. Cancer Res., 2014, 12: 571-582.

[14]

Stransky N, . The mutational landscape of head and neck squamous cell carcinoma. Science, 2011, 333: 1157-1160.

[15]

Pietras K, Östman A. Hallmarks of cancer: interactions with the tumor stroma. Exp. Cell Res., 2010, 316: 1324-1331.

[16]

Forster M, Devlin M. Immune checkpoint inhibition in head and neck cancer. Front Oncol., 2018, 29: 310.

[17]

Agrawal N, . Exome sequencing of head and neck squamous cell carcinoma reveals inactivating mutations in NOTCH1. Science, 2011, 333: 1154-1157.

[18]

Hammerman P, Hayes D, Grandis J. Therapeutic insights from genomic studies of head and neck squamous cell carcinomas. Cancer Discov., 2015, 5: 239-244.

[19]

Keck M, . Integrative analysis of head and neck cancer identifies two biologically distinct HPV and three non-HPV subtypes. Clin. Cancer Res., 2015, 21: 870-881.

[20]

Puram S, . Single-cell transcriptomic analysis of primary and metastatic tumor ecosystems in head and neck cancer. Cell, 2017, 171: 1611-1624.

[21]

Lindenbergh-Van Der Plas M, . Prognostic significance of truncating TP53 mutations in head and neck squamous cell carcinoma. Clin. Cancer Res., 2011, 17: 3733-3741.

[22]

Leemans C, Braakhuis B, Brakenhoff R. The molecular biology of head and neck cancer. Nat. Rev. Cancer, 2011, 11: 9-22.

[23]

Brown C, Lain S, Verma C, Fersht A, Lane D. Awakening guardian angels: drugging the p53 pathway. Nat. Rev. Cancer, 2009, 9: 862-873.

[24]

Leemans C, Snijders P, Brakenhoff R. The molecular landscape of head and neck cancer. Nat. Rev. Cancer, 2018, 18: 269-282.

[25]

Smeets S, . Genetic classification of oral and oropharyngeal carcinomas identifies subgroups with a different prognosis. Anal. Cell Pathol., 2009, 31: 291-300.

[26]

Plath M, Broglie M, Förbs D, Stoeckli S, Jochum W. Prognostic significance of cell cycle-associated proteins p16, pRB, cyclin D1 and p53 in resected oropharyngeal carcinoma. J. Otolaryngol. Head. Neck Surg., 2018, 47: 53-62.

[27]

Bray S. Notch signalling in context. Nat. Rev. Mol. Cell Biol., 2016, 17: 722-735.

[28]

Yap L, . The opposing roles of NOTCH signalling in head and neck cancer: a mini review. Oral. Dis., 2015, 21: 850-857.

[29]

Fukusumi T, Califano J. The NOTCH pathway in head and neck squamous cell carcinoma. J. Dent. Res., 2018, 97: 645-653.

[30]

Nowell C, Radtke F. Notch as a tumour suppressor. Nat. Rev. Cancer, 2017, 17: 145-159.

[31]

Cai Y, Dodhia S, Su G. Dysregulations in the PI3K pathway and targeted therapies for head and neck squamous cell carcinoma. Oncotarget, 2017, 8: 22203-22217.

[32]

Lui V, . Frequent mutation of the PI3K pathway in head and neck cancer defines predictive biomarkers. Cancer Discov., 2013, 3: 761-769.

[33]

Janku F, . PIK3CA mutation H1047R is associated with response to PI3K/AKT/mTOR signaling pathway inhibitors in early-phase clinical trials. Cancer Res., 2013, 73: 276-284.

[34]

Kim H, . Mouse–human co-clinical trials demonstrate superior anti-tumour effects of buparlisib (BKM120) and cetuximab combination in squamous cell carcinoma of head and neck. Br. J. Cancer, 2020, 23: 1-10.

[35]

Dunn L, . A Phase 1b Study of Cetuximab and BYL719 (Alpelisib) concurrent with intensity modulated radiation therapy in stage III–IVB head and neck squamous cell carcinoma. Int. J. Radiat. Oncol. Biol. Phys., 2020, 106: 564-570.

