ReviewInternational journal of molecular sciences2025
Molecular Mechanisms Driving Metastatic Progression Within the Aged Tumor Microenvironment.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Synthesis, anti-proliferative evaluation, DFT,RSC advances · 2026Article
- The central role of the β-cell in diabetes: from monogenic forms to type 1, type 2, and gestational diabetes.Reviews in endocrine & metabolic disorders · 2026Review
- Editorial: Immune-genetic dynamics in disease progression and therapeutic strategies.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastasis remains the leading cause of cancer deaths, heavily influenced by aging-related biological processes. As global life expectancy increases, cancer incidence and progression complexity in older adults also rise, emphasizing the urgent need to understand how the aging tumor microenvironment (TME) promotes metastasis. This review explores the molecular and cellular mechanisms behind metastatic development in the aged TME, focusing on the combined impacts of cellular senescence, chronic inflammation (inflammaging), immune system decline, extracellular matrix (ECM) changes, and abnormal blood vessel growth. Aging causes an accumulation of senescent cells that secrete a range of cytokines, growth factors, and enzymes (SASPs), which remodel the ECM, making it stiffer and more degradable, and activate pro-metastatic pathways like TGF-β, STAT3, and MAPK, aiding processes like EMT and tumor invasion. Meanwhile, persistent low-grade inflammation attracts immunosuppressive cells, and immune decline hampers tumor surveillance, allowing cancer cells to evade immune detection. The aged TME also undergoes significant vascular and metabolic changes, such as abnormal angiogenesis and hypoxia, supporting the growth of more aggressive, treatment-resistant cancer clones and spreading metastases. These changes are driven by hallmarks of molecular aging, including telomere shortening, oxidative DNA damage, and epigenetic alterations, which lead to genetic instability and turn the aged stroma into fertile ground for metastasis. The review also discusses new therapeutic approaches, including senolytics, anti-inflammatory treatments, immune system rejuvenation, and metabolic strategies, highlighting the importance of age-specific models and precision medicine to enhance outcomes for the growing number of elderly cancer patients.
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Registered trials
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