{"slug":"biological-ageing","tag":"biological-ageing","variants":["biological-ageing"],"description":"No description yet","count":5,"kinds":{"technology":5},"related":[{"slug":"rejuvenation","tag":"rejuvenation","shared":5},{"slug":"survivorship","tag":"survivorship","shared":5},{"slug":"biomarker","tag":"biomarker","shared":3},{"slug":"blood","tag":"blood","shared":1},{"slug":"childhood-cancer","tag":"childhood-cancer","shared":1},{"slug":"epigenetics","tag":"epigenetics","shared":1},{"slug":"late-effects","tag":"late-effects","shared":1},{"slug":"second-cancers","tag":"second-cancers","shared":1},{"slug":"senescence","tag":"senescence","shared":1}],"records":[{"id":"rejuv-age-epigenetic-clocks","kind":"technology","name":"Epigenetic age after cancer treatment","route":"/technologies/rejuv-age-epigenetic-clocks/","status":"emerging","tldr":"An epigenetic clock reads chemical marks on DNA and estimates how old the body looks, which is not always the age on a birth certificate. In survivors of childhood cancer the clock runs ahead of chronological age, and the gap is larger after radiotherapy and after certain chemotherapy drugs. What the gap means for any one person is not yet known, and the clocks do not agree with each other."},{"id":"rejuv-age-clonal-haematopoiesis-after-therapy","kind":"technology","name":"Clonal haematopoiesis after cancer treatment","route":"/technologies/rejuv-age-clonal-haematopoiesis-after-therapy/","status":"established","tldr":"Chemotherapy and radiotherapy do not select blood stem cells at random. They favour the ones carrying mutations in DNA-damage genes, which then expand. Most people with such a clone never develop a blood cancer, but the clone is a measurable mark of what treatment did, and in a minority it is the seed of a later leukaemia."},{"id":"rejuv-age-senescent-cells-after-treatment","kind":"technology","name":"Senescent cells and p16 after chemotherapy","route":"/technologies/rejuv-age-senescent-cells-after-treatment/","status":"emerging","tldr":"Chemotherapy pushes cells into senescence: they stop dividing but stay alive and keep releasing inflammatory signals. The usual marker, p16INK4a in blood T cells, rises sharply during treatment and is still raised a year later. In one study the rise matched about fifteen years of ordinary ageing, in another the gap in survivors was larger still."},{"id":"rejuv-age-frailty-and-late-effects","kind":"technology","name":"Frailty and late effects in survivors","route":"/technologies/rejuv-age-frailty-and-late-effects/","status":"established","tldr":"The clearest evidence that treatment ages people is not a laboratory marker, it is what happens to survivors decades later. In the St Jude Lifetime Cohort, one in eight women who had cancer as a child met the clinical definition of frailty at a mean age of 33, a rate usually seen after 65. Frailty predicted new chronic conditions and death."},{"id":"rejuv-age-telomere-length","kind":"technology","name":"Telomere length after treatment","route":"/technologies/rejuv-age-telomere-length/","status":"emerging","tldr":"Telomeres are the caps on chromosomes that shorten each time a cell divides. They are the oldest and best known measure of cellular ageing, and the one with the least to show for itself in cancer survivors so far: the measurements exist, the associations are inconsistent, and nothing follows from a result."}]}