Evidence map›Paper›PMID 29330550›Full record

ArticleScientific reports2018

A Metabolomics Pilot Study on Desmoid Tumors and Novel Drug Candidates.

Kelly A Mercier, Mushriq Al-Jazrawe, Raymond Poon, Zachery Acuff, Benjamin Alman

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. PDGFRβ Signaling Cooperates with β-Catenin to Modulate c-Abl and Biologic Behavior of Desmoid-Type Fibromatosis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. On the Relevance of Soft Tissue Sarcomas Metabolic Landscape Mapping.International journal of molecular sciences · 2022
    Review
  10. Article
  11. CRISPR-SID: Identifying EZH2 as a druggable target for desmoid tumors via in vivo dependency mapping.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. High-Throughput Metabolomics by 1D NMR.Angewandte Chemie (International ed. in English) · 2019
    Review
  18. 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

5 authors at 3 institutions in 2 countries.

Kelly A MercierRTI International, Research Triangle Park, Durham, NC, 27709, USA. kmercier@rti.org.
Mushriq Al-JazraweDevelopmental & Stem Cell Biology Program, Hospital for Sick Children, Toronto, ON, Canada.
Raymond PoonDevelopmental & Stem Cell Biology Program, Hospital for Sick Children, Toronto, ON, Canada.
Zachery AcuffRTI International, Research Triangle Park, Durham, NC, 27709, USA.
Benjamin AlmanDevelopmental & Stem Cell Biology Program, Hospital for Sick Children, Toronto, ON, Canada. ben.alman@dm.duke.edu.
Hospital for Sick Children · CARTI International · USUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Desmoid tumors (aggressive fibromatosis) are locally invasive soft tissue tumors that lack the ability to metastasize. There are no directed therapies or standard treatment plan, and chemotherapeutics, radiation, and surgery often have temporary effects. The majority of desmoid tumors are related to T41A and S45F mutations of the beta-catenin encoding gene (CTNNB1). Using broad spectrum metabolomics, differences were investigated between paired normal fibroblast and desmoid tumor cells from affected patients. There were differences identified, also, in the metabolomics profiles associated with the two beta-catenin mutations, T41A and S45F. Ongoing drug screening has identified currently available compounds which inhibited desmoid tumor cellular growth by more than 50% but did not affect normal fibroblast proliferation. Two drugs were investigated in this study, and Dasatinib and FAK Inhibitor 14 treatments resulted in unique metabolomics profiles for the normal fibroblast and desmoid tumor cells, in addition to the T41A and S45F. The biochemical pathways that differentiated the cell lines were aminoacyl-tRNA biosynthesis in mitochondria and cytoplasm and signal transduction amino acid-dependent mTORC1 activation. This study provides preliminary understanding of the metabolic differences of paired normal and desmoid tumors cells, their response to desmoid tumor therapeutics, and new pathways to target for therapy.

Indexed as

beta CateninCell Line, TumorDasatinibDesmoid TumorsDrug Screening Assays, AntitumorFemaleGene Expression Regulation, NeoplasticHumansMaleMetabolomeMetabolomicsMutationPilot ProjectsProtein Kinase Inhibitorsbeta CateninCTNNB1 protein, humanDasatinibProtein Kinase Inhibitors

Identifiers

PMID29330550
PMCPMC5766559
OpenAlexW2783140122

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.