%0 Journal Article
%T Interconnected Dynamics Among Inflammation, Immunity, and Cancer–From Tumor Suppression to Tumor Onset, Promotion, and Progression
%A Elena-Teodora Tâlvan
%A Liviuta Budișan
%A Călin Ilie Mohor
%A Valentin Grecu
%A Ioana Berindan-Neagoe
%A Victor Cristea
%A George Oprinca
%A Adrian Cristian
%J Archive of International Journal of Cancer and Allied Science
%@ 3108-4834
%D 2023
%V 3
%N 1
%R 10.51847/nbSWsJHJMZ
%P 25-28
%X Inflammation serves as the body’s defensive response to harmful stimuli. In the acute phase, immune cells such as neutrophils—which act as the principal responders—along with NK cells, DCs, and macrophages, secrete inflammatory mediators including cytokines, growth factors, and proteolytic enzymes, thereby facilitating tissue repair and regeneration. However, when this response becomes chronic, macrophages become the dominant immune population, succeeded by T and B cells, leading to the continuous release of cytokines, growth factors, and enzymatic mediators. This persistent inflammatory state initiates destructive effects on epithelial structures, immune cells, and vascular components, ultimately contributing to pro-tumoral processes. In the context of cancer, inflammation exhibits a dual nature: it can act as a protective mechanism or as a driving force behind tumor development. This dichotomy is largely regulated by key transcription factors such as nuclear factor-kappa beta (NF-KB) and signal transducer and activator of transcription-3 (STAT3), both of which are essential in modulating immune cell behavior and facilitating tumor progression at different stages of cancer. The present article focuses on the role of inflammatory mediators in both acute and chronic inflammatory microenvironments and their involvement in a wide array of cellular, immunological, and vascular alterations.
%U https://smerpub.com/article/interconnected-dynamics-among-inflammation-immunity-and-cancerfrom-tumor-suppression-to-tumor-ons-rrmvlzrlcopegrq