ReviewCancer genomics & proteomics
Histone Deacetylases as New Therapeutic Targets in Triple-negative Breast Cancer: Progress and Promises.
Review in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- Signaling Pathways and Natural Compounds in Triple-Negative Breast Cancer Cell Line.Molecules (Basel, Switzerland) · 2022Pooled it
- Chidamide combined with fulvestrant in the treatment of HR-positive, HER2-negative advanced breast cancer after failure of previous endocrine therapy: a single-arm, single-center, phase 2 study.Breast cancer research : BCR · 2026Trial
- Histone Deacetylase-2 Expression in Colorectal Cancer: An Immunohistochemical Study and Its Clinicopathological Significance.Cancers · 2026Article
- Steroidogenic Acute Regulatory Protein in Breast Cancer: Mechanistic Insights into Pathogenesis and Therapeutics.International journal of molecular sciences · 2026Review
- Repositioning Antihistamine for Cancer Therapy: Clemizole as a Template for the Design of Liver Tissue-Targeting Epigenetic-Modifying Agents.Journal of medicinal chemistry · 2026Article
- Crosstalk between acetylation modification and autophagy in cancer: roles, mechanisms, and therapeutic potential.Cell death discovery · 2025Review
- Guardians in the Gut: Mechanistic Insights into a Hidden Ally Against Triple-Negative Breast Cancer.Cancers · 2025Review
- The role of the gut microbiota in shaping the tumor microenvironment and immunotherapy of breast cancer.Frontiers in microbiology · 2025Review
- Acetylation-Mediated Epigenetic Consequences for Biological Control and Cancer.Results and problems in cell differentiation · 2025Review
- Apigenin and its combination with Vorinostat induces apoptotic-mediated cell death in TNBC by modulating the epigenetic and apoptotic regulators and related miRNAs.Scientific reports · 2024Article
- Dual inhibitors of DNMT and HDAC induce viral mimicry to induce antitumour immunity in breast cancer.Cell death discovery · 2024Article
- Catalysts of Healing: A Symphony of Synthesis and Clinical Artistry in Small-Molecule Agents for Breast Cancer Alleviation.Molecules (Basel, Switzerland) · 2024Review
- Unlocking the epigenetic code: new insights into triple-negative breast cancer.Frontiers in oncology · 2024Review
- Review
- Cytotoxic evaluation of YSL-109 in a triple negative breast cancer cell line and toxicological evaluations.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- The Role of Bitter Melon in Breast and Gynecological Cancer Prevention and Therapy.International journal of molecular sciences · 2023Review
- Review
- Control of Redox Homeostasis by Short-Chain Fatty Acids: Implications for the Prevention and Treatment of Breast Cancer.Pathogens (Basel, Switzerland) · 2023Review
- Emerging Epigenetic-Based Nanotechnology for Cancer Therapy: Modulating the Tumor Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) lacks expression of estrogen receptor (ER), progesterone receptor (PR) and HER2 gene. It comprises approximately 15-20% of breast cancers (BCs). Unfortunately, TNBC's treatment continues to be a clinical problem because of its relatively poor prognosis, its aggressiveness and the lack of targeted therapies, leaving chemotherapy as the mainstay of treatment. It is essential to find new therapies against TNBC, in order to surpass the resistance and the invasiveness of already existing therapies. Given the fact that epigenetic processes control both the initiation and progression of TNBC, there is an increasing interest in the mechanisms, molecules and signaling pathways that participate at the epigenetic modulation of genes expressed in carcinogenesis. The acetylation of histone proteins provokes the transcription of genes involved in cell growth, and the expression of histone deacetylases (HDACs) is frequently up-regulated in many malignancies. Unfortunately, in the field of BC, HDAC inhibitors have shown limited effect as single agents. Nevertheless, their use in combination with kinase inhibitors, autophagy inhibitors, ionizing radiation, or two HDAC inhibitors together is currently being evaluated. HDAC inhibitors such as suberoylanilidehydroxamic acid (SAHA), sodium butyrate, mocetinostat, panobinostat, entinostat, YCW1 and N-(2-hydroxyphenyl)-2-propylpentanamide have shown promising therapeutic outcomes against TNBC, especially when they are used in combination with other anticancer agents. More studies concerning HDAC inhibitors in breast carcinomas along with a more accurate understanding of the TNBC's pathobiology are required for the possible identification of new therapeutic strategies.
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Registered trials
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.