Evidence map›Paper›PMID 40006021›Full record

ReviewPharmaceuticals (Basel, Switzerland)2025

Cellular Epigenetic Targets and Epidrugs in Breast Cancer Therapy: Mechanisms, Challenges, and Future Perspectives.

Ibrahim S Alalhareth, Saleh M Alyami, Ali H Alshareef, Ahmed O Ajeibi, Manea F Al Munjem, Ahmad A Elfifi, Meshal M Alsharif, Seham A Alzahrani, Mohammed A Alqaad, Marwa B Bakir and 1 more

Abstract readReview
In one paragraph

Review in Pharmaceuticals (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–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

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. The role of epigenetic alterations in canine mammary cancer.The Journal of reproduction and development · 2026
    Review
  7. Article
  8. Review
  9. Review
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

11 authors.

Ibrahim S AlalharethCollege of Pharmacy, Najran University, Najran 66256, Saudi Arabia.
Saleh M AlyamiCollege of Pharmacy, Najran University, Najran 66256, Saudi Arabia.
Ali H AlshareefDepartment of Pharmaceuticals Care, Ministry of Defense, Najran 66281, Saudi Arabia.
Ahmed O AjeibiDepartment of Pharmaceuticals Care, Ministry of Defense, Najran 66281, Saudi Arabia.
Manea F Al MunjemKing Khaled Hospital -Najran Health Cluster, Najran 66261, Saudi Arabia.
Ahmad A ElfifiDepartment of Pharmaceuticals Care, Ministry of Defense, Najran 66281, Saudi Arabia.
Meshal M AlsharifDepartment of Pharmaceuticals Care, Ministry of Defense, Najran 66281, Saudi Arabia.
Seham A AlzahraniPharmacy Department, Khamis Mushait General Hospital, King Khalid Rd, Al Shifa, Khamis Mushait 62433, Saudi Arabia.
Mohammed A AlqaadDepartment of Pharmaceutical Care Services, Al Noor Specialized Hospital, Makkah Health, Cluster, Makkah 24241, Saudi Arabia.ORCID 0009-0007-9241-2035
Marwa B BakirDepartment of Medical Education, College of Medicine, Najran University, Najran 1988, Saudi Arabia.
Basel A Abdel-WahabDepartment of Pharmacology, College of Pharmacy, Najran University, Najran 1988, Saudi Arabia.ORCID 0000-0002-5545-6422

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is the most common malignancy affecting women, manifesting as a heterogeneous disease with diverse molecular characteristics and clinical presentations. Recent studies have elucidated the role of epigenetic modifications in the pathogenesis of breast cancer, including drug resistance and efflux characteristics, offering potential new diagnostic and prognostic markers, treatment efficacy predictors, and therapeutic agents. Key modifications include DNA cytosine methylation and the covalent modification of histone proteins. Unlike genetic mutations, reprogramming the epigenetic landscape of the cancer epigenome is a promising targeted therapy for the treatment and reversal of drug resistance. Epidrugs, which target DNA methylation and histone modifications, can provide novel options for the treatment of breast cancer by reversing the acquired resistance to treatment. Currently, the most promising approach involves combination therapies consisting of epidrugs with immune checkpoint inhibitors. This review examines the aberrant epigenetic regulation of breast cancer initiation and progression, focusing on modifications related to estrogen signaling, drug resistance, cancer progression, and the epithelial-mesenchymal transition (EMT). It examines existing epigenetic drugs for treating breast cancer, including agents that modify DNA, inhibitors of histone acetyltransferases, histone deacetylases, histone methyltransferases, and histone demethyltransferases. It also delves into ongoing studies on combining epidrugs with other therapies and addresses the upcoming obstacles in this field.

Indexed as

Breast cancerDNA methylationepidrugsepigeneticshistone acetyl-transferase and histone deacetylase inhibitorshistone methyltransferase and demethyltransferase inhibitorshistone modification

Identifiers

PMID40006021
PMCPMC11858621

What OpenQuestion holds

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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.