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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.
In plain words · The hormone switch that drives most breast cancers. Blocking or destroying it is the oldest and most effective targeted therapy.
Showing the target this term concerns: Estrogen receptor (ERα).
The glossary entry explains the word; the readout page carries the scoring rule, the thresholds approvals use, the companion diagnostics and the tests.
Shares EMBER-3, Imlunestrant, Camizestrant, Elacestrant.
Shares EMERALD, ESR1 mutation (ligand-binding domain, usually in ctDNA), SERENA-6, Elacestrant.
Shares Imlunestrant, Vepdegestrant, Camizestrant, Elacestrant.
Shares EMERALD, Elacestrant, Estrogen receptor (ERα), Liquid biopsy (ctDNA).
Shares EMERALD, ESR1 mutation (ligand-binding domain, usually in ctDNA), EMBER-3, Imlunestrant.
Shares EMERALD, Elacestrant, Estrogen receptor (ERα), Liquid biopsy (ctDNA).
Shares Molecular-progression switching beyond ESR1, Tumour heterogeneity and clonal evolution, Acquired resistance to every therapy, Liquid biopsy (ctDNA).
Shares SERENA-6, Camizestrant, Estrogen receptor (ERα), Liquid biopsy (ctDNA).