Estrogen receptor-positive (ER+) breast cancer is the most common molecularly-defined subtype of breast cancer, representing approximately 70-80% of cases. It is characterized by expression of estrogen receptor alpha (ERα), which drives tumor growth in response to estrogen. ER+ breast cancer encompasses the luminal A and luminal B intrinsic subtypes, with generally favorable prognosis especially for luminal A tumors. Treatment centers on endocrine therapy to block estrogen signaling, with CDK4/6 inhibitors revolutionizing treatment of metastatic disease.
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name: ER-Positive Breast Cancer
creation_date: '2026-01-26T02:55:13Z'
updated_date: '2026-04-22T20:53:03Z'
description: >-
Estrogen receptor-positive (ER+) breast cancer is the most common molecularly-defined
subtype of breast cancer, representing approximately 70-80% of cases. It is
characterized by expression of estrogen receptor alpha (ERα), which drives tumor
growth in response to estrogen. ER+ breast cancer encompasses the luminal A and
luminal B intrinsic subtypes, with generally favorable prognosis especially for
luminal A tumors. Treatment centers on endocrine therapy to block estrogen signaling,
with CDK4/6 inhibitors revolutionizing treatment of metastatic disease.
categories:
- Molecularly-Defined Cancer
- Breast Cancer Subtype
- Solid Tumor
parents:
- breast carcinoma
has_subtypes:
- name: Luminal A Breast Cancer
description: >-
ER+/HER2- with low proliferation (Ki-67 <20%). Best prognosis among breast
cancer subtypes with high endocrine sensitivity and low recurrence rates.
Often does not require chemotherapy.
evidence:
- reference: PMID:19436038
reference_title: "Ki67 index, HER2 status, and prognosis of patients with luminal B breast cancer."
supports: PARTIAL
snippet: >-
Luminal B tumors have higher proliferation and poorer prognosis than luminal
A tumors.
explanation: >-
Supports luminal A versus luminal B prognostic and proliferation differences,
but does not directly support all subtype-defining criteria in this descriptor.
- name: Luminal B Breast Cancer
description: >-
ER+/HER2- with high proliferation (Ki-67 ≥20%) or ER+/HER2+. Higher recurrence
risk than luminal A, often benefits from chemotherapy in addition to
endocrine therapy.
evidence:
- reference: PMID:19436038
reference_title: "Ki67 index, HER2 status, and prognosis of patients with luminal B breast cancer."
supports: PARTIAL
snippet: >-
the 10-year breast cancer-specific survival was 79% (95% CI = 76% to 83%)
for luminal A, 64% (95% CI = 59% to 70%) for luminal B
explanation: >-
Supports worse survival for luminal B versus luminal A, but does not directly
support all biomarker and treatment details in this descriptor.
pathophysiology:
- name: Estrogen Receptor Activation
description: >-
ER+ breast cancer is driven by estrogen-dependent activation of the estrogen
receptor alpha (ERα), a nuclear hormone receptor that functions as a
ligand-activated transcription factor. Estrogen binding induces receptor
dimerization, DNA binding, and transcriptional activation of target genes.
evidence:
- reference: PMID:41549581
reference_title: "Targeting Estrogen Pathways in Breast Cancer: A Review of Current Therapies and Emerging Strategies."
supports: PARTIAL
snippet: At the heart of this subtype is the estrogen signaling pathway, especially the estrogen receptor alpha (ERα), which plays a major role in the development, growth, and response to these cancers.
explanation: This supports ERalpha pathway centrality, but not the full mechanistic detail in this descriptor.
cell_types:
- preferred_term: luminal epithelial cell of mammary gland
term:
id: CL:0002326
label: luminal epithelial cell of mammary gland
biological_processes:
- preferred_term: intracellular estrogen receptor signaling pathway
modifier: INCREASED
term:
id: GO:0030520
label: estrogen receptor signaling pathway
downstream:
- target: Estrogen-Driven Transcription
description: Activated ER binds DNA and regulates target genes
- name: Estrogen-Driven Transcription
description: >-
Activated ERα binds estrogen response elements (EREs) in target gene promoters,
recruiting coactivators and driving transcription of genes promoting cell
cycle progression (CCND1), survival (BCL2), and growth factor signaling
(IGF1R, EGFR). This creates estrogen-dependent tumor growth.
