Kostic and Barker (2025). Re‐evaluating Stem Cell Roles in Homeostasis and Cancer of the Esophagus. BioEssays 47(9): e70044.
Abstract:
The localization and identity of esophageal stem cells remain highly debated, prompting the emergence of several hypotheses. Although early models proposed a homogeneous basal progenitor layer, recent evidence suggests a heterogeneous pool of stem/progenitor cells with diverse phenotypic and functional characteristics. We present a perspective on this heterogeneity and its implications for both normal tissue maintenance and disease susceptibility. Esophageal cancers can emerge as a result of random mutations or the activity of cancer stem cells (CSCs). The multifaceted interactions between genetic predisposition and environmental influences demonstrate that cancer onset can be driven not only by cell phenotype but also by various external pressures. Advances in in vivo and in vitro models now offer valuable tools to explore these stem cell dynamics and may pave the way for novel therapeutic approaches in esophageal cancer treatment.
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Publisher Copyright
Funding Info:
There was no specific funding for the research done
Description:
This is the peer reviewed version of the following article: Kostic and Barker (2025). Re‐evaluating Stem Cell Roles in Homeostasis and Cancer of the Esophagus. BioEssays 47(9): e70044., which has been published in final form at https://doi.org/10.1002/bies.70044. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. This article may not be enhanced, enriched or otherwise transformed into a derivative work, without express permission from Wiley or by statutory rights under applicable legislation. Copyright notices must not be removed, obscured or modified. The article must be linked to Wiley’s version of record on Wiley Online Library and any embedding, framing or otherwise making available the article or pages thereof by third parties from platforms, services and websites other than Wiley Online Library must be prohibited.