Evidence map›Paper›PMID 39542458›Full record

ArticleCell proliferation2025

The apoptotic and anti-proliferative effects of Neosetophomone B in T-cell acute lymphoblastic leukaemia via PI3K/AKT/mTOR pathway inhibition.

Shilpa Kuttikrishnan, Abdul W Ansari, Muhammad Suleman, Fareed Ahmad, Kirti S Prabhu, Tamam El-Elimat, Feras Q Alali, Ammira S Al Shabeeb Akil, Ajaz A Bhat, Maysaloun Merhi and 3 more

Abstract read
In one paragraph

Article in Cell proliferation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Chromatin regulatorsChinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. 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

13 authors.

Shilpa KuttikrishnanTranslational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.
Abdul W AnsariTranslational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.
Muhammad SulemanLaboratory of Animal Research Center, Qatar University, Doha, Qatar.
Fareed AhmadTranslational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.
Kirti S PrabhuTranslational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.
Tamam El-ElimatDepartment of Medicinal Chemistry and Pharmacognosy, Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Qatar.
Feras Q AlaliCollege of Pharmacy, QU Health, Qatar University, Doha, Qatar.
Ammira S Al Shabeeb AkilDepartment of Human Genetics-Precision Medicine in Diabetes, Obesity and Cancer Program, Sidra Medicine, Doha, Qatar.
Ajaz A BhatDepartment of Human Genetics-Precision Medicine in Diabetes, Obesity and Cancer Program, Sidra Medicine, Doha, Qatar.
Maysaloun MerhiTranslational Cancer Research Facility, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Said DermimeTranslational Cancer Research Facility, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Martin SteinhoffTranslational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.
Shahab UddinTranslational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.ORCID https://orcid.org/0000-0003-1886-6710

Funding

Hamad Medical Corporation MRC-01-21-301
6 · The paper itself

Abstract

The phosphatidylinositol 3-kinase/Protein Kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signalling pathway is pivotal in various cancers, including T-cell acute lymphoblastic leukaemia (T-ALL), a particularly aggressive type of leukaemia. This study investigates the effects of Neosetophomone B (NSP-B), a meroterpenoid fungal metabolite, on T-ALL cell lines, focusing on its anti-cancer mechanisms and therapeutic potential. NSP-B significantly inhibited the proliferation of T-ALL cells by inducing G0/G1 cell cycle arrest and promoting caspase-dependent apoptosis. Additionally, NSP-B led to the dephosphorylation and subsequent inactivation of the PI3K/AKT/mTOR signalling pathway, a critical pathway in cell survival and growth. Molecular docking studies revealed a strong binding affinity of NSP-B to the active site of AKT, primarily involving key residues crucial for its activity. Interestingly, NSP-B treatment also induced apoptosis and significantly reduced proliferation in phytohemagglutinin-activated primary human CD3

Indexed as

Antineoplastic AgentsApoptosisPrecursor T-Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesCell Line, TumorCell ProliferationHumansMolecular Docking SimulationPhosphatidylinositol 3-KinasesTerpenesAntineoplastic AgentsMTOR protein, humanneosetophomone BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTerpenesTOR Serine-Threonine Kinases

Identifiers

PMID39542458
PMCPMC11882758

What OpenQuestion holds

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LicenceCC BY
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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.