Central neurotoxicity in cancer chemotherapy: pharmacogenetic insights

Pharmacogenomics. 2011 Mar;12(3):379-95. doi: 10.2217/pgs.10.197.

Abstract

Central neurotoxicity of chemotherapy is likely to be multifactorial. There are two hypotheses regarding endogenous mechanisms that may be involved, namely the target and the blood-brain barrier transporter hypotheses. Here, we will review candidate genetic determinants for the risk of chemotherapy-induced neurotoxicity, such as polymorphisms involved in the target mechanism. These include polymorphisms in folate metabolizing enzymes and apolipoprotein E, as well as those in blood-brain barrier transporter genes. Currently, the exact role of pharmacogenetics in mechanisms that lead to central neurotoxicity of chemotherapy has not been fully unraveled. Larger, prospective, longitudinal and more uniform studies are needed, with prechemotherapy and follow-up measurements of neuropsychological performance, MRI, PET, genetic profiles and biomarkers relevant for the proposed target and transporter mechanisms.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Antineoplastic Agents / adverse effects*
  • Antineoplastic Agents / therapeutic use
  • Apolipoproteins E / genetics
  • Blood-Brain Barrier
  • Central Nervous System Diseases / chemically induced
  • Central Nervous System Diseases / genetics*
  • Humans
  • Metabolic Networks and Pathways / genetics
  • Methotrexate / adverse effects
  • Methotrexate / therapeutic use
  • Neoplasms / drug therapy*
  • Neurotoxicity Syndromes / genetics*
  • Pharmacogenetics / trends
  • Polymorphism, Genetic

Substances

  • Antineoplastic Agents
  • Apolipoproteins E
  • Methotrexate