biological_processes:
- preferred_term: positive regulation of transcription by RNA polymerase II
modifier: INCREASED
term:
id: GO:0045944
label: positive regulation of transcription by RNA polymerase II
downstream:
- target: Cell Cycle Progression
description: ER target genes drive proliferation
- name: Cell Cycle Progression
description: >-
ER signaling drives expression of cyclin D1 (CCND1), which complexes with
CDK4/6 to phosphorylate Rb and promote G1-S transition. This creates the
therapeutic rationale for CDK4/6 inhibitors in ER+ breast cancer.
biological_processes:
- preferred_term: G1/S transition of mitotic cell cycle
modifier: INCREASED
term:
id: GO:0000082
label: G1/S transition of mitotic cell cycle
- preferred_term: cell population proliferation
modifier: INCREASED
term:
id: GO:0008283
label: cell population proliferation
histopathology:
- name: Invasive Ductal Carcinoma
finding_term:
preferred_term: Invasive Breast Carcinoma of No Special Type
term:
id: NCIT:C4194
label: Invasive Breast Carcinoma of No Special Type
frequency: VERY_FREQUENT
description: Invasive ductal carcinoma is the most common type of breast cancer.
evidence:
- reference: PMID:39806949
reference_title: "An Overview of Invasive Ductal Carcinoma (IDC) in Women's Breast Cancer."
supports: PARTIAL
snippet: "Invasive ductal carcinoma (IDC) is the most common type of breast cancer,"
explanation: Supports IDC predominance in breast cancer overall, but not specifically ER-positive cohorts.
phenotypes:
- category: Neoplastic
name: Breast Carcinoma
frequency: OBLIGATE
diagnostic: true
description: >-
ER+ breast cancers are typically invasive ductal or lobular carcinomas.
Luminal A tumors are often lower grade with favorable histologic features.
phenotype_term:
preferred_term: Breast carcinoma
term:
id: HP:0003002
label: Breast carcinoma
- category: Molecular
name: Estrogen Receptor Expression
frequency: OBLIGATE
diagnostic: true
description: >-
Defining feature is ER expression ≥1% by immunohistochemistry. Higher ER
expression (>10%) correlates with greater endocrine sensitivity. PR expression
often accompanies ER positivity and indicates functional ER signaling.
evidence:
- reference: PMID:22291085
reference_title: "Estrogen receptor (ER) mRNA and ER-related gene expression in breast cancers that are 1% to 10% ER-positive by immunohistochemistry."
supports: PARTIAL
snippet: "defined as having 1% to 10% positivity by immunohistochemistry (IHC)"
explanation: "Supports ER IHC threshold discussion, but only partially covers the broader descriptor."
phenotype_term:
preferred_term: Neoplasm
term:
id: HP:0002664
label: Neoplasm
- category: Clinical
name: Late Recurrence Pattern
frequency: FREQUENT
description: >-
Unlike TNBC, ER+ breast cancer can recur many years (10-20+) after initial
diagnosis, necessitating long-term surveillance and extended adjuvant
endocrine therapy.
evidence:
- reference: PMID:30054636
reference_title: "Association of Circulating Tumor Cells With Late Recurrence of Estrogen Receptor-Positive Breast Cancer: A Secondary Analysis of a Randomized Clinical Trial."
supports: SUPPORT
snippet: "Late recurrence 5 or more years after diagnosis accounts for at least one-half of all cases of recurrent hormone receptor-positive breast cancer."
explanation: "Abstract reports that late recurrences account for at least half of recurrent hormone receptor-positive cases."
phenotype_term:
preferred_term: Neoplasm
term:
id: HP:0002664
label: Neoplasm
biochemical:
- name: Estrogen and Progesterone Receptor Testing
notes: >-
ER and PR status determined by immunohistochemistry. ER+ defined as ≥1%
nuclear staining, though clinical benefit greatest with higher expression.
PR positivity indicates functional ER pathway.
- name: Genomic Assays
notes: >-
Gene expression assays (Oncotype DX, MammaPrint, Prosigna) help determine
chemotherapy benefit in early-stage ER+/HER2- disease by assessing
proliferation and recurrence risk.
genetic:
- name: ESR1
association: Acquired Mutations (Resistance)
inheritance:
- name: Somatic
notes: >-
ESR1 mutations are rare in primary tumors but emerge in ~30-40% of metastatic
ER+ breast cancer after aromatase inhibitor therapy. Mutations in the
ligand-binding domain (Y537S, D538G) cause constitutive receptor activation
and endocrine resistance.
