Adaptive antitumor immune responses, either cellular or humoral, aim at eliminating tumor cells expressing the cognate antigens. There are some instances, however, where these same immune responses have tumor-promoting effects. These effects can lead to the expansion of antigen-negative tumor cells, tumor cell proliferation and tumor growth, metastatic dissemination, resistance to antitumor therapy and apoptotic stimuli, acquisition of tumor-initiating potential and activation of various forms of survival mechanisms. We describe the basic mechanisms that underlie tumor-promoting adaptive immune responses and try to identify the variables that induce the switching of a tumor-inhibitory, cellular or humoral immune response, into a tumor-promoting one. We suggest that tumor-promoting adaptive immune responses may be at the origin of at least a fraction of hyperprogressive diseases (HPD) that are observed in cancer patients during therapy with immune checkpoint inhibitors (ICI) and, less frequently, with single-agent chemotherapy. We also propose the use of non-invasive biomarkers allowing to predict which patients may undergo HPD during ICI and other forms of antitumor therapy. Eventually, we suggest possibilities of therapeutic intervention allowing to inhibit tumor-promoting adaptive immune responses.

细胞或体液的适应性抗肿瘤免疫应答旨在消除表达同源抗原的肿瘤细胞。但是，在某些情况下，这些相同的免疫反应也具有促肿瘤作用。这些作用可导致抗原阴性肿瘤细胞扩增，肿瘤细胞增殖和肿瘤生长，转移性扩散，对抗肿瘤治疗和凋亡刺激的抵抗力，获得肿瘤起始潜力并激活各种形式的生存机制。我们描述了促进肿瘤的适应性免疫应答基础的基本机制，并试图确定诱导诱导肿瘤抑制性，细胞或体液免疫应答转换为促进肿瘤的变量。我们建议，在免疫检查点抑制剂（ICI）和单药化疗较少见的癌症患者中，促进肿瘤的适应性免疫应答可能至少是一部分过度进展性疾病（HPD）的起源。我们还建议使用非侵入性生物标志物，以预测哪些患者可能在ICI和其他形式的抗肿瘤治疗期间经历HPD。最终，我们提出了治疗干预的可能性，以抑制肿瘤促进的适应性免疫反应。我们还建议使用非侵入性生物标志物，以预测哪些患者可能在ICI和其他形式的抗肿瘤治疗期间经历HPD。最终，我们提出了治疗干预的可能性，以抑制肿瘤促进的适应性免疫反应。我们还建议使用非侵入性生物标志物，以预测哪些患者可能在ICI和其他形式的抗肿瘤治疗期间经历HPD。最终，我们提出了治疗干预的可能性，以抑制肿瘤促进的适应性免疫反应。