Evidence map›Paper›PMID 41894035›Full record

ReviewCancer metastasis reviews2026

The role of Notch signalling and its crosstalk with oestrogen receptor signalling in breast cancer.

Aygun Azadova, Orkhan Isayev, Antonio Marco, Greg N Brooke

Abstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Aygun AzadovaSchool of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.
Orkhan IsayevDepartment of Cytology, Embryology, and Histology, Azerbaijan Medical University, Baku, AZ1022, Azerbaijan.
Antonio MarcoSchool of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.
Greg N BrookeSchool of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK. gbrooke@essex.ac.uk.

Funding

Biotechnology and Biological Sciences Research Council BB/W020033/1Biotechnology and Biological Sciences Research Council BB/X511171/1
6 · The paper itself

Abstract

Breast cancer (BCa) is the most frequently diagnosed malignancy in women worldwide, with approximately 70% of cases driven by oestrogen receptor alpha (ERα). Endocrine therapies aim to suppress ERα signalling activity and form the foundation of current therapeutic strategies. However, a substantial proportion of patients either fail to respond due to intrinsic resistance or acquire resistance over the course of the treatment. This resistance arises through a complex interplay of factors including crosstalk with other signalling pathways such as Notch. Notch signalling, essential for mammary gland development, is aberrantly activated in breast tumours, where it contributes to cancer stem cell maintenance, epithelial-mesenchymal transition, angiogenesis, and metastasis. Notch receptors exert context- and subtype-specific roles: Notch1 and 4 promote tumour aggressiveness, whereas Notch2 often exhibits tumour-suppressive roles. In ERα-positive BCa, ERα and Notch signalling cooperate to drive resistance, whereas in ERα-negative disease, Notch promotes stemness and angiogenesis. While anti-oestrogen therapies effectively inhibit tumour growth, they can paradoxically activate Notch signalling and promote therapeutic resistance. Co-targeting Notch alongside endocrine therapy has been proposed as a strategy to delay the onset of therapeutic resistance. However, clinical development of Notch inhibitors has been limited by toxicity associated with pan-Notch blockade. More selective approaches, such as paralogue-specific antibodies, transcription-complex disruption, rational drug combinations, and advanced delivery platforms, are under active development to overcome these limitations. This review outlines the ERα-Notch crosstalk in BCa and examines current and emerging strategies for targeting Notch to overcome endocrine resistance and improve clinical outcomes.

Indexed as

Breast NeoplasmsEstrogen Receptor alphaReceptors, EstrogenReceptors, NotchAnimalsDrug Resistance, NeoplasmFemaleHumansReceptor Cross-TalkSignal TransductionEstrogen Receptor alphaReceptors, EstrogenReceptors, NotchBreast cancerCrosstalkEndocrine resistanceEndocrine therapyNotchNotch inhibitorsOestrogen receptor

Identifiers

PMID41894035
PMCPMC13031202

What OpenQuestion holds

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Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.