Evidence map›Paper›PMID 39021957›Full record

ReviewHeliyon2024

Stochasticity of anticancer mechanisms underlying clinical effectiveness of vorinostat.

Nasreddine El Omari, Asaad Khalid, Hafiz A Makeen, Hassan A Alhazmi, Mohammed Albratty, Syam Mohan, Ching Siang Tan, Long Chiau Ming, Jack Bee Chook, Abdelhakim Bouyahya

Abstract readReview
In one paragraph

Review in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Epigenetic regulation in gynecological cancers: a paradigm shift in immunotherapy strategies.Journal of experimental & clinical cancer research : CR · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. 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

10 authors.

Nasreddine El OmariHigh Institute of Nursing Professions and Health Techniques of Tetouan, Tetouan, Morocco.
Asaad KhalidSubstance Abuse and Toxicology Research Center, Jazan University, P.O. Box 114, Postal Code 45142, Jazan, Saudi Arabia.
Hafiz A MakeenPharmacy Practice Research Unit, Clinical Pharmacy Department, Faculty of Pharmacy, Jazan University, Jazan, Saudi Arabia.
Hassan A AlhazmiSubstance Abuse and Toxicology Research Center, Jazan University, P.O. Box 114, Postal Code 45142, Jazan, Saudi Arabia.
Mohammed AlbrattyDepartment of Pharmaceutical Chemistry and Pharmacognosy, College of Pharmacy, Jazan University, P.O. Box 114, Postal Code 45142, Jazan, Saudi Arabia.
Syam MohanSubstance Abuse and Toxicology Research Center, Jazan University, P.O. Box 114, Postal Code 45142, Jazan, Saudi Arabia.
Ching Siang TanSchool of Pharmacy, KPJ Healthcare University, Nilai, Malaysia.
Long Chiau MingSchool of Medical and Life Sciences, Sunway University, Sunway City, Malaysia.
Jack Bee ChookSchool of Medical and Life Sciences, Sunway University, Sunway City, Malaysia.
Abdelhakim BouyahyaLaboratory of Human Pathologies Biology, Faculty of Sciences, Mohammed V University in Rabat, Rabat, 10106, Morocco.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Food and Drug Administration (FDA) has approved vorinostat, also called Zolinza®, for its effectiveness in fighting cancer. This drug is a suberoyl-anilide hydroxamic acid belonging to the class of histone deacetylase inhibitors (HDACis). Its HDAC inhibitory potential allows it to accumulate acetylated histones. This, in turn, can restore normal gene expression in cancer cells and activate multiple signaling pathways. Experiments have proven that vorinostat induces histone acetylation and cytotoxicity in many cancer cell lines, increases the level of p21 cell cycle proteins, and enhances pro-apoptotic factors while decreasing anti-apoptotic factors. Additionally, it regulates the immune response by up-regulating programmed death-ligand 1 (PD-L1) and interferon gamma receptor 1 (IFN-γR1) expression, and can impact proteasome and/or aggresome degradation, endoplasmic reticulum function, cell cycle arrest, apoptosis, tumor microenvironment remodeling, and angiogenesis inhibition. In this study, we sought to elucidate the precise molecular mechanism by which Vorinostat inhibits HDACs. A deeper understanding of these mechanisms could improve our understanding of cancer cell abnormalities and provide new therapeutic possibilities for cancer treatment.

Indexed as

ApoptosisCancerCell deathClinical efficacyEpigenetic pathwaysHuman and diseaseMedicineOncology

Identifiers

PMID39021957
PMCPMC11253278

What OpenQuestion holds

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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.