Background

Tumor initiation and subsequent progression are usually long-term processes, spread over time and conditioned by diverse aspects. Many cancers develop on the basis of chronic inflammation; however, despite dozens of years of research, little is known about the factors triggering neoplastic transformation under these conditions. Molecular characterization of both pathogenetic states, i.e., similarities and differences between chronic inflammation and cancer, is also poorly defined. The secretory activity of tumor cells may change the immunophenotype of immune cells and modify the extracellular microenvironment, which allows the bypass of host defense mechanisms and seems to have diagnostic and prognostic value. The phenomenon of immunosuppression is also present during chronic inflammation, and the development of cancer, due to its duration, predisposes patients to the promotion of chronic inflammation. The aim of our work was to discuss the above issues based on the latest scientific insights. A theoretical mechanism of cancer immunosuppression is also proposed.

Conclusions

Development of solid tumors may occur both during acute and chronic phases of inflammation. Differences in the regulation of immune responses between precancerous states and the cancers resulting from them emphasize the importance of immunosuppressive factors in oncogenesis. Cancer cells may, through their secretory activity and extracellular transport mechanisms, enhance deterioration of the immune system which, in turn, may have prognostic implications.

中文翻译：

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实体瘤发病机制中免疫反应的建模及其预后意义。

背景

肿瘤的发生和随后的进展通常是长期的过程，随着时间的推移而扩散，并受到不同方面的影响。许多癌症是在慢性炎症的基础上发展起来的。然而，尽管进行了数十年的研究，但对于在这些条件下触发肿瘤转化的因素知之甚少。两种致病状态的分子特征，即慢性炎症和癌症之间的相似性和差异性，也尚不清楚。肿瘤细胞的分泌活性可能会改变免疫细胞的免疫表型并改变细胞外微环境，从而绕过宿主防御机制，似乎具有诊断和预后价值。慢性炎症期间也存在免疫抑制现象，而癌症的发展由于其持续时间，使患者易于促进慢性炎症。我们工作的目的是根据最新的科学见解讨论上述问题。还提出了癌症免疫抑制的理论机制。

结论

实体瘤的发展可能发生在炎症的急性期和慢性期。癌前状态和由此产生的癌症之间免疫反应调节的差异强调了免疫抑制因素在肿瘤发生中的重要性。癌细胞可能通过其分泌活性和细胞外运输机制，加剧免疫系统的恶化，进而可能产生预后影响。