Altered metabolism in head and neck squamous cell carcinoma: an opportunity for identification of novel biomarkers and drug targets

Head Neck. 2012 Feb;34(2):282-90. doi: 10.1002/hed.21664. Epub 2011 Feb 14.

Abstract

Tumor cells were first shown to exhibit a distinct metabolic phenotype over 80 years ago. Since then, it has become clear that multiple oncogenic events contribute to the development of a metabolic phenotype that supports rapid proliferation. Because this phenotype represents an essential component of tumorigenesis and disease progression, it also represents a potential source of biomarkers associated with aggressive disease. In addition, the addiction of tumor cells to specific nutrients and the up-regulation of key metabolic enzymes provide unique opportunities for pharmacologic manipulation. Despite the use of multimodality treatment, survival rates for patients with advanced head and neck squamous cell carcinoma (HNSCC) remain low, partially attributed to the development of drug resistance. In this review, we evaluate the role of altered HNSCC metabolism as both a source of novel biomarkers and a means to bypass resistance mechanisms to conventional forms of therapy.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Biomarkers, Tumor / metabolism*
  • Carcinoma, Squamous Cell / drug therapy
  • Carcinoma, Squamous Cell / genetics
  • Carcinoma, Squamous Cell / metabolism*
  • Carcinoma, Squamous Cell / mortality
  • Cell Proliferation
  • Cell Transformation, Neoplastic / metabolism*
  • Drug Resistance, Neoplasm
  • Glucose Transport Proteins, Facilitative / metabolism
  • Glycolysis / physiology
  • Head and Neck Neoplasms / drug therapy
  • Head and Neck Neoplasms / genetics
  • Head and Neck Neoplasms / metabolism*
  • Head and Neck Neoplasms / mortality
  • Humans
  • Oncogene Protein v-akt / physiology
  • Phenotype
  • Phosphatidylinositol 3-Kinases / physiology
  • Squamous Cell Carcinoma of Head and Neck

Substances

  • Biomarkers, Tumor
  • Glucose Transport Proteins, Facilitative
  • Phosphatidylinositol 3-Kinases
  • Oncogene Protein v-akt