[36]

Soulières D, . Buparlisib and paclitaxel in patients with platinum-pretreated recurrent or metastatic squamous cell carcinoma of the head and neck (BERIL-1): a randomised, double-blind, placebo-controlled phase 2 trial. Lancet Oncol., 2017, 18: 323-335.

[37]

Dubot C, . Comprehensive genomic profiling of head and neck squamous cell carcinoma reveals FGFR1 amplifications and tumour genomic alterations burden as prognostic biomarkers of survival. Eur. J. Cancer, 2018, 91: 47-55.

[38]

Tan Y, . Mitigating SOX2-potentiated immune escape of head and neck squamous cell carcinoma with a STING-inducing nanosatellite vaccine. Clin. Cancer Res., 2018, 24: 4242-4255.

[39]

Wuebben E, Rizzino A. The dark side of SOX2: cancer-a comprehensive overview. Oncotarget, 2017, 8: 44917-44943.

[40]

Balkwill F, Mantovani A. Inflammation and cancer: back to Virchow?. Lancet, 2001, 357: 539-545.

[41]

Bissell M, Hall H, Parry G. How does the extracellular matrix direct gene expression?. J. Theor. Biol., 1982, 99: 31-68.

[42]

Peltanova B, Raudenska M, Masarik M. Effect of tumor microenvironment on pathogenesis of the head and neck squamous cell carcinoma: a systematic review. Mol. Cancer, 2019, 18: 63-87.

[43]

Joyce J, Pollard J. Microenvironmental regulation of metastasis. Nat. Rev. Cancer, 2009, 9: 239-252.

[44]

Weinberg R. The Biology of Cancer (Garland Science, 2013).

[45]

Liu T, Zhou L, Li D, Andl T, Zhang Y. Cancer-associated fibroblasts build and secure the tumor microenvironment. Front Cell Dev. Biol., 2019, 24: 60.

[46]

Qin X, . Cancer-associated fibroblast-derived IL-6 promotes head and neck cancer progression via the osteopontin-NF-kappa B signaling pathway. Theranostics, 2018, 8: 92-940.

[47]

Elmusrati A, Pilborough A, Khurram S, Lambert D. Cancer-associated fibroblasts promote bone invasion in oral squamous cell carcinoma. Br. J. Cancer, 2017, 117: 867-875.

[48]

Yu B, . Periostin secreted by cancer-associated fibroblasts promotes cancer stemness in head and neck cancer by activating protein tyrosine kinase 7. Cell Death Dis., 2018, 9: 1-8.

[49]

New J, . Secretory autophagy in cancer-associated fibroblasts promotes head and neck cancer progression and offers a novel therapeutic target. Cancer Res., 2017, 77: 6679-6691.

[50]

Takahashi H, . Immunosuppressive activity of cancer-associated fibroblasts in head and neck squamous cell carcinoma. Cancer Immunol. Immunother., 2015, 64: 1407-1417.

[51]

Greten F, Grivennikov S. Inflammation and cancer: triggers, mechanisms, and consequences. Immunity, 2019, 51: 27-41.

[52]

Cillo A, . Immune landscape of viral-and carcinogen-driven head and neck cancer. Immunity, 2020, 52: 183-199.

[53]

Mantovani A, Marchesi F, Malesci A, Laghi L, Allavena P. Tumour-associated macrophages as treatment targets in oncology. Nat. Rev. Clin. Oncol., 2017, 14: 399-416.

[54]

Tan H, Wang N, Feng Y. Autophagy mediated activation of RelB/p52 responsible for the reprogramming of tumour associated macrophages. Eur. J. Cancer, 2016, 61: S49.

[55]

Curry J, . Tumor microenvironment in head and neck squamous cell carcinoma. Semin Oncol., 2014, 41: 217-234.

[56]

Koontongkaew S. The tumor microenvironment contribution to development, growth, invasion and metastasis of head and neck squamous cell carcinomas. J. Cancer, 2013, 4: 66-83.

[57]

Senovilla L, . Trial watch: prognostic and predictive value of the immune infiltrate in cancer. Oncoimmunology, 2012, 1: 1323-1343.

