Jump to ContentJump to Main Navigation
Show Summary Details
More options …

Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board Member: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Sies, Helmut / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred

12 Issues per year


IMPACT FACTOR 2016: 3.273

CiteScore 2016: 3.01

SCImago Journal Rank (SJR) 2016: 1.679
Source Normalized Impact per Paper (SNIP) 2016: 0.800

Online
ISSN
1437-4315
See all formats and pricing
More options …
Volume 389, Issue 1 (Jan 2008)

Issues

Differential effects of novel tumour-derived p53 mutations on the transformation of NIH-3T3 cells

Howard Donninger
  • 1Division of Medical Biochemistry, Institute for Infectious Disease and Molecular Medicine, Faculty of Health Sciences, University of Cape Town, Observatory 7925, South Africa
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Anke Binder
  • 2Division of Virology, Institute for Infectious Disease and Molecular Medicine, Faculty of Health Sciences, University of Cape Town, Observatory 7925, South Africa
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Lothar Bohm
  • 3Department of Radiation Oncology, Faculty of Medicine, University of Stellenbosch, Tygerberg 7505, South Africa
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ M. Iqbal Parker
  • 4Division of Medical Biochemistry, Institute for Infectious Disease and Molecular Medicine, Faculty of Health Sciences, University of Cape Town, Observatory 7925, South Africa
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
Published Online: 2007-12-20 | DOI: https://doi.org/10.1515/BC.2008.010

Abstract

The p53 tumour suppressor gene is frequently mutated in human tumours and different tumour-derived mutations have varying effects on cells. The effect of a novel tumour-derived p53 mutation and two recently described mutations from South African breast cancer patients on the growth rate, colony formation, cell cycle arrest after irradiation and response to chemotherapeutic drugs was investigated. None of the p53 mutations had any significant effect on the inherent growth rate of the cells; however, contact inhibition of growth in two of the mutants was lost. These same two mutants formed colonies in soft agar, whereas the third mutant did not. All three of the mutants failed to show a G1 cell cycle arrest after exposure to 7 Gy of [60Co] radiation, albeit to different degrees. Cells expressing the p53 mutants were either more sensitive to cisplatin and melphalan or more resistant than the untransfected cells, depending on the mutation. However, there was no difference in response to daunorubicin treatment. These results demonstrate that different p53 mutations exert varying biological effects on normal cells, with some altering checkpoint activation more effectively than others. The data also suggest that the nature of the p53 mutation influences the sensitivity to cytostatic drugs.

Keywords: breast cancer; cell cycle; chemotherapeutic agents

About the article

Corresponding author


Received: 2007-07-04

Accepted: 2007-10-01

Published Online: 2007-12-20

Published in Print: 2008-01-01


Citation Information: Biological Chemistry, ISSN (Online) 14374315, ISSN (Print) 14316730, DOI: https://doi.org/10.1515/BC.2008.010.

Export Citation

Citing Articles

Here you can find all Crossref-listed publications in which this article is cited. If you would like to receive automatic email messages as soon as this article is cited in other publications, simply activate the “Citation Alert” on the top of this page.

[1]
Howard Donninger, Jennifer A. Clark, Megan K. Monaghan, M. Lee Schmidt, Michele Vos, and Geoffrey J. Clark
Journal of Biological Chemistry, 2014, Volume 289, Number 45, Page 31287
[2]
Claus M Schlotter, Ulf Vogt, Heike Allgayer, and Burkhard Brandt
Breast Cancer Research, 2008, Volume 10, Number 4

Comments (0)

Please log in or register to comment.
Log in