Is loss of p53 a driver of ductal carcinoma in situ progression?

Cet article passe en revue les données mettant en évidence la prévalence de gènes TP53 mutés dans les cellules des carcinomes canalaires in situ (DCIS), analyse la pertinence des modèles murins pour les études concernant ce type de cancer du sein et souligne la nécessité d'études fonctionnelles sur le rôle de la protéine TP53 dans le développement d'un DCIS et sa progression vers une forme invasive

Résumé en anglais

Ductal carcinoma in situ (DCIS) is a non-obligate precursor of invasive carcinoma. Multiple studies have shown that DCIS lesions typically possess a driver mutation associated with cancer development. Mutation in the TP53 tumour suppressor gene is present in 15–30% of pure DCIS lesions and in ~30% of invasive breast cancers. Mutations in TP53 are significantly associated with high-grade DCIS, the most likely form of DCIS to progress to invasive carcinoma. In this review, we summarise published evidence on the prevalence of mutant TP53 in DCIS (including all DCIS subtypes), discuss the availability of mouse models for the study of DCIS and highlight the need for functional studies of the role of TP53 in the development of DCIS and progression from DCIS to invasive disease.