- name: PIK3CA
association: Somatic Mutations
inheritance:
- name: Somatic
notes: >-
PIK3CA hotspot mutations (E545K, H1047R) occur in approximately 40% of ER+
breast cancers. Confer partial endocrine resistance and identify patients
who benefit from PI3K inhibitor alpelisib.
- name: CCND1
association: Amplification
inheritance:
- name: Somatic
notes: >-
CCND1 (cyclin D1) amplification occurs in ~15% of ER+ breast cancers and
may confer sensitivity to CDK4/6 inhibitors.
treatments:
- name: Aromatase Inhibitors
description: >-
First-line endocrine therapy in postmenopausal women. Letrozole, anastrozole,
and exemestane block peripheral estrogen synthesis by inhibiting aromatase.
Superior to tamoxifen in postmenopausal patients.
evidence:
- reference: PMID:15894097
reference_title: "Effects of chemotherapy and hormonal therapy for early breast cancer on recurrence and 15-year survival: an overview of the randomised trials."
supports: NO_EVIDENCE
snippet: >-
For ER-positive disease only, allocation to about 5 years of adjuvant
tamoxifen reduces the annual breast cancer death rate by 31% (SE 3)
explanation: >-
Snippet supports tamoxifen benefit in ER-positive disease, but does not directly support aromatase inhibitors.
treatment_term:
preferred_term: hormone modifying therapy
term:
id: MAXO:0000283
label: hormone modifying therapy
- name: Tamoxifen
description: >-
Selective estrogen receptor modulator (SERM) that competitively blocks
estrogen binding to ER. First-line in premenopausal women, alternative
in postmenopausal patients. Also used for risk reduction.
evidence:
- reference: PMID:15894097
reference_title: "Effects of chemotherapy and hormonal therapy for early breast cancer on recurrence and 15-year survival: an overview of the randomised trials."
supports: SUPPORT
snippet: >-
For ER-positive disease only, allocation to about 5 years of adjuvant
tamoxifen reduces the annual breast cancer death rate by 31% (SE 3)
explanation: >-
Landmark EBCTCG meta-analysis of 194 trials shows 5 years of tamoxifen
reduces breast cancer mortality by 31%.
treatment_term:
preferred_term: pharmacotherapy
term:
id: MAXO:0000058
label: pharmacotherapy
therapeutic_agent:
- preferred_term: tamoxifen
term:
id: CHEBI:41774
label: tamoxifen
- name: CDK4/6 Inhibitors
description: >-
Palbociclib, ribociclib, and abemaciclib inhibit CDK4/6, blocking Rb
phosphorylation and G1-S transition. Combined with endocrine therapy,
dramatically improved outcomes in metastatic ER+/HER2- breast cancer.
Abemaciclib and ribociclib also approved in high-risk early-stage disease.
evidence:
- reference: PMID:26947331
reference_title: "Fulvestrant plus palbociclib versus fulvestrant plus placebo for treatment of hormone-receptor-positive, HER2-negative metastatic breast cancer that progressed on previous endocrine therapy (PALOMA-3): final analysis of the multicentre, double-blind, phase 3 randomised controlled trial."
supports: PARTIAL
snippet: >-
Median progression-free survival was 9·5 months (95% CI 9·2-11·0) in the
fulvestrant plus palbociclib group and 4·6 months (3·5-5·6) in the
fulvestrant plus placebo group (hazard ratio 0·46, 95% CI 0·36-0·59,
p<0·0001).
explanation: >-
Supports palbociclib efficacy in metastatic HR+/HER2- disease, but does not directly support the full CDK4/6 class-level descriptor.
treatment_term:
preferred_term: targeted therapy
term:
id: NCIT:C93352
label: Targeted Therapy
- name: Fulvestrant
description: >-
Selective estrogen receptor degrader (SERD) that binds ER, blocking its
function and promoting its degradation. Used in metastatic disease,
particularly after progression on other endocrine therapy.
evidence:
- reference: PMID:26947331
reference_title: "Fulvestrant plus palbociclib versus fulvestrant plus placebo for treatment of hormone-receptor-positive, HER2-negative metastatic breast cancer that progressed on previous endocrine therapy (PALOMA-3): final analysis of the multicentre, double-blind, phase 3 randomised controlled trial."
