A network of genetic events sufficient to convert normal human cells to a tumorigenic state.

Journal Article

Although great progress has been made at identifying and characterizing individual genes involved in cancer, less is known about how the combination of such genes collaborate to form tumors in humans. To this end, we sought to genetically recreate tumorigenesis in normal human cells using genes altered in human cancer. We now show that expression of mammalian proteins that inactivate the tumor suppressors Rb and p53 in conjunction with the oncoproteins Ras and Myc and the telomerase subunit hTERT is sufficient to drive a number of normal human somatic cells to a tumorigenic fate. This provides a blueprint of the events that lead to human cancer, allowing different cancers to be genetically modeled from normal human cells.

Full Text

Duke Authors

Cited Authors

  • Kendall, SD; Linardic, CM; Adam, SJ; Counter, CM

Published Date

  • November 1, 2005

Published In

Volume / Issue

  • 65 / 21

Start / End Page

  • 9824 - 9828

PubMed ID

  • 16267004

International Standard Serial Number (ISSN)

  • 0008-5472

Digital Object Identifier (DOI)

  • 10.1158/0008-5472.CAN-05-1543

Language

  • eng

Conference Location

  • United States