Magali Olivier

TL;DR: It is shown that loss of transactivation capacity is a key factor for the selection of missense mutations, and that difference in mutation frequencies is closely related to nucleotide substitution rates along TP53 coding sequence, which provides new insights into the factors that shape mutation patterns and influence mutation phenotype.

TL;DR: Current knowledge on TP53 gene variations observed in human cancers and populations, and current clinical applications derived from this knowledge are summarized.

TL;DR: Recent developments of the IARC TP53 mutation dataset are described, which include restructuring of the database, which is now patient‐centered, with more detailed annotations on the patient (carcinogen exposure, virus infection, genetic background).

TL;DR: The available data suggest that p53 mutations in lung cancers can be attributed to direct DNA damage from cigarette smoke carcinogens rather than to selection of pre-existing endogenous mutations.

TL;DR: It is shown that intrinsic mutagenicity rates, loss of transactivation activities, and to a lesser extent, dominant-negative activities are the main driving forces that determine TP53 mutation patterns and influence tumor phenotype.