supports: NO_EVIDENCE
snippet: >-
Fulvestrant plus palbociclib was associated with significant and consistent
improvement in progression-free survival compared with fulvestrant plus
placebo
explanation: >-
PALOMA-3 confirms fulvestrant's role as backbone therapy in HR+/HER2-
metastatic breast cancer, demonstrating activity when combined with CDK4/6i.
treatment_term:
preferred_term: pharmacotherapy
term:
id: MAXO:0000058
label: pharmacotherapy
therapeutic_agent:
- preferred_term: fulvestrant
term:
id: CHEBI:31638
label: fulvestrant
- name: Alpelisib
description: >-
PI3K alpha-selective inhibitor approved for PIK3CA-mutated ER+/HER2-
metastatic breast cancer in combination with fulvestrant.
evidence:
- reference: PMID:26947331
reference_title: "Fulvestrant plus palbociclib versus fulvestrant plus placebo for treatment of hormone-receptor-positive, HER2-negative metastatic breast cancer that progressed on previous endocrine therapy (PALOMA-3): final analysis of the multicentre, double-blind, phase 3 randomised controlled trial."
supports: SUPPORT
snippet: >-
PIK3CA mutation was detected in the plasma DNA of 129 (33%) of 395 patients
explanation: >-
Snippet supports PIK3CA mutation prevalence only, not alpelisib efficacy or indication.
treatment_term:
preferred_term: targeted therapy
term:
id: NCIT:C93352
label: Targeted Therapy
therapeutic_agent:
- preferred_term: alpelisib
term:
id: CHEBI:231324
label: alpelisib
- name: Elacestrant
description: >-
Oral SERD approved for ER+/HER2- metastatic breast cancer with ESR1 mutations
after progression on prior endocrine therapy. Active against common ESR1
resistance mutations.
evidence:
- reference: PMID:26947331
reference_title: "Fulvestrant plus palbociclib versus fulvestrant plus placebo for treatment of hormone-receptor-positive, HER2-negative metastatic breast cancer that progressed on previous endocrine therapy (PALOMA-3): final analysis of the multicentre, double-blind, phase 3 randomised controlled trial."
supports: NO_EVIDENCE
snippet: >-
women aged 18 years or older with hormone-receptor-positive, HER2-negative
metastatic breast cancer that had progressed on previous endocrine therapy
explanation: >-
Snippet describes PALOMA-3 eligibility context but does not provide direct evidence for elacestrant.
treatment_term:
preferred_term: pharmacotherapy
term:
id: MAXO:0000058
label: pharmacotherapy
therapeutic_agent:
- preferred_term: elacestrant
term:
id: CHEBI:229213
label: elacestrant
disease_term:
preferred_term: luminal A breast carcinoma
term:
id: MONDO:0021116
label: luminal A breast carcinoma
classifications:
icdo_morphology:
classification_value: Adenocarcinoma
harrisons_chapter:
- classification_value: cancer
- classification_value: solid tumor
ER+ breast cancer is driven by estrogen receptor alpha (ERα; ESR1)–dependent transcriptional programs primed by pioneer factors (FOXA1, GATA3) and modulated by oncogenic crosstalk (PI3K/AKT/mTOR, RTKs such as FGFR/HER2) and the tumor microenvironment. Under selective pressure from aromatase inhibitors (AIs) and other endocrine therapies, tumors frequently acquire ESR1 ligand-binding domain (LBD) mutations or rearrangements that sustain ligand-independent ER signaling and promote endocrine resistance; combination strategies targeting PI3K/AKT/mTOR and cell cycle (CDK4/6) have become foundational, with biomarker-guided escalation to oral SERDs (e.g., elacestrant) and AKT inhibition (capivasertib) in defined molecular subsets (ESR1-mutated; PIK3CA/AKT1/PTEN-altered). High-level summaries of these mechanisms and therapeutic linkages are consolidated in the embedded table artifact. (ferro2024noveltreatmentstrategies pages 23-24, santangelo2025secondlinestrategiesto pages 7-7, ferrari2025molecularmechanismsand pages 1-2)
| Mechanism | Key genes/proteins (HGNC) | Pathway / GO terms (suggested) | Therapeutic classes (CHEBI / example drugs) | Evidence (citation IDs) |
|---|---|---|---|---|
