A genetically tractable model of human glioma formation.

Published

Journal Article

Gliomas remain one of the deadliest forms of cancer. Improved therapeutics will require a better understanding of the molecular nature of these tumors. We, therefore, mimicked the most common genetic changes found in grade III-IV gliomas, disruption of the p53 and RB pathways and activation of telomere maintenance and independence from growth factors, through the ectopic expression of the SV40 T/t-Ag oncogene, an oncogenic form of H-ras (H-ras(V12G)), and the human telomerase catalytic subunit hTERT in normal human astrocytes. The resulting cells displayed many of the hallmarks of grade III-IV gliomas, including greatly expanded life span and growth in soft agar and, most importantly, were tumorigenic with pathology consistent with grade III-IV neuroectodermal tumors in mice. This model system will, for the first time, allow the biological significance of selected genetic alterations to be studied in human gliomas.

Full Text

Duke Authors

Cited Authors

  • Rich, JN; Guo, C; McLendon, RE; Bigner, DD; Wang, XF; Counter, CM

Published Date

  • May 2001

Published In

Volume / Issue

  • 61 / 9

Start / End Page

  • 3556 - 3560

PubMed ID

  • 11325817

Pubmed Central ID

  • 11325817

Electronic International Standard Serial Number (EISSN)

  • 1538-7445

International Standard Serial Number (ISSN)

  • 0008-5472

Language

  • eng