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Abstract
Genotoxic chemotherapy kills proliferating tumor cells but also drives a substantial fraction of surrounding stromal and normal cells into senescence, a permanently arrested but metabolically active state. Senescent cells secrete a senescence-associated secretory phenotype (SASP), a cocktail of pro-inflammatory cytokines, chemokines, and matrix-remodeling enzymes that actively contributes to chemotherapy side effects and, critically, can reactivate dormant disseminated tumor cells and promote cancer relapse. This paper synthesizes a decade of evidence: from the original identification of senolytic drugs (compounds that selectively clear senescent cells) through direct demonstration that senolytic clearance reduces cancer relapse and metastasis in mice, to a completed first-in-human senolytic trial and a 2025 mechanistic study directly linking chemotherapy-induced senescence to neutrophil extracellular trap (NET)-mediated reactivation of dormant breast cancer cells. Because the leading senolytic combination (dasatinib plus quercetin) uses two agents already in clinical use — an approved oncology drug and a well-tolerated flavonoid — this represents an unusually mature repurposing opportunity: the missing step is not drug discovery but a dedicated oncology trial testing senolytic administration in the peri-chemotherapy window as a relapse-prevention strategy. We present the mechanistic cascade, tabulate the evidence timeline, and propose a general intervention framework and trial design.
Keywords: cellular senescence; SASP; senolytics; dasatinib; quercetin; neutrophil extracellular traps; tumor dormancy; cancer relapse
Authors: Khalid Omer Alfarouk, PhD
Affiliation: Zamzam University College, Khartoum, Sudan
Accepted: 29 September 2026 · Published: 6 October 2026 · Vol. 1, Issue 2 · pp. 5–8