[58]

Fridman W, Pagès F, Sautes-Fridman C, Galon J. The immune contexture in human tumours: impact on clinical outcome. Nat. Rev. Cancer, 2012, 12: 298-306.

[59]

Ferrandino R, . Neutrophil‐to‐lymphocyte ratio as a prognostic indicator for overall and cancer‐specific survival in squamous cell carcinoma of the head and neck. Head Neck, 2020, 42: 2839-2840.

[60]

Hanakawa H, . Regulatory T-cell infiltration in tongue squamous cell carcinoma. Acta Otolaryngol., 2014, 134: 859-864.

[61]

Boucek J, . Regulatory T cells and their prognostic value for patients with squamous cell carcinoma of the head and neck. J. Cell Mol. Med., 2010, 14: 426-433.

[62]

Sasidharan Nair V, Elkord E. Immune checkpoint inhibitors in cancer therapy: a focus on T‐regulatory cells. Immunol. Cell Biol., 2018, 96: 21-33.

[63]

Jaillon S, . Neutrophil diversity and plasticity in tumour progression and therapy. Nat. Rev. Cancer, 2020, 20: 485-503.

[64]

Mascarella M, Mannard E, Silva S, Zeitouni A. Neutrophil‐to‐lymphocyte ratio in head and neck cancer prognosis: a systematic review and meta‐analysis. Head Neck, 2018, 40: 1091-1100.

[65]

Shaul M, Fridlender Z. Tumour-associated neutrophils in patients with cancer. Nat. Rev. Clin. Oncol., 2019, 16: 601-620.

[66]

Valero C, . Pretreatment count of peripheral neutrophils, monocytes, and lymphocytes as independent prognostic factor in patients with head and neck cancer. Head Neck, 2017, 39: 219-226.

[67]

Michaeli J, . Tumor-associated neutrophils induce apoptosis of non-activated CD8 T-cells in a TNFα and NO-dependent mechanism, promoting a tumor-supportive environment. Oncoimmunology, 2017, 6: e1356965-12.

[68]

Moses K, Brandau S. Human neutrophils: their role in cancer and relation to myeloid-derived suppressor cells. Semin. Immunol., 2016, 28: 187-196.

[69]

Fridlender Z, . Polarization of tumor-associated neutrophil phenotype by TGF-β: “N1” versus “N2” TAN. Cancer Cell., 2009, 16: 183-194.

[70]

Sionov R, Fridlender Z, Granot Z. The multifaceted roles neutrophils play in the tumor microenvironment. Cancer Microenviron., 2015, 8: 125-158.

[71]

Yasumatsu R, . Monitoring the neutrophil‐to‐lymphocyte ratio may be useful for predicting the anticancer effect of nivolumab in recurrent or metastatic head and neck cancer. Head Neck, 2019, 41: 2610-2618.

[72]

Rachidi S, . Neutrophil‐to‐lymphocyte ratio and overall survival in all sites of head and neck squamous cell carcinoma. Head Neck, 2016, 38: E1068-E1074.

[73]

Bhatia A, Burtness B. Human papillomavirus–associated oropharyngeal cancer: defining risk groups and clinical trials. J. Clin. Oncol., 2015, 33: 3243-3250.

[74]

Keskinov A, Shurin M. Myeloid regulatory cells in tumor spreading and metastasis. Immunobiology, 2015, 220: 236-242.

[75]

Umansky V, Blattner C, Gebhardt C, Utikal J. The role of myeloid-derived suppressor cells (MDSC) in cancer progression. Vaccines, 2016, 4: 36.

[76]

Parker K, Beury D, Ostrand-Rosenberg S. Myeloid-derived suppressor cells: critical cells driving immune suppression in the tumor microenvironment. Adv. Cancer Res., 2015, 128: 95-139.

[77]

Weber R, . Myeloid-derived suppressor cells hinder the anti-cancer activity of immune checkpoint inhibitors. Front. Immunol., 2018, 9: 1310.

