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SHR Neuro Cancer Cardio Lipid Metab Microb

Houben, R; Hesbacher, S; Schmid, CP; Kauczok, CS; Flohr, U; Haferkamp, S; Müller, CS; Schrama, D; Wischhusen, J; Becker, JC.
High-level expression of wild-type p53 in melanoma cells is frequently associated with inactivity in p53 reporter gene assays.
PLoS One. 2011; 6(7):e22096-e22096 Doi: 10.1371/journal.pone.0022096 [OPEN ACCESS]
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Co-authors Med Uni Graz
Becker Jürgen Christian
Schrama David
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Abstract:
Inactivation of the p53 pathway that controls cell cycle progression, apoptosis and senescence, has been proposed to occur in virtually all human tumors and p53 is the protein most frequently mutated in human cancer. However, the mutational status of p53 in melanoma is still controversial; to clarify this notion we analysed the largest series of melanoma samples reported to date. Immunohistochemical analysis of more than 180 melanoma specimens demonstrated that high levels of p53 are expressed in the vast majority of cases. Subsequent sequencing of the p53 exons 5-8, however, revealed only in one case the presence of a mutation. Nevertheless, by means of two different p53 reporter constructs we demonstrate transcriptional inactivity of wild type p53 in 6 out of 10 melanoma cell lines; the 4 other p53 wild type melanoma cell lines exhibit p53 reporter gene activity, which can be blocked by shRNA knock down of p53. In melanomas expressing high levels of wild type p53 this tumor suppressor is frequently inactivated at transcriptional level.
Find related publications in this database (using NLM MeSH Indexing)
Base Sequence -
Cell Cycle -
Cell Line, Tumor -
DNA Mutational Analysis -
Genes, Reporter - genetics
Genetic Techniques -
Humans -
Melanoma - metabolism
Melanoma - pathology
Molecular Sequence Data -
Mutation - genetics
Skin Neoplasms - metabolism
Skin Neoplasms - pathology
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism

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