From:  More than alternative estrogen receptors: the emerging role of GPER-1 and ERα36 in breast cancer

 GPER-1 and ERα36 in expanded ERα/PR/EGFR biomarker frameworks.

BiomarkerRoleEvidence typeTumor evidenceSubtypeFunctional implicationDiagnostic valueMain references
ERαClassical nuclear estrogen receptorPrimary experimental + clinical + genomicDefines luminal tumorsLuminal A/BHormone-dependent transcriptional regulationCore clinical markerClinical standard
PRERα downstream effectorClinical + mechanisticER axis integrityLuminal A/BFunctional ER signalingPredicts endocrine responseClinical standard
EGFRRTKExperimental + clinicalAggressive tumorsTNBC/HER2MAPK/PI3K signalingAggressive marker[10, 27, 79, 86, 106, 160]
GPER-1GPCR non-genomicExperimental + pharmacology + translational~50–60% tumorsLuminal resistant/TNBCPlasticity, resistanceER-independent signaling[22, 26, 28, 56, 66, 70, 85, 86, 90, 92, 93, 9599, 101103, 135, 160, 161]
ERα36Splice variant ESR1Experimental + translational~30–40% tumorsLuminal B/TNBCEMT, resistanceNon-classical ER signaling[10, 21, 25, 27, 104106, 108112, 114117, 139]
GPER-1 +
ERα36
Crosstalk axisMechanistic integrationNot unified clinicallyLuminal resistant/TNBCAdaptive plasticityCandidate axis[24, 29, 54, 93, 121, 127]
IntegrationNetwork signalingSystems biologyCorrelative datasetsAllMAPK/PI3K-transcriptionMulti-marker support[29, 79, 81, 97, 117, 143, 144, 162]
LimitationTranslational gapMethodologicalLimited validationContext dependenceNeeds clinical validation[6, 163]