[78]

Greene S, . Inhibition of MDSC trafficking with SX-682, a CXCR1/2 inhibitor, enhances NK-cell immunotherapy in head and neck cancer models. Clin. Cancer Res., 2020, 26: 1420-1431.

[79]

Sawa-Wejksza K, Kandefer-Szerszeń M. Tumor-associated macrophages as target for antitumor therapy. Arch. Immunol. Ther. Exp., 2018, 66: 97-111.

[80]

Sun H, . TGF-β1/TβRII/Smad3 signaling pathway promotes VEGF expression in oral squamous cell carcinoma tumor-associated macrophages. Biochem. Biophys. Res. Commun., 2018, 497: 583-590.

[81]

Gao L, . Tumor associated macrophages induce epithelial to mesenchymal transition via the EGFR/ERK1/2 pathway in head and neck squamous cell carcinoma. Oncol. Rep., 2018, 40: 2558-2572.

[82]

Petruzzi M, Cherubini K, Salum F, De Figueiredo M. Role of tumour-associated macrophages in oral squamous cells carcinoma progression: an update on current knowledge. Diagn. Pathol., 2017, 12: 1-7.

[83]

Lewis C, Pollard J. Distinct role of macrophages in different tumor microenvironments. Cancer Res., 2006, 66: 605-612.

[84]

Mantovani A, Schioppa T, Porta C, Allavena P, Sica A. Role of tumor-associated macrophages in tumor progression and invasion. Cancer Metastasis Rev., 2006, 25: 315-322.

[85]

Laoui D, . Tumor-associated macrophages in breast cancer: distinct subsets, distinct functions. Int J. Dev. Biol., 2011, 55: 861-867.

[86]

Mosser D, Edwards J. Exploring the full spectrum of macrophage activation. Nat. Rev. Immunol., 2008, 8: 958-969.

[87]

Mantovani A, . The chemokine system in diverse forms of macrophage activation and polarization. Trends Immunol., 2004, 25: 677-686.

[88]

Zhang Q, . Prognostic significance of tumor-associated macrophages in solid tumor: a meta-analysis of the literature. PloS ONE, 2012, 7: e50946.

[89]

Kouketsu A, . Regulatory T cells and M2-polarized tumour-associated macrophages are associated with the oncogenesis and progression of oral squamous cell carcinoma. Int J. Oral. Maxillofac. Surg., 2019, 48: 1279-1288.

[90]

Petty A, Yang Y. Tumor-associated macrophages: implications in cancer immunotherapy. Immunotherapy, 2017, 9: 289-302.

[91]

Morvan M, Lanier L. NK cells and cancer: you can teach innate cells new tricks. Nat. Rev. Cancer, 2016, 16: 7-19.

[92]

Santos E, de Matos F, de Morais E, Galvão H, de Almeida Freitas R. Evaluation of Cd8+ and natural killer cells defense in oral and oropharyngeal squamous cell carcinoma. J. Craniomaxillofac. Surg., 2019, 47: 676-681.

[93]

Mandal R, . The head and neck cancer immune landscape and its immunotherapeutic implications. JCI Insight, 2016, 1: 1-18.

[94]

Muntasell A, . Targeting NK-cell checkpoints for cancer immunotherapy. Curr. Opin. Immunol., 2017, 45: 73-81.

[95]

Ralli M, . The role of cytokines in head and neck squamous cell carcinoma: a review. Clin. Ter., 2020, 171: e268-e274.

[96]

Pang X, Tang Y, Liang X. Transforming growth factor-β signaling in head and neck squamous cell carcinoma: Insights into cellular responses. Oncol. Lett., 2018, 16: 4799-4806.

[97]

Ma H, . Interferon-alpha promotes immunosuppression through IFNAR1/STAT1 signalling in head and neck squamous cell carcinoma. BJC, 2019, 120: 317-330.

[98]

Johnson D, O’Keefe R, Grandis J. Targeting the IL-6/JAK/STAT3 signalling axis in cancer. Nat. Rev. Clin. Oncol., 2018, 15: 234-248.

[99]

Geiger J, Grandis J, Bauman J. The STAT3 pathway as a therapeutic target in head and neck cancer: Barriers and innovations. Oral. Oncol., 2016, 56: 84-92.

