Evidence map›Paper›PMID 33003540›Full record

ReviewCells2020

Notch Signaling in Breast Cancer: A Role in Drug Resistance.

McKenna BeLow, Clodia Osipo

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 4% of its field
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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Multi-omic Profiling of Recurrence Risk Across Breast Cancer Subtypes.medRxiv : the preprint server for health sciences · 2026
    Article
  6. Article
  7. The miRNA-4330/ABCG2 axis overcomes drug resistance and cancer progression in both ER-positive and ER-negative resistant breast cancer cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Mechanistic insights into the lncRNA-Notch signaling axis in tumors.Frontiers in cell and developmental biology · 2026
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Role of Estrogen Signaling in Notch Pathway Activation in Sertoli Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2025
    Article
  20. Article

15 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

McKenna BeLowIntegrated Cell Biology Program, Loyola University Chicago, Maywood, IL 60513, USA.ORCID 0000-0002-2656-5187
Clodia OsipoIntegrated Cell Biology Program, Loyola University Chicago, Maywood, IL 60513, USA.ORCID 0000-0003-1979-8465
Loyola University Chicago · US

Funding

Training in Neuroimmunoendocrine Effects of AlcoholT32AA013527 · NIAAA · LOYOLA UNIVERSITY CHICAGO · PI CHOUDHRY, MASHKOOR A · 2002 to 2021
$4.4M
NIAAA NIH HHS T32 AA013527
6 · The paper itself

Abstract

Breast cancer is a heterogeneous disease that can be subdivided into unique molecular subtypes based on protein expression of the Estrogen Receptor, Progesterone Receptor, and/or the Human Epidermal Growth Factor Receptor 2. Therapeutic approaches are designed to inhibit these overexpressed receptors either by endocrine therapy, targeted therapies, or combinations with cytotoxic chemotherapy. However, a significant percentage of breast cancers are inherently resistant or acquire resistance to therapies, and mechanisms that promote resistance remain poorly understood. Notch signaling is an evolutionarily conserved signaling pathway that regulates cell fate, including survival and self-renewal of stem cells, proliferation, or differentiation. Deregulation of Notch signaling promotes resistance to targeted or cytotoxic therapies by enriching of a small population of resistant cells, referred to as breast cancer stem cells, within the bulk tumor; enhancing stem-like features during the process of de-differentiation of tumor cells; or promoting epithelial to mesenchymal transition. Preclinical studies have shown that targeting the Notch pathway can prevent or reverse resistance through reduction or elimination of breast cancer stem cells. However, Notch inhibitors have yet to be clinically approved for the treatment of breast cancer, mainly due to dose-limiting gastrointestinal toxicity. In this review, we discuss potential mechanisms of Notch-mediated resistance in breast cancer cells and breast cancer stem cells, and various methods of targeting Notch through γ-secretase inhibitors, Notch signaling biologics, or transcriptional inhibitors. We also discuss future plans for identification of novel Notch-targeted therapies, in order to reduce toxicity and improve outcomes for women with resistant breast cancer.

Indexed as

Amyloid Precursor Protein SecretasesAntineoplastic AgentsBreast NeoplasmsCell Line, TumorCell ProliferationDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMolecular Targeted TherapyNeoplastic Stem CellsReceptors, NotchSignal TransductionAmyloid Precursor Protein SecretasesAntineoplastic AgentsReceptors, Notchbreast cancercancer stem cellsNotchresistance

Identifiers

PMID33003540
PMCPMC7601482
OpenAlexW3091346371

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.