![]() 10 However, vaccine‐induced regression of high‐risk HPV infection is related to high‐grade CIN lesions, 11 but not established cervical cancers. ![]() 9Ĭancer therapeutic vaccines aim at eliciting effector T cells, especially tumor antigen‐specific CD8 + T cells that target tumor cells, without affecting the normal cells or tissues as demonstrated in clinical trials, such as those against melanoma. 8 Clinical trials also showed synergetic results of immune checkpoint blockade and therapeutic vaccination. 6 PD‐1 blockade combined with therapeutic vaccines synergises with each other to induce T‐cell‐mediated tumor control, as animal models have demonstrated, 7 including HPV16 E6/7‐transformed TC‐1 tumor models. 4 However, immune checkpoint inhibitor monotherapy, such as PD‐1 2 and CTLA‐4 blockade, 5 is less effective in the management of advanced cervical cancers. The use of immune checkpoint inhibitors has resulted in unprecedented rates of long‐lasting tumor responses in patients with a variety of solid tumors. 3 HPV‐related cancers are most severe in developing countries where HPV prophylactic vaccination rates are low. 2 Moreover, high‐risk HPV infection, especially HPV16 infection, is related to a fraction of head and neck epithelial carcinoma in both developed and undeveloped countries. 1 Cervical cancers are the third‐most common cancer in women worldwide. ![]() ![]() Human papillomavirus (HPV) infection accounted for 4.6% of 14 million new cancer cases reported worldwide in 2012, and HPV‐associated cancers comprise 29.1% of all 2.2 million infection‐related cancers, including nearly 100% of cervical cancers. ![]()
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