[100]

Oweida A, . STAT3 modulation of regulatory T cells in response to radiation therapy in head and neck cancer. J. Natl Cancer Inst., 2019, 111: 1339-1349.

[101]

Vassilakopoulou M, Psyrri A, Argiris A. Targeting angiogenesis in head and neck cancer. Oral. Oncol., 2015, 51: 409-415.

[102]

Ferris R. Immunology and immunotherapy of head and neck cancer. J. Clin. Oncol., 2015, 33: 3293-3304.

[103]

Jie H, . Intratumoral regulatory T cells upregulate immunosuppressive molecules in head and neck cancer patients. Br. J. Cancer, 2013, 109: 2629-2635.

[104]

Ma S, . Blockade of adenosine A2A receptor enhances CD8+ T cells response and decreases regulatory T cells in head and neck squamous cell carcinoma. Mol. Cancer, 2017, 16: 99-114.

[105]

Kansy B, . PD-1 status in CD8+ T cells associates with survival and anti-PD-1 therapeutic outcomes in head and neck cancer. Cancer Res., 2017, 77: 6353-6364.

[106]

Togashi Y, Shitara K, Nishikawa H. Regulatory T cells in cancer immunosuppression—implications for anticancer therapy. Nat. Rev. Clin. Oncol., 2019, 16: 356-371.

[107]

Allen C, Clavijo P, Van Waes C, Chen Z. Anti-tumor immunity in head and neck cancer: understanding the evidence, how tumors escape and immunotherapeutic approaches. Cancers, 2015, 7: 2397-2414.

[108]

Komohara Y, Jinushi M, Takeya M. Clinical significance of macrophage heterogeneity in human malignant tumors. Cancer Sci., 2014, 105: 1-8.

[109]

Brooks J, . Development and validation of a combined hypoxia and immune prognostic classifier for head and neck cancer. Clin. Cancer Res., 2019, 25: 5315-5328.

[110]

Zhu G, . Long noncoding RNA HAS2‐AS1 mediates hypoxia‐induced invasiveness of oral squamous cell carcinoma. Mol. Carcinog., 2017, 56: 2210-2222.

[111]

Coliat P, . Constitutive or induced HIF-2 addiction is involved in resistance to Anti-EGFR treatment and radiation therapy in HNSCC. Cancers, 2019, 11: 1607-1623.

[112]

Mirghani H, . Oropharyngeal cancers: relationship between epidermal growth factor receptor alterations and human papillomavirus status. Eur. J. Cancer, 2014, 50: 1100-1111.

[113]

Chouaib S, Noman M, Kosmatopoulos K, Curran M. Hypoxic stress: obstacles and opportunities for innovative immunotherapy of cancer. Oncogene, 2017, 36: 439-445.

[114]

Burnet M. Cancer—a biological approach: III. viruses associated with neoplastic conditions. IV. Practical applications. Br. Med. J., 1957, 13: 841-847.

[115]

Kiessling R, Klein E, Pross H, Wigzell H. “Natural’’□ killer cells in the mouse. II. Cytotoxic cells with specificity for mouse Moloney leukemia cells. Characteristics of the killer cell. Eur. J. Immunol., 1975, 5: 117-121.

[116]

D’Souza G, . Epidemiology of head and neck squamous cell cancer among HIV-infected patients. J. Acquir Immune Defic. Syndr., 2014, 65: 603-619.

[117]

Gillison M. Oropharyngeal cancer: a potential consequence of concomitant HPV and HIV infection. Curr. Opin. Oncol., 2009, 21: 439-444.

[118]

Rabinovics N, . Cancer of the head and neck region in solid organ transplant recipients. Head Neck, 2014, 36: 181-186.

[119]

Mittal D, Gubin M, Schreiber R, Smyth M. New insights into cancer immunoediting and its three component phases—elimination, equilibrium and escape. Curr. Opin. Immunol., 2014, 27: 16-25.

[120]

Seliger B. Novel insights into the molecular mechanisms of HLA class I abnormalities. Cancer Immunol. Immunother., 2012, 61: 249-254.

