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Wild-type p53: tumors can't stand it.

Publication ,  Journal Article
Kastan, MB
Published in: Cell
March 9, 2007

Most malignant tumors disrupt the p53 signaling pathway in order to grow and survive. Although many genes in addition to p53 are mutated in tumors, recent studies by Ventura et al. (2007) and Xue et al. (2007) suggest that restoring p53 function alone is sufficient to cause regression of several different tumor types in mice and thus might represent a potent therapeutic strategy to treat certain human cancers. Martins et al. (2006) also demonstrate that restoration of p53 activity results in tumor regression but add the sobering caveat that tumors may be able to quickly generate resistance by finding other ways to disrupt the p53 pathway.

Duke Scholars

Published In

Cell

DOI

ISSN

0092-8674

Publication Date

March 9, 2007

Volume

128

Issue

5

Start / End Page

837 / 840

Location

United States

Related Subject Headings

  • Tumor Suppressor Protein p53
  • Signal Transduction
  • Oncogenes
  • Neoplasms
  • Mice
  • Humans
  • Genes, p53
  • Developmental Biology
  • Cellular Senescence
  • Cell Transformation, Neoplastic
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Kastan, M. B. (2007). Wild-type p53: tumors can't stand it. Cell, 128(5), 837–840. https://doi.org/10.1016/j.cell.2007.02.022
Kastan, Michael B. “Wild-type p53: tumors can't stand it.Cell 128, no. 5 (March 9, 2007): 837–40. https://doi.org/10.1016/j.cell.2007.02.022.
Kastan MB. Wild-type p53: tumors can't stand it. Cell. 2007 Mar 9;128(5):837–40.
Kastan, Michael B. “Wild-type p53: tumors can't stand it.Cell, vol. 128, no. 5, Mar. 2007, pp. 837–40. Pubmed, doi:10.1016/j.cell.2007.02.022.
Kastan MB. Wild-type p53: tumors can't stand it. Cell. 2007 Mar 9;128(5):837–840.
Journal cover image

Published In

Cell

DOI

ISSN

0092-8674

Publication Date

March 9, 2007

Volume

128

Issue

5

Start / End Page

837 / 840

Location

United States

Related Subject Headings

  • Tumor Suppressor Protein p53
  • Signal Transduction
  • Oncogenes
  • Neoplasms
  • Mice
  • Humans
  • Genes, p53
  • Developmental Biology
  • Cellular Senescence
  • Cell Transformation, Neoplastic