Cold tumors generally show low mutational burden and low infiltration of effector T cells. The pancreas, prostate, ovary, breast, and colon are placed into the category of cold tumors. In such tumors, effector T cells are either excluded from the tumor area or taken away from being in contact with tumor cells. The stromal reaction in the form of desmoplasia is important for the pathogenesis of tumors like the pancreas. Besides acting as a barrier for the penetration of drugs into the tumor area, the dense stroma presumably creates an immunosuppressive tumor microenvironment (TME), which accounts for low responses from tumor to immunotherapy. Cancer stem cells (CSCs) are an important part of the immunosuppressive complex within the TME. The presence of CSCs within the TME is related negatively to the activity of the antitumor immune system. Here, the question is how desmoplastic aggregates can influence the functionality of CSCs for promoting a cold pancreatic tumor immunity? This review is aimed at responding to this question, the disruption of which can be an effective strategy for improving responses from cold tumors to immunotherapy.

中文翻译：

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丰富的癌症干细胞、致密基质和冷免疫：胰腺癌中的相关事件


冷肿瘤通常表现出低突变负荷和低效应 T 细胞浸润。胰腺、前列腺、卵巢、乳腺和结肠都属于冷肿瘤的范畴。在此类肿瘤中，效应T细胞要么被排除在肿瘤区域之外，要么被剥夺与肿瘤细胞的接触。结缔组织形成形式的间质反应对于胰腺等肿瘤的发病机制很重要。除了充当药物渗透到肿瘤区域的屏障之外，致密基质可能会产生免疫抑制肿瘤微环境（TME），这是肿瘤对免疫治疗反应低的原因。癌症干细胞 (CSC) 是 TME 内免疫抑制复合物的重要组成部分。 TME 内 CSC 的存在与抗肿瘤免疫系统的活性呈负相关。这里的问题是促纤维聚集体如何影响CSC促进冷胰腺肿瘤免疫的功能？本综述旨在回答这个问题，破坏这个问题可能是改善冷肿瘤对免疫治疗反应的有效策略。