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Aim. The paper aimed to update the study on accelerated biological aging as a complication of cancer therapy with a focus on diagnosing and prognosing the disease course. The authors independently searched scientific literature for the systematic review within databases PubMed, Scopus and Cochrane in the period from 2018 to 2024, using combinations of keywords “cancer”, “biological aging”, “replicative aging”, “antitumor therapy”, “markers of cellular senescence”, “coronary artery calcium” and selected full-text publications written in English and Ukrainian with level 1–3 evidence. People affected by cancer grow old faster. This could be related to malignant growth biology as well as to methods of anticancer therapy received. Cytostatics, targeted, hormonal and immune drugs damage not only malignant, but also benign cells, which leads to violations of replication with sustained cell cycle arrest and other phenotypic signs – macromolecular damage, metabolic changes, production of a specific senescence-associated secretome. Clinically, this is manifested by reduced work capacity, weakness, chronic organ dysfunction, cardiovascular disorders, progression of coronary atherosclerosis, hypertension, diabetes, dyslipidemia, sarcopenia, cognitive disorders, a de novo development of tumors and premature death. Biological markers of cellular senescence include the expression of lipofuscin, Ki67, p21 WAF1/Cip1 or p16 INK4a. A clinical marker of aging is the deposition of calcium salts within coronary arteries based on the Agatston score detected using multidetector computed tomography. Conclusions. A better understanding of the cancer consequences associated with accelerated biological aging might suggest new therapeutic strategies and improve the quality of life among cancer survivors. Rehabilitation measures through changes in diet, caloric restriction, aerobic exercises and pharmacological senolytic therapy should be a part of a patient’s daily routine after completion of radical cancer treatment.

Aim. The paper aimed to update the study on accelerated biological aging as a complication of cancer therapy with a focus on diagnosing and prognosing the disease course. The authors independently searched scientific literature for the systematic review within databases PubMed, Scopus and Cochrane in the period from 2018 to 2024, using combinations of keywords "cancer", "biological aging", "replicative aging", "antitumor therapy", "markers of cellular senescence", "coronary artery calcium" and selected full-text publications written in English and Ukrainian with level 1-3 evidence. People affected by cancer grow old faster. This could be related to malignant growth biology as well as to methods of anticancer therapy received. Cytostatics, targeted, hormonal and immune drugs damage not only malignant, but also benign cells, which leads to violations of replication with sustained cell cycle arrest and other phenotypic signs - macromolecular damage, metabolic changes, production of a specific senescence-associated secretome. Clinically, this is manifested by reduced work capacity, weakness, chronic organ dysfunction, cardiovascular disorders, progression of coronary atherosclerosis, hypertension, diabetes, dyslipidemia, sarcopenia, cognitive disorders, a de novo development of tumors and premature death. Biological markers of cellular senescence include the expression of lipofuscin, Ki67, p21 WAF1/Cip1 or p16 INK4a. A clinical marker of aging is the deposition of calcium salts within coronary arteries based on the Agatston score detected using multidetector computed tomography. Conclusions. A better understanding of the cancer consequences associated with accelerated biological aging might suggest new therapeutic strategies and improve the quality of life among cancer survivors. Rehabilitation measures through changes in diet, caloric restriction, aerobic exercises and pharmacological senolytic therapy should be a part of a patient's daily routine after completion of radical cancer treatment. [ABSTRACT FROM AUTHOR]