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Updated: Feb 15, 2026

On-Site Sampling and Extraction of Brain Tumors for Metabolomics and Lipidomics Analysis
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A Metabolomics Pilot Study on Desmoid Tumors and Novel Drug Candidates

Kelly A Mercier1, Mushriq Al-Jazrawe2,3, Raymond Poon2

  • 1RTI International, Research Triangle Park, Durham, NC, 27709, USA. kmercier@rti.org.

Scientific Reports
|January 14, 2018
PubMed

Insights

This study reveals distinct metabolic profiles in desmoid tumors, linked to specific beta-catenin mutations. Researchers identified targeted therapies that inhibit tumor growth without harming normal cells, offering new treatment avenues.

Area of Science:

  • Oncology
  • Biochemistry
  • Genetics

Background:

  • Desmoid tumors (aggressive fibromatosis) are locally invasive soft tissue neoplasms with no standard treatment.
  • Current therapies like chemotherapy, radiation, and surgery offer only temporary relief.
  • Most desmoid tumors are associated with mutations in the beta-catenin gene (CTNNB1), specifically T41A and S45F.

Purpose of the Study:

  • To investigate metabolic differences between normal fibroblasts and desmoid tumor cells.
  • To analyze metabolic profiles associated with specific CTNNB1 mutations (T41A and S45F).
  • To identify potential therapeutic targets by evaluating drug responses in desmoid tumor cells.

Main Methods:

  • Utilized broad-spectrum metabolomics to compare paired normal fibroblast and desmoid tumor cells.
  • Analyzed metabolomic profiles related to T41A and S45F beta-catenin mutations.
  • Screened compounds for their effect on desmoid tumor cell proliferation versus normal fibroblasts.

Main Results:

  • Identified significant metabolic differences between normal and desmoid tumor cells, varying with CTNNB1 mutation type.
  • Dasatinib and FAK Inhibitor 14 demonstrated >50% inhibition of desmoid tumor cell growth without affecting normal fibroblasts.
  • Drug treatments induced unique metabolomic profiles, highlighting differences between cell types and mutation statuses.

Conclusions:

  • Established preliminary understanding of metabolic distinctions in desmoid tumors and their response to therapeutics.
  • Identified aminoacyl-tRNA biosynthesis and mTORC1 signaling as key differentiating biochemical pathways.
  • Suggests novel therapeutic strategies targeting these metabolic pathways for desmoid tumor treatment.

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