Is Loss of p53 a Driver of Ductal Carcinoma In Situ Progression?

Authors

Rhiannon L Morrissey
Alastair M Thompson
Guillermina Lozano

Publication Date

11-1-2022

Journal

British Journal of Cancer

DOI

10.1038/s41416-022-01885-5

PMID

35764786

PMCID

PMC9643347

PubMedCentral® Posted Date

6-28-2022

PubMedCentral® Full Text Version

Post-print

Abstract

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.

Keywords

Animals, Mice, Humans, Carcinoma, Intraductal, Noninfiltrating, Tumor Suppressor Protein p53, Mutation, Carcinoma, Ductal, Breast, Carcinoma in Situ, Disease Progression

Published Open-Access

yes

Recommended Citation

Rhiannon L Morrissey, Alastair M Thompson, and Guillermina Lozano, "Is Loss of p53 a Driver of Ductal Carcinoma In Situ Progression?" (2022). Faculty, Staff and Student Publications. 4794.
https://digitalcommons.library.tmc.edu/uthgsbs_docs/4794