A network of genetic events sufficient to convert normal human cells to a tumorigenic state
SDS Kendall, CM Linardic, SJ Adam, CM Counter - Cancer research, 2005 - AACR
SDS Kendall, CM Linardic, SJ Adam, CM Counter
Cancer research, 2005•AACRAlthough 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 …
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 …
Abstract
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.
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