ESR1 mutation
A change in the oestrogen receptor gene that lets the cancer grow without oestrogen, so aromatase inhibitors stop working. Found in the blood in about a third of patients after hormone therapy.
Ligand-binding-domain mutations (Y537S, D538G, E380Q and others) arise under aromatase-inhibitor pressure in 30-40% of endocrine-resistant tumours and are rare at diagnosis (<5%). Detected by ctDNA (Guardant360 CDx is the companion diagnostic). Predicts resistance to AIs but retained sensitivity to SERDs, oral SERDs, and PROTAC degraders; the basis for elacestrant, imlunestrant, vepdegestrant, and camizestrant labels.
Pages like this
not linked directly; found by shared links- TermOral SERD
Shares Imlunestrant, EMBER-3, Camizestrant, Elacestrant.
- PersonFrançois-Clément Bidard
Shares EMERALD, Elacestrant, Estrogen receptor (ERα), Liquid biopsy (ctDNA).
- TermSelective oestrogen receptor degrader (SERD)
Shares EMERALD, Elacestrant, SERENA-6, Estrogen receptor (ERα).
- PersonNicholas Turner
Shares Camizestrant, SERENA-6, Estrogen receptor (ERα), Liquid biopsy (ctDNA).
- IdeaLook for the resistant sub-population before the first dose
Shares Estrogen receptor (ERα), Tumour heterogeneity and clonal evolution, Acquired resistance to every therapy, Liquid biopsy (ctDNA).
- IdeaA clone report from blood at every treatment cycle
Shares Molecular-progression switching beyond ESR1, Tumour heterogeneity and clonal evolution, Acquired resistance to every therapy, Liquid biopsy (ctDNA).
- TrialVERITAC-2
Shares Vepdegestrant, Estrogen receptor (ERα), HR-positive / HER2-negative breast cancer.
- PathwayOestrogen receptor signalling
Shares Vepdegestrant, Elacestrant, Transcriptional machinery & addiction, Estrogen receptor (ERα).