Biological aspects of chondrosarcoma: Leaps and hurdles

Crit Rev Oncol Hematol. 2018 Jun:126:32-36. doi: 10.1016/j.critrevonc.2018.03.009. Epub 2018 Mar 22.

Abstract

Chondrosarcomas are characterized by their chemo- and radioresistance leading to a therapeutic surgical approach which remains the only available treatment with a 10-year survival between 30% and 80% depending on the grade. Non-surgical treatments are under investigation and rely on an accurate biological understanding of drug resistance mechanisms. Novel targeted therapy which represents a new relevant therapeutic approach will open new treatment options by targeting several pathways responsible for processes of proliferation and invasion. Survival pathways such as PI3K, AKT, mTOR and VEGF have been shown to be involved in proliferation of chondrosarcoma cells and antiapoptotic proteins may also play a relevant role. Other proteins such as p53 or COX2 have been identified as potential new targets. This review provides an insight into the biological substantial treatment challenges of CHS and focuses on improving our understanding of CH biology through an overview of major signaling pathways that could represent targets for new therapeutic approaches.

Keywords: Biology; Chemo and radiation resistance; Chondrosarcoma; Signaling pathways.

Publication types

  • Review

MeSH terms

  • Bone Neoplasms / metabolism*
  • Bone Neoplasms / pathology*
  • Bone Neoplasms / therapy*
  • Chondrosarcoma / metabolism*
  • Chondrosarcoma / pathology*
  • Chondrosarcoma / therapy*
  • Drug Resistance, Neoplasm / physiology
  • Drugs, Investigational / therapeutic use
  • Humans
  • Molecular Targeted Therapy / methods
  • Molecular Targeted Therapy / trends
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction / physiology
  • TOR Serine-Threonine Kinases / metabolism
  • Therapies, Investigational / methods
  • Therapies, Investigational / trends

Substances

  • Drugs, Investigational
  • MTOR protein, human
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases