Cancer Cachexia and Antitumor Immunity: Common Mediators and Potential Targets for New Therapies

Cancer cachexia syndrome (CCS) is a multifactorial metabolic syndrome affecting a significant proportion of patients. CCS is characterized by progressive weight loss, alterations of body composition and a systemic inflammatory status, which exerts a major impact on the host’s innate and adaptive imm...

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Bibliographic Details
Published in:Life (Basel, Switzerland) Switzerland), 2022-06, Vol.12 (6), p.880
Main Authors: Rounis, Konstantinos, Makrakis, Dimitrios, Gioulbasanis, Ioannis, Ekman, Simon, De Petris, Luigi, Mavroudis, Dimitris, Agelaki, Sofia
Format: Article
Language:English
Subjects:
Adaptive immunity
Antitumor activity
antitumor immunity
Biological activity
Body composition
Body fat
Body weight loss
Cachexia
Cancer
cancer cachexia
Cancer therapies
Cytokines
Deregulation
Genotype & phenotype
Growth factors
Health services
Homeostasis
Hypothalamus
Immune checkpoint inhibitors
Immune response
Immune system
Immunity
Immunotherapy
Infectious diseases
Inflammation
Lymphocytes
Medicin och hälsovetenskap
Melanoma
Metabolic disorders
Metabolic syndrome
Metabolism
Monoclonal antibodies
Pathophysiology
Patients
PD-1
Proteins
resistance to immunotherapy
Review
Subgroups
Tumor microenvironment
Tumor necrosis factor-TNF
Tumors
Weight loss
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Summary:Cancer cachexia syndrome (CCS) is a multifactorial metabolic syndrome affecting a significant proportion of patients. CCS is characterized by progressive weight loss, alterations of body composition and a systemic inflammatory status, which exerts a major impact on the host’s innate and adaptive immunity. Over the last few years, the development of immune checkpoint inhibitors (ICIs) transformed the treatment landscape for a wide spectrum of malignancies, creating an unprecedented opportunity for long term remissions in a significant subset of patients. Early clinical data indicate that CCS adversely impairs treatment outcomes of patients receiving ICIs. We herein reviewed existing evidence on the potential links between the mechanisms that promote the catabolic state in CCS and those that impair the antitumor immune response. We show that the biological mediators and processes leading to the development of CCS may also participate in the modulation and the sustainment of an immune suppressive tumor microenvironment and impaired anti-tumor immunity. Moreover, we demonstrate that the deregulation of the host’s metabolic homeostasis in cancer cachexia is associated with resistance to ICIs. Further research on the interrelation between cancer cachexia and anti-tumor immunity is required for the effective management of resistance to immunotherapy in this specific but large subgroup of ICI treated individuals.
ISSN:2075-1729
2075-1729
DOI:10.3390/life12060880