[121]

Whiteside T. Tumor-induced death of immune cells: its mechanisms and consequences. Semin Cancer Biol., 2002, 12: 43-50.

[122]

Tong C, Kao J, Sikora A. Recognizing and reversing the immunosuppressive tumor microenvironment of head and neck cancer. Immunol. Res., 2012, 54: 266-274.

[123]

Duechler M, Peczek L, Szubert M, Suzin J. Influence of hypoxia inducible factors on the immune microenvironment in ovarian cancer. Anticancer Res., 2014, 34: 2811-2819.

[124]

Barsoum I, Koti M, Siemens D, Graham C. Mechanisms of hypoxia mediated immune escape in cancer. Cancer Res., 2014, 74: 7185-7190.

[125]

Barsoum I, Smallwood C, Siemens D, Graham C. A mechanism of hypoxia-mediated escape from adaptive immunity in cancer cells. Cancer Res., 2014, 74: 665-674.

[126]

Vaupel, P. & Multhoff, G. Hypoxia-/HIF-1α-driven factors of the tumor microenvironment impeding antitumor immune responses and promoting malignant progression. in Oxygen Transport to Tissue XL. 171–175 (Springer, 2018).

[127]

Schilling D, Tetzlaff F, Konrad S, Li W, Multhoff G. A hypoxia-induced decrease of either MICA/B or Hsp70 on the membrane of tumor cells mediates immune escape from NK cells. Cell Stress Chaperones, 2015, 20: 139-147.

[128]

Garrido F, Algarra I, García-Lora A. The escape of cancer from T lymphocytes: immunoselection of MHC class I loss variants harboring structural-irreversible “hard” lesions. Cancer Immunol. Immunother., 2010, 59: 1601-1606.

[129]

Ferris R, Whiteside T, Ferrone S. Immune escape associated with functional defects in antigen-processing machinery in head and neck cancer. Clin. Cancer Res., 2006, 12: 3890-3895.

[130]

Ribas A, Wolchok J. Cancer immunotherapy using checkpoint blockade. Science, 2018, 359: 1350-1355.

[131]

Postow M, Callahan M, Wolchok J. Immune checkpoint blockade in cancer therapy. J. Clin. Oncol., 2015, 33: 974.

[132]

Abril-Rodriguez G, Ribas A. SnapShot: immune checkpoint inhibitors. Cancer Cell, 2017, 31: 848-848.

[133]

Zandberg D, Strome S. The role of the PD-L1: PD-1 pathway in squamous cell carcinoma of the head and neck. Oral. Oncol., 2014, 50: 627-632.

[134]

Deng W, . LAG-3 confers poor prognosis and its blockade reshapes antitumor response in head and neck squamous cell carcinoma. Oncoimmunology, 2016, 5: 1239005-1239014.

[135]

Strauss L, Bergmann C, Gooding W, Johnson J, Whiteside T. The frequency and suppressor function of CD4+ CD25highFoxp3+ T cells in the circulation of patients with squamous cell carcinoma of the head and neck. Clin. Cancer Res., 2007, 13: 6301-6311.

[136]

Zhou Q, . Coexpression of Tim-3 and PD-1 identifies a CD8+ T-cell exhaustion phenotype in mice with disseminated acute myelogenous leukemia. Am. J. Hematol., 2011, 117: 4501-4510.

[137]

Jie H, . Increased PD-1+ and TIM-3+ TILs during cetuximab therapy inversely correlate with response in head and neck cancer patients. Cancer Immunol. Res., 2017, 5: 408-416.

[138]

Wang, C., et al. CD276 expression enables squamous cell carcinoma stem cells to evade immune surveillance. Cell Stem Cell. https://doi.org/10.1016/j.stem.2021.04.011 (2021).

[139]

Bauml J, . Pembrolizumab for platinum-and cetuximab-refractory head and neck cancer: results from a single arm, phase II study. J. Clin. Oncol., 2017, 35: 1542-1549.

[140]

Bonner J, . Radiotherapy plus cetuximab for locoregionally advanced head and neck cancer: 5-year survival data from a phase 3 randomised trial, and relation between cetuximab-induced rash and survival. Lancet Oncol., 2010, 11: 21-28.

