The paradox of neoplastic glial cell invasion of the brain and apparent metastatic failure

Anticancer Res. Nov-Dec 1997;17(6B):4103-5.


Brain tumours fall into 3 major categories: a) secondary tumours which have originated in distant parts of the body, b) meningiomas, which generally grow on, rather than in, the substance of the brain and c) intrinsic tumours which are generally composed of neoplastic glial cells. Secondary tumours show a marked propensity for metastasis to, and growth in, the brain; up to 24% of cancers are thought to metastasize to the brain. These metastatic deposits are frequently multiple but are usually well circumscribed lesions. Meningiomas are usually benign lesions which grow by expansion and seeding along the leptomeninges on the surface of the brain. Such tumours may, however, recur and show some degree of invasion of the underlying cerebral cortex. The most common form of brain tumour is the glioma, of which there are various histological types. These tumours generally fail to metastasize out of the nervous system. Two plausable explanations for this failure have been recently proposed. Firstly, the vascular basal laminae of the brain appears to exclude intravasation of neoplastic glia and secondly, if such cells do enter the vascular system they are prevented from binding to the endothelial cells of "target" organs by virtue of a lack of appropriate cell adhesion molecules, including CD 15. While intrinsic glial tumours fail to metastasize they are, however, characterised by diffuse local invasion of the normal nervous tissues. This important biological feature hampers all current therapeutic approaches. Local invasion is a multi-faceted phenomenon of interactive mechanisms including cell motility, adhesion and enzymic remodelling of the extracellular matrix components and involves paracrine interaction between normal and neoplastic cellular elements.

Publication types

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

MeSH terms

  • Blood-Brain Barrier
  • Brain Neoplasms / secondary*
  • Cell Communication
  • Cell Movement / physiology
  • Glioma / secondary*
  • Humans
  • Lewis X Antigen / metabolism
  • Neoplasm Invasiveness
  • Neoplasm Metastasis
  • Neuroglia / pathology*
  • Time Factors


  • Lewis X Antigen