Article
p53 mutation in normal esophagus promotes multiple stages of carcinogenesis but is constrained by clonal competition.
Nature communications - 20 Oct 2022
Murai Kasumi, Dentro Stefan, Ong Swee Hoe, Sood Roshan, Fernandez-Antoran David, Herms Albert, Kostiou Vasiliki, Abnizova Irina, Hall Benjamin A, Gerstung Moritz, Jones Philip H
Abstract excerpt
Aging normal human oesophagus accumulates TP53 mutant clones. These are the origin of most oesophageal squamous carcinomas, in which biallelic TP53 disruption is almost universal. However, how p53 mutant clones expand and contribute to cancer development is unclear. Here we show that inducing the p53R245W mutant in single oesophageal progenitor cells in transgenic mice confers a proliferative advantage and clonal...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.
