慢性炎症是持续的炎性刺激和调节机制紊乱的病理结果。它增加了肿瘤发展的风险，并在特定器官中编排了肿瘤发生的所有阶段。在某些癌症中，炎症过程为新生物转化创造了适当的条件。而在其他类型的癌症中，致癌性变化为导致肿瘤发展的炎性微环境铺平了道路。有趣的是，促进肿瘤和癌相关炎症的特征非常相似，共享复杂的基质（成纤维细胞和血管细胞）和炎症免疫细胞网络，共同形成肿瘤微环境（TME）。最初发展用于支持稳态的信号通路与TME中的转录和调节途径发生变化，促进非典型增殖、存活、血管生成和对适应性免疫的压制。这些转录和调节途径不可避免地促进了慢性炎症性疾病中的促癌炎症，并在各种肿瘤类型的微环境中滋生着"潜伏"炎症。除了确定多种癌症共同的靶位点外，调控免疫细胞可塑性和功能多样性的信号程序及其相互作用还可用于开发新的命运标记以及谱系追踪机制。在本文中，我们综述了建立炎症与肿瘤发展、进展和转移之间关联的重要分子机制和途径。我们还讨论了信号通路之间的相互作用及其设计的策略，重点关注这些相互作用机制，以利用合成致命药物组合进行靶向癌症治疗。版权所有 © 2023 Attiq and Afzal.

Unresolved inflammation is a pathological consequence of persistent inflammatory stimulus and perturbation in regulatory mechanisms. It increases the risk of tumour development and orchestrates all stages of tumorigenesis in selected organs. In certain cancers, inflammatory processes create the appropriate conditions for neoplastic transformation. While in other types, oncogenic changes pave the way for an inflammatory microenvironment that leads to tumour development. Of interest, hallmarks of tumour-promoting and cancer-associated inflammation are striking similar, sharing a complex network of stromal (fibroblasts and vascular cells) and inflammatory immune cells that collectively form the tumour microenvironment (TME). The cross-talks of signalling pathways initially developed to support homeostasis, change their role, and promote atypical proliferation, survival, angiogenesis, and subversion of adaptive immunity in TME. These transcriptional and regulatory pathways invariably contribute to cancer-promoting inflammation in chronic inflammatory disorders and foster "smouldering" inflammation in the microenvironment of various tumour types. Besides identifying common target sites of numerous cancer types, signalling programs and their cross-talks governing immune cells' plasticity and functional diversity can be used to develop new fate-mapping and lineage-tracing mechanisms. Here, we review the vital molecular mechanisms and pathways that establish the connection between inflammation and tumour development, progression, and metastasis. We also discussed the cross-talks between signalling pathways and devised strategies focusing on these interaction mechanisms to harness synthetic lethal drug combinations for targeted cancer therapy.Copyright © 2023 Attiq and Afzal.