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Acute Myeloid Leukemia Research / Retinoids in Leukemia and Cellular Processes · Journal article
International Journal of Innovative Science and Research Technology · August 13, 2026
Raises a question worth testing. It does not answer one.
This is a narrative review of cellular senescence as a cancer therapy target, discussing biological mechanisms, contrasting roles in tumorigenesis, and emerging therapeutic strategies (senolytic and senomorphic agents combined with conventional therapies). The source presents conceptual frameworks and therapeutic hypotheses rather than empirical evidence from controlled trials or clinical outcomes data.
Journal article.
Persistent senescent cells release bioactive molecules (SASP) that may promote chronic inflammation, tumor progression, metastasis, and therapy resistance Emerging strategies include inducing senescence in malignant cells or selectively eliminating senescent cells using senolytic agents Combination approaches pairing senescence-targeted interventions with chemotherapy, radiotherapy, immunotherapy, and molecularly targeted therapies are proposed to improve efficacy and reduce recurrence
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
This is a narrative review summarizing biological mechanisms and therapeutic concepts without reporting original experimental data, clinical trials, or comparative efficacy evidence.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Cellular senescence is a permanent state of growth arrest that develops when cells encounter various forms of physiological or pathological stress. Although senescence initially functions as a protective mechanism by preventing the proliferation of damaged cells, persistent senescent cells can alter the surrounding tissue environment through the release of bioactive molecules collectively known as the senescence-associated secretory phenotype (SASP). These secretions may promote chronic inflammation, tumor progression, metastasis, and resistance to anticancer therapy. Consequently, cellular senescence has emerged as both a biological barrier to cancer and a promising therapeutic target. Recent advances have led to the development of strategies that either induce senescence in malignant cells or selectively eliminate harmful senescent cells using senolytic agents while suppressing detrimental SASP signaling through senomorphic therapies. In addition, combining senescence-targeted interventions with chemotherapy, radiotherapy, immunotherapy, and molecularly targeted therapies offers new opportunities to improve treatment efficacy and reduce disease recurrence. This review summarizes the biological mechanisms regulating cellular senescence, highlights its contrasting roles in cancer development, discusses emerging therapeutic approaches, and outlines current challenges and future directions for translating senescence-based therapies into clinical oncology.
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