Epithelial-to-mesenchymal transition drives cancer genomic instability

Julienne L Carstens; Sara Lovisa

doi:10.1186/s13046-025-03402-x

Epithelial-to-mesenchymal transition drives cancer genomic instability

J Exp Clin Cancer Res. 2025 Apr 30;44(1):135. doi: 10.1186/s13046-025-03402-x.

Authors

Julienne L Carstens^{1

2

3}, Sara Lovisa^{4

5}

Affiliations

¹ Department of Medicine, Division of Hematology & Oncology, University of Alabama at Birmingham, Birmingham, AL, USA. jcarstens@uabmc.edu.
² O'Neal Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA. jcarstens@uabmc.edu.
³ Immunology Institute, University of Alabama at Birmingham, Birmingham, AL, USA. jcarstens@uabmc.edu.
⁴ Department of Biomedical Sciences, Humanitas University, 20072 Pieve Emanuele, Milan, Italy. sara.lovisa@humanitasresearch.it.
⁵ Department of Gastroenterology, IRCCS Humanitas Research Hospital, 20089 Rozzano, Milan, Italy. sara.lovisa@humanitasresearch.it.

Abstract

Epithelial-to-Mesenchymal Transition (EMT) is a form of embryonic cell plasticity reactivated in adult cells during injury and cancer. A recent study by Perelli et al. demonstrates that EMT confers an evolutionary advantage to tumors by inducing chromosomal instability, structural genomic rearrangements and chromothripsis, thus favoring the emergence of high-fitness malignant clones.

Keywords: Cancer; Cell plasticity; EMT; Epithelial-to-mesenchymal transition; Genomic instability.

MeSH terms

Animals
Epithelial-Mesenchymal Transition* / genetics
Genomic Instability*
Humans
Neoplasms* / genetics
Neoplasms* / pathology