Mutations in p53 gene could lead to loss of function, negative complementation, or to gain-of-oncogenic functions, thus leading to the increase of tumorigenicity and invasiveness of cancer. This study focused on cancer-related p53 mutants, including A138T, C141Y, R158L, G245C, and R248Q. Using a modified differential display technique, response profiles of plasmid-expressed wild-type as well as mutated p53, in comparison to p53-null cells, are being established. These profiles can help our understanding of p53 involvement in cancer, leading to accurate diagnosis, treatment, and prognostic analysis by: 1) comprehensive knowledge of p53 network gene expression profiles; 2) finding the most significant gene expression profiles of p53 mutants; 3) revealing genes that only respond to p53 mutants (gain of function). Our results showed significant differences in the expression patterns among p53-null, wild-type p53, and p53 mutants A138T, C141Y, R158L, G245C, and R248Q samples. We also report here the first found p53 mutant-triggered alternative splicing.
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Document Type: Research Article
Department of Biotechnology, Institute of Medical Biology, University of Tromsø, 9037 Tromsø, Norway
Publication date: January 1, 2003
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Formerly: Oncology Research Incorporating Anti-Cancer Drug Design
Oncology Research Featuring Preclinical and Clincal Cancer Therapeutics publishes research of the highest quality that contributes to an understanding of cancer in areas of molecular biology, cell biology, biochemistry, biophysics, genetics, biology, endocrinology, and immunology, as well as studies on the mechanism of action of carcinogens and therapeutic agents, reports dealing with cancer prevention and epidemiology, and clinical trials delineating effective new therapeutic regimens.
From Volume 23, Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics is Open Access under the terms of the Creative Commons CC BY-NC-ND license.