2024
DOI: 10.1016/j.jare.2023.04.018
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Immunoregulation in cancer-associated cachexia

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Cited by 10 publications
(8 citation statements)
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“…Furthermore, altered immune responses that support tumor growth and metastasis also play critical roles in the development of cachexia. These findings support further investigation ( 9 , 10 ). Therefore, the current Research Topic entitled “ Immunology of cachexia ” is a step in this direction.…”
supporting
confidence: 91%
“…Furthermore, altered immune responses that support tumor growth and metastasis also play critical roles in the development of cachexia. These findings support further investigation ( 9 , 10 ). Therefore, the current Research Topic entitled “ Immunology of cachexia ” is a step in this direction.…”
supporting
confidence: 91%
“…Cancer-associated cachexia (CAC) is the persistent loss of skeletal muscle mass, with or without fat loss, that is not reversed by nutritional support [1]. In CAC, immune dysfunction caused by inflammation leads to a cytokine storm, raising the risk of multiple organ failure, and eventually impacting muscle and adipose tissue [2,3].…”
Section: Introductionmentioning
confidence: 99%
“…These factors, either in isolation or conjunction, expedite the deterioration of the tumor microenvironment, further propelling systemic inflammation, precipitating immune dysregulation, and engendering metabolic aberrations across multiple organ systems. 27 In the context wherein organs and neoplasms are at a comparatively balanced stage, the emergence of anorexia, characterized by diminished dietary intake, manifests as an initial symptomatology. The etiological mechanism governing anorexia is multifactorial, encompassing cellular components secreted by both the neoplasm and host, which predominantly contribute to this phenomenon.…”
Section: Introductionmentioning
confidence: 99%
“…An imbalance between pro‐inflammatory cytokines and anti‐inflammatory cytokines, modulated by inflammatory cells derived from the host and cancer cells (such as macrophages, neutrophils, fibroblasts, lymphocytes, and monocytes), culminates in the synthesis of pro‐inflammatory cytokines (such as interleukin‐1, interleukin‐6, interferon‐gamma, tumor necrosis factor‐α, TGF‐β, etc.). These factors, either in isolation or conjunction, expedite the deterioration of the tumor microenvironment, further propelling systemic inflammation, precipitating immune dysregulation, and engendering metabolic aberrations across multiple organ systems 27 …”
Section: Introductionmentioning
confidence: 99%
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