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Related Concept Videos

The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...

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Related Experiment Video

Updated: May 11, 2026

Molecular and Immunologic Techniques in a Genetically Engineered Mouse Model of Gastrointestinal Stromal Tumor
07:21

Molecular and Immunologic Techniques in a Genetically Engineered Mouse Model of Gastrointestinal Stromal Tumor

Published on: May 2, 2022

Gastrointestinal stromal tumors.

Markku Miettinen1, Jerzy Lasota

  • 1Laboratory of Pathology, NCI/NIH, Bethesda, MD 20892, USA. miettinenmm@mail.nih.gov

Gastroenterology Clinics of North America
|May 4, 2013
PubMed
Summary

Gastrointestinal stromal tumors (GISTs) are common. Early GIST treatments targeted KIT mutations, but new research reveals other causes like SDH deficiencies and BRAF mutations.

Area of Science:

  • Gastroenterology
  • Oncology
  • Molecular Biology

Background:

  • Gastrointestinal stromal tumors (GISTs) represent the most frequent mesenchymal neoplasms within the gastrointestinal tract.
  • GISTs were initially identified as tumors driven by mutations in KIT or platelet-derived growth factor receptor (PDGFR).
  • This understanding established GISTs as a primary target for tyrosine kinase inhibitor (TKI) therapies in solid tumors.

Purpose of the Study:

  • To review the evolving understanding of GIST pathogenesis.
  • To highlight newly discovered molecular mechanisms driving GIST development.
  • To provide an updated perspective on GISTs beyond KIT/PDGFR mutations.

Main Methods:

  • Literature review of GIST pathogenesis.
  • Analysis of recent molecular discoveries in GISTs.

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  • Synthesis of information on succinate dehydrogenase (SDH) deficiencies, NF1 alterations, and BRAF mutations in GISTs.

    • Main Results:

    • GISTs are primarily driven by KIT or PDGFR mutations, leading to successful TKI therapies.
    • Alternative molecular pathways, including succinate dehydrogenase (SDH) complex deficiencies, are implicated in GIST pathogenesis.
    • NF1-gene alterations associated with neurofibromatosis type 1 and rare BRAF oncogene mutations also contribute to GIST development.

    Conclusions:

    • The molecular landscape of GISTs is more complex than initially recognized.
    • Understanding these diverse molecular drivers is crucial for advancing GIST treatment strategies.
    • Further research into non-KIT/PDGFR driven GISTs may uncover novel therapeutic targets.