Metaplasia as a Precursor to Dysplasia and Cancer: Mechanisms and Screening Implications
This review examines how environmental stimuli and inflammation trigger replacement of one cell type by another, with metaplasia serving as a precursor to the dysplasia-cancer sequence in esophagus, stomach, and pancreas. The work has implications for pathology labs performing surveillance biopsies, highlighting how transcription factor signatures and epigenetic reprogramming markers could improve early detection of malignant transformation.
The original study
Metaplasia: tissue injury adaptation and a precursor to the dysplasia-cancer sequence.
- Authors
- Giroux V, Rustgi AK
- Journal
- Nature reviews. Cancer
- Type
- Journal Article, Review, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't
- PMID
- 28860646
Original abstract
Metaplasia is the replacement of one differentiated somatic cell type with another differentiated somatic cell type in the same tissue. Typically, metaplasia is triggered by environmental stimuli, which may act in concert with the deleterious effects of microorganisms and inflammation. The cell of origin for intestinal metaplasia in the oesophagus and stomach and for pancreatic acinar-ductal metaplasia has been posited through genetic mouse models and lineage tracing but has not been identified in other types of metaplasia, such as squamous metaplasia. A hallmark of metaplasia is a change in cellular identity, and this process can be regulated by transcription factors that initiate and/or maintain cellular identity, perhaps in concert with epigenetic reprogramming. Universally, metaplasia is a precursor to low-grade dysplasia, which can culminate in high-grade dysplasia and carcinoma. Improved clinical screening for and surveillance of metaplasia might lead to better prevention or early detection of dysplasia and cancer.