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Metabolic Pathways and Targets in Chondrosarcoma

Ida Micaily1, Megan Roche1, Mohammad Y Ibrahim2

  • 1Department of Medical Oncology, Thomas Jefferson University, Philadelphia, PA, United States.

Frontiers in Oncology
|December 23, 2021
PubMed

Insights

Chondrosarcomas, a rare bone cancer, exhibit poor outcomes due to resistance to standard treatments. This review explores metabolic alterations and signaling pathways driving cancer aggressiveness and resistance, offering new therapeutic targets.

Area of Science:

  • Oncology
  • Cancer Metabolism
  • Epigenetics

Background:

  • Chondrosarcomas are the second most common primary bone cancer.
  • These tumors produce cartilaginous matrix and are typically resistant to radiation and chemotherapy, leading to poor patient outcomes.
  • Understanding the mechanisms behind chondrosarcoma aggressiveness and therapeutic resistance is crucial.

Purpose of the Study:

  • To review metabolic alterations in chondrosarcoma.
  • To explore the relationship between metabolic changes, epigenetic state, and the tumor microenvironment.
  • To discuss potential therapeutic strategies targeting metabolism, including immunotherapy combinations.

Main Methods:

  • Literature review focusing on metabolic pathways in chondrosarcoma.
  • Analysis of signaling pathways including isocitrate dehydrogenase 1 and 2 (IDH1/IDH2), hedgehog, PI3K-mTOR-AKT, and SRC.
  • Examination of the role of histone acetylation and angiogenesis.

Main Results:

  • Metabolic alterations are linked to epigenetic state and tumor microenvironment in chondrosarcoma.
  • Specific signaling pathways (IDH1/IDH2, hedgehog, PI3K-mTOR-AKT, SRC) are implicated in cancer aggressiveness and resistance.
  • Histone acetylation and angiogenesis are associated with chondrosarcoma progression.

Conclusions:

  • Metabolic reprogramming is a key driver of chondrosarcoma aggressiveness and treatment resistance.
  • Targeting metabolic pathways presents a promising therapeutic avenue.
  • Combination therapies, potentially including immunotherapies, may enhance treatment efficacy.
Keywords:
IDHLdhAPI3K - AKT pathwaychondrosarcomalactate dehydrogenasemTORmetabolism

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