| ER / ESR1 signaling & activating LBD mutations | ESR1 (ESR1) | Steroid hormone receptor signaling (GO:0030520); transcriptional activation (GO:0006351) | SERMs / SERDs (tamoxifen, fulvestrant, elacestrant) | (ferro2024noveltreatmentstrategies pages 23-24, santangelo2025secondlinestrategiesto pages 7-7, ferrari2025molecularmechanismsand pages 1-2) |
| ESR1 gene fusions (ligand‑binding loss) | ESR1 fusions (e.g., ESR1::CCDC170) | Fusion-driven constitutive transcription (GO:0006351) | Indirect targeting: downstream kinase inhibitors / pathway-directed therapies | (santangelo2025secondlinestrategiesto pages 7-7, ramezani2025mechanismsofendocrine pages 13-15, ferro2024noveltreatmentstrategies pages 26-27) |
| Pioneer transcription factors (chromatin priming) | FOXA1, GATA3 (FOXA1, GATA3) | Chromatin binding / pioneer factor activity (GO:0000978; GO:0030901) | Epigenetic modulators; ER-directed agents (to disrupt reprogrammed ER cistrome) | (ramezani2025mechanismsofendocrine pages 13-15, ferrari2025molecularmechanismsand pages 1-2, ferro2024noveltreatmentstrategies pages 26-27) |
| PI3K / AKT / mTOR signaling axis | PIK3CA, AKT1, PTEN, MTOR | PI3K/AKT signaling (GO:0014065); mTOR signaling (GO:0031929) | PI3K inhibitors (alpelisib), AKT inhibitors (capivasertib), mTOR inhibitors (everolimus) | (ferro2024noveltreatmentstrategies pages 23-24, santangelo2025secondlinestrategiesto pages 7-7, ferrari2025molecularmechanismsand pages 1-2) |
| CDK4/6-driven cell-cycle control | CDK4, CDK6, CCND1, RB1 | G1/S cell-cycle transition (GO:0044843) | CDK4/6 inhibitors (palbociclib, ribociclib, abemaciclib) ± ET | (ferro2024noveltreatmentstrategies pages 23-24, ferrari2025molecularmechanismsand pages 1-2, ferro2024noveltreatmentstrategies pages 26-27) |
| RTK crosstalk: FGFR / HER family | FGFR1–4, ERBB2 (HER2), FGF ligands | Receptor tyrosine kinase signaling (GO:0007169); MAPK/PI3K pathway cross-talk | FGFR inhibitors (tasurgratinib, others); HER2 ADCs (trastuzumab deruxtecan) | (ramezani2025mechanismsofendocrine pages 13-15, ferrari2025molecularmechanismsand pages 1-2, ferro2024noveltreatmentstrategies pages 26-27) |
| Epigenetic & chromatin remodeling | ARID1A, KMT2C, EZH2, SWI/SNF components | Chromatin remodeling (GO:0006338); histone modification (GO:0016570) | Epigenetic drugs (HDACi, DNMTi) and combination approaches (preclinical/clinical) | (ramezani2025mechanismsofendocrine pages 11-13, ramezani2025mechanismsofendocrine pages 13-15, ferrari2025molecularmechanismsand pages 1-2) |
| Tumor microenvironment & immune features | CD274 (PD-L1), TIL markers, CAF markers (FAP), cytokines (CCL2, IL6) | Immune response (GO:0006955); cell–cell signaling (GO:0007267) | Immune checkpoint inhibitors (selected settings), ADCs, stroma-targeting strategies | (ramezani2025mechanismsofendocrine pages 13-15, ferrari2025molecularmechanismsand pages 1-2, ferro2024noveltreatmentstrategies pages 26-27) |
| Imaging biomarker: 18F‑FES PET (ER functional imaging) | ER / ESR1 (imaged ligand binding) | Diagnostic molecular imaging; ER ligand binding assessment | 18F‑FES PET to guide endocrine therapy selection / assess ER heterogeneity | (santangelo2025secondlinestrategiesto pages 7-7, santangelo2025secondlinestrategiesto pages 1-3) |
| Clinical biomarkers & testing (therapy selection) | ESR1, PIK3CA, AKT1, PTEN (HGNC: ESR1, PIK3CA, AKT1, PTEN) | Clinical molecular diagnostics; actionable mutation annotation | Biomarker-driven drugs: elacestrant (ESR1-mut), alpelisib (PIK3CA), capivasertib (AKT), PARPi for BRCA | (santangelo2025secondlinestrategiesto pages 7-7, ferro2024noveltreatmentstrategies pages 23-24, ferrari2025molecularmechanismsand pages 1-2) |
Table: Table summarizing core ER-positive breast cancer mechanisms, key genes/proteins with suggested GO pathway terms, linked therapeutic classes (examples), and supporting evidence from recent reviews and studies (2023–2025 reviews cited). This consolidates mechanistic-to-clinical links useful for knowledge-base annotation and therapeutic decision contexts.
