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When hormone therapy stops controlling a hormone-driven breast cancer, either quickly (primary) or after years (acquired).
Primary resistance: relapse within 2 years of adjuvant ET or progression within 6 months of first-line metastatic ET. Secondary: later relapse or progression. Mechanisms: ESR1 mutations, PI3K/AKT/mTOR activation, cyclin D1/CDK4 amplification, RB loss, FGFR1 amplification, HER2 activation, lineage plasticity. Determines eligibility for INAVO120-type regimens (relapse on/within 12 months of adjuvant ET).
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).
Shares Aromatase inhibitor, Hormone receptor status (ER / PR), Estrogen receptor (ERα).
Shares CDK4/6, Estrogen receptor (ERα), HR-positive / HER2-negative breast cancer.
Shares Receptor conversion: when the receptors change between the primary and a recurrence, Hormone receptor status (ER / PR), HR-positive / HER2-negative breast cancer.
Shares CDK4/6, Estrogen receptor (ERα), HR-positive / HER2-negative breast cancer.
Shares Selective oestrogen receptor degrader (SERD), Hormone receptor status (ER / PR), Estrogen receptor (ERα), HR-positive / HER2-negative breast cancer.
Shares CDK4/6, Estrogen receptor (ERα), HR-positive / HER2-negative breast cancer.
Shares Selective oestrogen receptor degrader (SERD), Estrogen receptor (ERα), HR-positive / HER2-negative breast cancer.
Shares Selective oestrogen receptor degrader (SERD), Estrogen receptor (ERα), HR-positive / HER2-negative breast cancer.