Evidence map›Paper›PMID 37294406›Full record

ReviewMedical oncology (Northwood, London, England)2023

Recent advancement of HDAC inhibitors against breast cancer.

Syed Abdulla Mehmood, Kantrol Kumar Sahu, Sounok Sengupta, Sangh Partap, Rajshekhar Karpoormath, Brajesh Kumar, Deepak Kumar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. ACS pharmacology & translational science · 2025
    Article
  5. Article
  6. Article
  7. Histone acetylation modulators in breast cancer.Breast cancer research : BCR · 2025
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
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

7 authors at 5 institutions in 2 countries.

Syed Abdulla MehmoodDepartment of Pharmacology, School of Pharmaceutical Education & Research, Jamia Humdard University, New Delhi, India.
Kantrol Kumar SahuDepartment of Pharmacology, Institute of Pharmaceutical Research, GLA University, Mathura, Uttar Pradesh, India.
Sounok SenguptaDepartment of Pharmacology, School of Pharmaceutical Sciences, Shoolini University, Solan, Himachal Pradesh, India.
Sangh PartapDepartment of Pharmaceutical Chemistry, Discipline of Pharmaceutical Sciences, College of Health Sciences, University of KwaZulu-Natal, Durban, 4000, South Africa.
Rajshekhar KarpoormathDepartment of Pharmaceutical Chemistry, Discipline of Pharmaceutical Sciences, College of Health Sciences, University of KwaZulu-Natal, Durban, 4000, South Africa.
Brajesh KumarDepartment of Chemistry, TATA College, Kolhan University, Chaibasa, India.
Deepak KumarDepartment of Pharmaceutical Chemistry, School of Pharmaceutical Sciences, Shoolini University, Solan, Himachal Pradesh, India. guptadeepak002@gmail.com.ORCID http://orcid.org/0000-0003-2241-0054
Shoolini University · INUniversity of KwaZulu-Natal · ZAGLA University · INJamia Hamdard · INKolhan University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies highlight the great potential impact of HDAC inhibitors (HDACis) in suppressing TNBC, even though clinical trials including a single HDACis demonstrated unsatisfactory outcomes against TNBC. New compounds created to achieve isoform selectivity and/or a polypharmacological HDAC strategy have also produced interesting results. The current study discusses the HDACis pharmacophoric models and the structural alterations that produced drugs with strong inhibitory effects on TNBC progression. With more than 2 million new cases reported in 2018, breast cancer-the most common cancer among women worldwide-poses a significant financial burden on an already deteriorating public health system. Due to a lack of therapies being developed for triple-negative breast cancers and the development of resistance to the current treatment options, it is imperative to plan novel therapeutics in order to bring new medications to the pipeline. Additionally, HDACs deacetylate a large number of nonhistone cellular substrates that control a variety of biological processes, such as the beginning and development of cancer. The significance of HDACs in cancer and the therapeutic potential of HDAC inhibitor. Furthermore, we also reported molecular docking study with four HDAC inhibitors and performed molecular dynamic stimulation of the best dock score compound. Among the four ligands belinostat compound showed best binding affinity with histone deacetylase protein which was -8.7 kJ/mol. It also formed five conventional hydrogen bond with Gly 841, His 669, His 670, pro 809, and His 709 amino acid residues.

Indexed as

Histone Deacetylase InhibitorsTriple Negative Breast NeoplasmsFemaleHistone DeacetylasesHumansMolecular Docking SimulationProtein IsoformsHistone Deacetylase InhibitorsHistone DeacetylasesProtein IsoformsCancerCell lineHDACMd simulationMolecular dockingTNBC

Identifiers

PMID37294406
OpenAlexW4379967583

What OpenQuestion holds

Textmetadata
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.