About this Biochemistry, Genetics and Molecular Biology article

Use of Wild-type P53 to Achieve Complete Treatment Sensitization of Tumor Cells Expressing Endogenous Mutant P53 by Ruth A. Gjerset; Sally T. Turla; Robert E. Sobol; Jason J. Scalise; Dan Mercola; Heli Collins; Penelope J. Hopkins is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

## Abstract It is known that transfer of the wild‐type __p53__ gene into __p53__‐negative cells from transgenic mice increases their sensitivity to drug and radiation‐induced apoptosis. However, unlike many human tumors, these transgenic cells do not express mutant p53, and it is not known from these earlier studies whether wild‐type p53 dominates the effects of mutant p53 with respect to drug and radiation sensitivity. We addressed this question in glioblastoma, a disease characterized by an unusually high level of intrinsic resistance to therapy and poor prognosis: mean survival time from diagnosis is only about 1 yr. We introduced the gene for wild‐type __p53__ into human T98G glioblastoma cells, which express endogenous mutant p53 but not wild‐type p53. Stable transfectants that co‐expressed mutant and wild‐type p53 had enhanced sensitivity to cisplatin and gamma radiation, compared with parental cells, control vector‐transduced cells, and transduced cells that had lost expression of wild‐type p53. Transient wild‐type p53 expression after high‐efficiency gene transfer by a p53 adenovirus also sensitized the cells to cisplatin and correlated with the induction of apoptosis. The

Author

Ruth A. Gjerset; Sally T. Turla; Robert E. Sobol; Jason J. Scalise; Dan Mercola; Heli Collins; Penelope J. Hopkins

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0899-1987)

Published

1995

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)