Literature DB >> 2005181

p53 mutations: gains or losses?

D Michalovitz1, O Halevy, M Oren.   

Abstract

Although the case for p53 as a tumor suppressor gene appears very strong, one should still keep an open eye for the possibility that mutations in p53 do not necessarily imply a mere loss of "suppressor" activity. It is still possible that the presence of a p53 mutation in a tumor contributes, in a dominant positive manner, to tumorigenesis. In other words, certain p53 mutants may well be oncogenic in their own right, and carry distinct activities that promote growth deregulation and malignant progression. Elucidating this issue also has practical implications, since the nature of the resident mutations may greatly dictate the consequences of attempts to reintroduce wild-type (wt) p53 into particular types of tumor cells. There are two major obstacles along the road to meaningful answers: the limitations of the experimental systems used for evaluating the biological activities of wt and mutant p53 and a fundamental lack of knowledge about the relevant biochemistry of the p53 protein. These two aspects constitute primary experimental challenges for investigators in the field.

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Year:  1991        PMID: 2005181     DOI: 10.1002/jcb.240450108

Source DB:  PubMed          Journal:  J Cell Biochem        ISSN: 0730-2312            Impact factor:   4.429


  31 in total

1.  Identification of a minimal transforming domain of p53: negative dominance through abrogation of sequence-specific DNA binding.

Authors:  E Shaulian; A Zauberman; D Ginsberg; M Oren
Journal:  Mol Cell Biol       Date:  1992-12       Impact factor: 4.272

2.  Simian virus 40 can overcome the antiproliferative effect of wild-type p53 in the absence of stable large T antigen-p53 binding.

Authors:  D Michael-Michalovitz; F Yehiely; E Gottlieb; M Oren
Journal:  J Virol       Date:  1991-08       Impact factor: 5.103

3.  Dominant-negative p53 mutations selected in yeast hit cancer hot spots.

Authors:  R K Brachmann; M Vidal; J D Boeke
Journal:  Proc Natl Acad Sci U S A       Date:  1996-04-30       Impact factor: 11.205

4.  Specific interaction of mutant p53 with regions of matrix attachment region DNA elements (MARs) with a high potential for base-unpairing.

Authors:  K Will; G Warnecke; L Wiesmüller; W Deppert
Journal:  Proc Natl Acad Sci U S A       Date:  1998-11-10       Impact factor: 11.205

5.  p53 regulates Ki-67 promoter activity through p53- and Sp1-dependent manner in HeLa cells.

Authors:  Mei-Juan Wang; Dong-Sheng Pei; Guo-Wei Qian; Xiao-Xing Yin; Qian Cheng; Lian-Tao Li; Hui-Zhong Li; Jun-Nian Zheng
Journal:  Tumour Biol       Date:  2011-05-25

Review 6.  Microenvironment and pathogenesis of epithelial ovarian cancer.

Authors:  Antonio F Saad; Wei Hu; Anil K Sood
Journal:  Horm Cancer       Date:  2010-12       Impact factor: 3.869

7.  Accumulation of p53 in a mutant cell line defective in the ubiquitin pathway.

Authors:  D R Chowdary; J J Dermody; K K Jha; H L Ozer
Journal:  Mol Cell Biol       Date:  1994-03       Impact factor: 4.272

8.  Transactivation of the human p53 tumor suppressor gene by c-Myc/Max contributes to elevated mutant p53 expression in some tumors.

Authors:  B Roy; J Beamon; E Balint; D Reisman
Journal:  Mol Cell Biol       Date:  1994-12       Impact factor: 4.272

9.  Mutation of p53 in primary biopsy material and cell lines from Hodgkin disease.

Authors:  R K Gupta; K Patel; W F Bodmer; J G Bodmer
Journal:  Proc Natl Acad Sci U S A       Date:  1993-04-01       Impact factor: 11.205

10.  Repression of the interleukin 6 gene promoter by p53 and the retinoblastoma susceptibility gene product.

Authors:  U Santhanam; A Ray; P B Sehgal
Journal:  Proc Natl Acad Sci U S A       Date:  1991-09-01       Impact factor: 11.205

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