Evidence map›Paper›PMID 32336756›Full record

ArticleBritish journal of cancer2020

Targeted therapy for mTORC1-driven tumours through HDAC inhibition by exploiting innate vulnerability of mTORC1 hyper-activation.

Fuchun Yang, Shaogang Sun, Chenran Wang, Michael Haas, Syn Yeo, Jun-Lin Guan

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. 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

6 authors at 2 institutions in 1 country.

Fuchun YangDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Shaogang SunDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Chenran WangDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.ORCID http://orcid.org/0000-0003-4181-2729
Michael HaasDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Syn YeoDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Jun-Lin GuanDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA. guanjl@uc.edu.
University of Cincinnati Medical Center · USUniversity of Cincinnati · US

Funding

Mechanisms of progression of vascular malformation to lymphangiosarcomaR01HL073394 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUAN, JUN-LIN · 2003 to 2025
$8.4M
Regulation of Neural Stem Cells and Neurogenesis by Autophagy GenesR01NS094144 · NINDS · UNIVERSITY OF CINCINNATI · PI GUAN, JUN-LIN · 2015 to 2024
$3.6M
Mechanisms of FIP200 regulation of breast cancer through its autophagy and non-autophagy functionsR01CA211066 · NCI · UNIVERSITY OF CINCINNATI · PI JUN-LIN GUAN · 2017 to 2026
$3.4M
Regulation of Lipid Catabolism by Autophagy in Neural Stem Cell of Tuberous Sclerosis ComplexR01NS103981 · NINDS · UNIVERSITY OF CINCINNATI · PI WANG, CHENRAN · 2018 to 2022
$1.8M
Genetic Analysis of FAK kinase and scaffold functions in breast cancerR01CA163493 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUAN, JUN-LIN · 2012 to 2016
$1.6M
NCI NIH HHS R01 CA163493NCI NIH HHS R01 CA211066NHLBI NIH HHS R01 HL073394NINDS NIH HHS R01 NS094144NINDS NIH HHS R01 NS103981U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) 2R01HL073394-14A1U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL073394-14A1U.S. Department of Health & Human Services | NIH | NCI | Division of Cancer Epidemiology and Genetics, National Cancer Institute (National Cancer Institute Division of Cancer Epidemiology and Genetics) R01CA211066-01A1
6 · The paper itself

Abstract

backgoundThe mechanistic target of rapamycin complex 1 (mTORC1) is important in the development and progression of many cancers. Targeted cancer therapy using mTORC1 inhibitors is used for treatment of cancers; however, their clinical efficacies are still limited.

methodsWe recently created a new mouse model for human lymphangiosarcoma by deleting Tsc1 in endothelial cells and consequent hyper-activation of mTORC1. Using Tsc1

resultsUnlike the cytostatic effect of mTORC1 inhibitors, HDAC inhibitors induced Tsc1

conclusionThese studies suggest a potential new treatment strategy for mTORC1-driven cancers like lymphangiosarcoma through an alternative mechanism.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell ProliferationDisease Models, AnimalHistone Deacetylase InhibitorsLymphangiosarcomaMechanistic Target of Rapamycin Complex 1MiceMolecular Targeted TherapyNeoplasms, ExperimentalAntineoplastic AgentsHistone Deacetylase InhibitorsMechanistic Target of Rapamycin Complex 1

Identifiers

PMID32336756
PMCPMC7283252
OpenAlexW3018841325

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.