{"slug":"blood","tag":"blood","variants":["blood"],"description":"No description yet","count":5,"kinds":{"technology":1,"term":4},"related":[{"slug":"rejuvenation","tag":"rejuvenation","shared":5},{"slug":"second-cancers","tag":"second-cancers","shared":5},{"slug":"survivorship","tag":"survivorship","shared":5},{"slug":"chemotherapy","tag":"chemotherapy","shared":2},{"slug":"biological-ageing","tag":"biological-ageing","shared":1},{"slug":"biomarker","tag":"biomarker","shared":1},{"slug":"targeted-therapy","tag":"targeted-therapy","shared":1}],"records":[{"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-second-alkylating-agents-and-myeloid-neoplasms","kind":"term","name":"Alkylating agents and therapy-related myeloid neoplasms","route":"/terms/rejuv-second-alkylating-agents-and-myeloid-neoplasms/","tldr":"Alkylating chemotherapy can damage a blood stem cell in a way that shows up years later as myelodysplastic syndrome or acute myeloid leukaemia. It is uncommon, it depends on the total dose, and the risk falls away after about ten years. Knowing the cumulative dose you were given is the single most useful thing on your treatment summary."},{"id":"rejuv-second-topoisomerase-inhibitors-short-latency","kind":"term","name":"Topoisomerase II inhibitors and the shorter latency","route":"/terms/rejuv-second-topoisomerase-inhibitors-short-latency/","tldr":"Etoposide and the anthracyclines can cause a leukaemia too, but a different one: it arrives after about two years rather than six, it starts as acute leukaemia without a myelodysplastic phase, and it carries a balanced break in a chromosome rather than a missing piece. So the first two or three years after this chemotherapy are when a blood count matters most."},{"id":"rejuv-second-platinum-and-parp-inhibitors","kind":"term","name":"Platinum drugs and PARP inhibitors: the newer leukaemia risk","route":"/terms/rejuv-second-platinum-and-parp-inhibitors/","tldr":"The leukaemia risk after chemotherapy was described in the era of mustards and etoposide, and it did not stay there. Platinum drugs carry it, PARP inhibitors raise it about two and a half times against placebo, and lenalidomide with oral melphalan raises it nearly fivefold against melphalan alone. The absolute numbers are small, but the choice of partner drug is sometimes a real decision."},{"id":"rejuv-second-from-clone-to-disease","kind":"term","name":"From a clone in the blood to a leukaemia: what is known, and what is done","route":"/terms/rejuv-second-from-clone-to-disease/","tldr":"Chemotherapy and radiotherapy select for blood stem cells carrying particular mutations, and in a small minority one of those clones becomes a leukaemia. The useful question is not whether a clone is there but whether it will progress: most never do, and nothing has been shown to stop one that does."}]}