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These processes converge to generate T cell populations exhibiting CD28 loss, killer cell lectin-like receptor G1 positivity, telomere attrition, and functional exhaustion characteristic of elderly individuals. Concurrently, inflammaging pathways and senescence-associated secretory phenotypes establish pro-tumorigenic microenvironments. Consequently, pediatric recipients demonstrate 4- to 20-fold elevated cancer incidence, with standardized incidence ratios for post-transplant lymphoproliferative disease exceeding 200 in some cohorts. Beyond hematological malignancies, significant increases in solid tumors suggest fundamental immunosurveillance failure. Emerging biomarkers including flow cytometric senescence panels, telomere length measurement, and epigenetic clocks enable personalized risk stratification. Therapeutic horizons encompass senolytic agents, checkpoint inhibitor modulation, thymic regeneration strategies, and metabolic interventions targeting aging pathways. This paradigm shift necessitates reconceptualizing pediatric transplantation through the aging lens, integrating precision medicine approaches that balance graft survival, immune competence preservation, and cancer prevention in this vulnerable population.<\/jats:p>","DOI":"10.5500\/wjt.v16.i2.117357","type":"journal-article","created":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T01:19:11Z","timestamp":1780017551000},"source":"Crossref","is-referenced-by-count":0,"title":["Immunosenescence and cancer predisposition in pediatric transplant recipients: An emerging paradigm"],"prefix":"10.5500","volume":"16","author":[{"given":"Aya Mohamed Adel","family":"Arafat","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Soliman M 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