ReviewBiomolecules2026
Immunosenescence in Aging and Cancer: Molecular Mechanisms, Tumor Microenvironment Remodeling, and Therapeutic Implications.
Review in Biomolecules, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
0 citing papers in PubMed.
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunosenescence is the decline in immune function with age, which influences cancer progression and treatment outcomes. This process arises from multiple, interconnected molecular and cellular alterations. Among these, mitochondrial dysfunction in aged immune cells may contribute to impaired immune function through altered metabolism, redox imbalance, and inflammatory signaling. This review discusses mitochondrial alterations alongside other age-related mechanisms that shape immune cell function and may promote cancer development. We examine how DNA damage, telomere shortening, epigenetic changes, altered proteostasis, and mitochondrial dysfunction contribute to immune aging and potentially compromise antitumor immunity. The aged tumor microenvironment is characterized by increased immunosuppressive cell populations, persistent inflammatory signaling, and metabolic alterations that can influence tumor development and therapeutic responses. We also examine how aging affects response to current cancer immunotherapies. While some treatments show comparable efficacy in older and younger patients, others may be less effective in the context of age-related immune dysfunction. Older patients may also experience distinct toxicity profiles that require careful clinical management. Understanding how mitochondrial alterations interact with other mechanisms of aging to shape immunosenescence may help identify therapeutic strategies for cancer in older adults. Future approaches may combine interventions targeting mitochondrial fitness, chronic inflammation, and cellular senescence. However, clinical studies specifically designed to include older populations are needed to establish the relevance of these mechanisms in cancer and to guide age-specific therapeutic strategies.
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