Limitations and scope note: While the narrative prioritizes 2023–2024 topics and clinical practices (SERDs, CDK4/6, PI3K/AKT/mTOR, imaging), several integrative reviews summarizing 2024 data were published in early 2025; these were included when they synthesized 2023–2024 primary evidence. Citations track to available context IDs above.
References
(ferro2024noveltreatmentstrategies pages 23-24): Antonella Ferro, Michela Campora, Alessia Caldara, Delia De Lisi, Martina Lorenzi, Sara Monteverdi, Raluca Mihai, Alessandra Bisio, Mariachiara Dipasquale, Orazio Caffo, and Yari Ciribilli. Novel treatment strategies for hormone receptor (hr)-positive, her2-negative metastatic breast cancer. Journal of Clinical Medicine, 13:3611, Jun 2024. URL: https://doi.org/10.3390/jcm13123611, doi:10.3390/jcm13123611. This article has 23 citations and is from a poor quality or predatory journal.
(santangelo2025secondlinestrategiesto pages 7-7): Samantha Santangelo. Second-line strategies to overcome resistance to oestrogen therapy in patients with er+/her2- metastatic breast cancer: a year in review. EMJ Oncology, pages 2-9, May 2025. URL: https://doi.org/10.33590/emjoncol/njqz9723, doi:10.33590/emjoncol/njqz9723. This article has 0 citations.
(ferrari2025molecularmechanismsand pages 1-2): Paola Ferrari, Maria Luisa Schiavone, Cristian Scatena, and Andrea Nicolini. Molecular mechanisms and therapeutic strategies to overcome resistance to endocrine therapy and cdk4/6 inhibitors in advanced er+/her2− breast cancer. International Journal of Molecular Sciences, Apr 2025. URL: https://doi.org/10.3390/ijms26073438, doi:10.3390/ijms26073438. This article has 7 citations and is from a poor quality or predatory journal.
(ramezani2025mechanismsofendocrine pages 13-15): Sepehr Ramezani and Faezeh soheili azad. Mechanisms of endocrine resistance in hormone receptor–positive breast cancer: an integrated genomic and translational review. The Cancer Review, 1:56-73, Nov 2025. URL: https://doi.org/10.61882/tcr.202501.01.05, doi:10.61882/tcr.202501.01.05. This article has 0 citations.
(ferro2024noveltreatmentstrategies pages 26-27): Antonella Ferro, Michela Campora, Alessia Caldara, Delia De Lisi, Martina Lorenzi, Sara Monteverdi, Raluca Mihai, Alessandra Bisio, Mariachiara Dipasquale, Orazio Caffo, and Yari Ciribilli. Novel treatment strategies for hormone receptor (hr)-positive, her2-negative metastatic breast cancer. Journal of Clinical Medicine, 13:3611, Jun 2024. URL: https://doi.org/10.3390/jcm13123611, doi:10.3390/jcm13123611. This article has 23 citations and is from a poor quality or predatory journal.
(ramezani2025mechanismsofendocrine pages 11-13): Sepehr Ramezani and Faezeh soheili azad. Mechanisms of endocrine resistance in hormone receptor–positive breast cancer: an integrated genomic and translational review. The Cancer Review, 1:56-73, Nov 2025. URL: https://doi.org/10.61882/tcr.202501.01.05, doi:10.61882/tcr.202501.01.05. This article has 0 citations.
(santangelo2025secondlinestrategiesto pages 1-3): Samantha Santangelo. Second-line strategies to overcome resistance to oestrogen therapy in patients with er+/her2- metastatic breast cancer: a year in review. EMJ Oncology, pages 2-9, May 2025. URL: https://doi.org/10.33590/emjoncol/njqz9723, doi:10.33590/emjoncol/njqz9723. This article has 0 citations.
(ramezani2025mechanismsofendocrine pages 17-18): Sepehr Ramezani and Faezeh soheili azad. Mechanisms of endocrine resistance in hormone receptor–positive breast cancer: an integrated genomic and translational review. The Cancer Review, 1:56-73, Nov 2025. URL: https://doi.org/10.61882/tcr.202501.01.05, doi:10.61882/tcr.202501.01.05. This article has 0 citations.