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Epigenetic and transcriptional therapy changes how genes are read rather than the genes themselves.
Epigenetic and transcriptional therapy changes how genes are read rather than the genes themselves. The section brings together DNMT and HDAC inhibitors used in haematological malignancies, EZH2 inhibitors, IDH inhibitors, menin inhibitors such as revumenib, BET inhibitors and emerging transcription-factor degraders, a class mostly established in blood cancers with solid tumours catching up. Linked records include the technologies epigenetic drugs and epigenetic editing, the term hypomethylating agents, the paper on the 2022 Hallmarks of Cancer, and the institutions USC Norris and Ruijin Hospital. Companies pointing here are Kura Oncology, Taiho Oncology, Servier, Syndax Pharmaceuticals, MorphoSys and Chipscreen Biosciences.
Drugs that change how genes are switched on and off without changing the DNA itself.
Switching a gene off for good without changing the DNA sequence, by writing chemical marks onto it.
First-in-class drugs against the histone acetyltransferases KAT6A and KAT6B, in late trials for hormone receptor-positive breast cancer that has stopped responding to endocrine therapy.
Drugs against the histone demethylase LSD1, which keeps blood and neuroendocrine cancer cells from maturing; being tested in myelofibrosis, leukaemia and small cell lung cancer.
Cancer is now understood to change its identity and behaviour without new mutations, to be shaped by bacteria inside and around it, and to be helped along by ageing cells. This explains why some tumours escape targeted drugs by changing cell type and why gut bacteria affect immunotherapy response.
A mechanism for the most feared form of treatment resistance in prostate cancer, and the reason combined TP53 and RB1 loss is worth knowing about before a man starts an androgen receptor drug rather than after his biopsy comes back neuroendocrine. Reversibility in the laboratory is also an argument that the switch is a target and not just a prognosis.
The explanation for why prostate cancer has so few targeted drugs outside the hormone axis and the DNA-repair genes: it is a quiet genome with structural rather than point-mutational damage, and the recurrent changes sit in the machinery that reads DNA rather than in kinases.
Open-source software, hardware and data projects catalogued by a third party, the Open Medical Registry, that bear on this front. Listing is not endorsement; check each project's own licence and validation before clinical use.
EpiMethEx (Epigenetic Methylation and Expression), a R package to perform a large-scale integrated analysis by cyclic correlation analyses between...
From the Open Medical Registry (openmedical.sh), an MIT-licensed catalogue of open-source medicine. Blurbs are one line from each registry record; every project keeps its own licence.