Classification of Glioblastoma Multiforme in Adults by... : The Cancer Journal (original) (raw)

GLIOBLASTOMA

Benjamin, Ramsis MD, MPHa,b; Capparella, Joanna DOa; Brown, Alice MD, PhDa

aMassachusetts General Hospital, Brain Tumor Center, Boston, Massachusetts

bCarolina Neurosurgery & Spine Associates, Charlotte, North Carolina.

Reprint requests: Alice Brown, MD, PhD, Massachusetts General Hospital, Brain Tumor Center, 100 Blossom Street Cox 315, Boston, MA 02114.

No benefits in any form have been or will be received from a commercial party related directly or indirectly to the subject of this article.

Received on March 11, 2003; accepted for publication March 12, 2003.

Abstract

Recent advances in cytogenetic and molecular methodologies have elucidated certain principal characteristics of oncogenesis in glioblastoma multiforme. The earliest clues implicate gene sequence alterations, such as gene amplification and numerical gain or loss of function in specific chromosomes. Genetic classification and expression patterns have thus been constructed, conferring the likelihood of two types of glioblastoma, primary (de novo) as opposed to secondary (evolving from a pre-existing low-grade glioma). The former group of tumors exhibits more frequent occurrences of EGFR gene amplification, whereas the latter group relies strongly on _TP53_gene inactivation. Many other tumor suppressor genes and oncogenes have been discovered. Most gene alterations induce cell cycle dysfunction on a complex molecular level. Further insight into tumor genesis by means of genomic assays may aid in predicting the clinical behavior of glioblastoma and in providing individualized potential targets for therapeutic agents.