Evidence map›Paper›PMID 34523696›Full record

ArticleInternational journal of oncology2021

Targeting the mTOR pathway using novel ATP‑competitive inhibitors, Torin1, Torin2 and XL388, in the treatment of glioblastoma.

Anubhav G Amin, Seung Won Jeong, John L Gillick, Tolga Sursal, Raj Murali, Chirag D Gandhi, Meena Jhanwar-Uniyal

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2021. 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
1.4field-weighted citation impact, top 19% 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
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  6. Inhibition of TRAF3IP2 Modulates NAMPT and NAD Metabolism in Glioblastoma.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
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  16. The Role of NRF2/KEAP1 Pathway in Glioblastoma: Pharmacological Implications.Medical oncology (Northwood, London, England) · 2022
    Review
  17. 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

7 authors at 2 institutions in 1 country.

Anubhav G Amin *Department of Neurosurgery, New York Medical College/Westchester Medical Center, Valhalla, NY 10595, USA.
Seung Won Jeong *Department of Neurosurgery, New York Medical College/Westchester Medical Center, Valhalla, NY 10595, USA.
John L Gillick *Department of Neurosurgery, New York Medical College/Westchester Medical Center, Valhalla, NY 10595, USA.
Tolga SursalDepartment of Neurosurgery, New York Medical College/Westchester Medical Center, Valhalla, NY 10595, USA.
Raj MuraliDepartment of Neurosurgery, New York Medical College/Westchester Medical Center, Valhalla, NY 10595, USA.
Chirag D GandhiDepartment of Neurosurgery, New York Medical College/Westchester Medical Center, Valhalla, NY 10595, USA.
Meena Jhanwar-UniyalDepartment of Neurosurgery, New York Medical College/Westchester Medical Center, Valhalla, NY 10595, USA.
Westchester Medical Center · USNew York Medical College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mechanistic target of rapamycin (mTOR), which functions via two multiprotein complexes termed mTORC1 and mTORC2, is positioned in the canonical phosphoinositide 3‑kinase‑related kinase (PI3K)/AKT (PI3K/AKT) pathways. These complexes exert their actions by regulating other important kinases, such as 40S ribosomal S6 kinases (S6K), eukaryotic translation initiation factor 4E (elF4E)‑binding protein 1 (4E‑BP1) and AKT, to control cell growth, proliferation, migration and survival in response to nutrients and growth factors. Glioblastoma (GB) is a devastating form of brain cancer, where the mTOR pathway is deregulated due to frequent upregulation of the Receptor Tyrosine Kinase/PI3K pathways and loss of the tumor suppressor phosphatase and tensin homologue (PTEN). Rapamycin and its analogs were less successful in clinical trials for patients with GB due to their incomplete inhibition of mTORC1 and the activation of mitogenic pathways via negative feedback loops. Here, the effects of selective ATP‑competitive dual inhibitors of mTORC1 and mTORC2, Torin1, Torin2 and XL388, are reported. Torin2 exhibited concentration‑dependent pharmacodynamic effects on inhibition of phosphorylation of the mTORC1 substrates S6K

Indexed as

Brain NeoplasmsCell Line, TumorCell MovementCell ProliferationGlioblastomaHumansMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2MTOR InhibitorsNaphthyridinesSulfones1-(4-(4-propionylpiperazin-1-yl)-3-(trifluoromethyl)phenyl)-9-(quinolin-3-yl)benzo(h)(1,6)naphthyridin-2(1H)-one9-(6-aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo(h)(1,6)naphthyridin-2(1H)-oneMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2MTOR InhibitorsNaphthyridinesSulfonesXL388glioblastomamTORmTOR inhibitorsPRAS40Torin1Torin2

Identifiers

PMID34523696
PMCPMC8448541
OpenAlexW3199996507

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.