[141]

Tumeh P, . PD-1 blockade induces responses by inhibiting adaptive immune resistance. Nature, 2014, 515: 568-571.

[142]

Hamid O, . Safety and tumor responses with lambrolizumab (anti–PD-1) in melanoma. Engl. J. Med., 2013, 369: 134-144.

[143]

Herbst R, . Predictive correlates of response to the anti-PD-L1 antibody MPDL3280A in cancer patients. Nature, 2014, 515: 563-567.

[144]

Clara J, Monge C, Yang Y, Takebe N. Targeting signalling pathways and the immune microenvironment of cancer stem cells—a clinical update. Nat. Rev. Clin. Oncol., 2020, 17: 204-232.

[145]

Jia L, Zhang W, Wang C. BMI1 inhibition eliminates residual cancer stem cells after PD1 blockade and activates antitumor immunity to prevent metastasis and relapse. Cell Stem Cell, 2020, 27: 1-16.

[146]

Prager B, Xie Q, Bao S, Rich J. Cancer stem cells: the architects of the tumor ecosystem. Cell Stem Cell, 2019, 24: 41-53.

[147]

Chen D, Wang C. Targeting cancer stem cells in squamous cell carcinoma. Precis. Clin. Med., 2019, 2: 152-165.

[148]

Zhang D, Tang D, Rycaj K. Cancer stem cells: regulation programs, immunological properties and immunotherapy. Semin. Cancer Biol., 2018, 52: 94-106.

[149]

Batlle E, Clevers H. Cancer stem cells revisited. Nat. Med., 2017, 23: 1124-1134.

[150]

Chen D, . Targeting BMI1+ cancer stem cells overcomes chemoresistance and inhibits metastases in squamous cell carcinoma. Cell Stem Cell, 2017, 20: 621-634.

[151]

Makena M, Ranjan A, Thirumala V, Reddy A. Cancer stem cells: road to therapeutic resistance and strategies to overcome resistance. Biochimic. Biophys. Acta Mol. Basis Dis., 2020, 1866: 165339.

[152]

Zhang W, . Targeting KDM4A epigenetically activates tumor-cell-intrinsic immunity by inducing DNA replication stress. Mol. Cel., 2021, 81: 2148-2165.e9.

[153]

D’Souza G, Dempsey A. The role of HPV in head and neck cancer and review of the HPV vaccine. Prev. Med., 2011, 53: S5-S11.

[154]

Rehman H, Silk A, Kane M, Kaufman H. Into the clinic: Talimogene laherparepvec (T-VEC), a first-in-class intratumoral oncolytic viral therapy. J. Immunother. Cancer, 2016, 4: 1-8.

[155]

Harrington K, . Phase I/II study of oncolytic HSVGM-CSF in combination with radiotherapy and cisplatin in untreated stage III/IV squamous cell cancer of the head and neck. Clin. Cancer Res., 2010, 16: 4005-4015.

[156]

Knochelmann H, . CAR T cells in solid tumors: blueprints for building effective therapies. Front. Immunol., 2018, 27: 1740.

[157]

Qureshi H, Lee S. Immunotherapy approaches beyond PD-1 inhibition: the future of cellular therapy for head and neck squamous cell carcinoma. Curr. Treat. Options Oncol., 2019, 20: 31.

[158]

Stevanovic S, . Treatment of metastatic human papillomavirus-associated epithelial cancers with adoptive transfer of tumor-infiltrating T cells. J. Clin. Oncol., 2018, 36: 3004-3004.

[159]

Papa S, . A phase I trial of T4 CAR T-cell immunotherapy in head and neck squamous cancer (HNSCC). J. Clin. Oncol., 2018, 36: 3046-3046.

[160]

Jenkins R, Barbie D, Flaherty K. Mechanisms of resistance to immune checkpoint inhibitors. BJC, 2018, 118: 9-16.

[161]

Kalafati L, . Innate immune training of granulopoiesis promotes anti-tumor activity. Cell, 2020, 29: 771-785.

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