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It highlights critical proteins and biomechanical cues, examines interactions with immune surveillance, and quantifies cellular proportions required for EDAC efficacy. 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\n[https://doi.org/10.1007/s12672-025-03519-7](https://doi.org/10.1007/s12672-025-03519-7)  \nDiscover Oncology  \nREVIEW Open Access  \nEpithelial guardians against cancer: integrating  cell competition and extrusion in early tumor control  \nGrecia Riofrio-Chung 1 and César Rivera 1*  \n*Correspondence: César Rivera[cerivera@utalca.cl](cerivera@utalca.cl)  \n1Oral and Maxillofacial Histopathology Laboratory, Department of Stomatology, Faculty of Dentistry, Universidad de Talca, Avenida Lircay S/N, Campus Norte, Oficina N°4, Talca, Chile  \nAbstract  \nEpithelial tissues maintain homeostasis by employing sophisticated mechanisms to promote clearance of precancerous cells, thus preventing tumorigenesis. Two key processes—cell competition and extrusion—collectively termed epithelial defense against cancer (EDAC), enable normal epithelial cells to outcompete or physically expel transformed counterparts. This review integrates recent advances in EDAC, detailing critical proteins, biomechanical cues, and their interplay with immune surveillance. We quantify cellular proportions essential for EDAC efficacy and examine cancer models, focusing on pancreatic, colorectal, and mammary cancers. By linking molecular mechanisms to clinical potential, we position EDAC as a promising frontier for cancer prevention and therapy.  \nKeywords Epithelial cells, Cell competition, Cell extrusion, Tumor suppressor proteins, Neoplasms  \n1 Introduction  \nEpithelial defense against cancer (EDAC) is an emerging paradigm that describes how epithelial tissues actively prevent tumor initiation by integrating two complementary processes: cell competition and extrusion as early, strategies to eliminate transformed cells from epithelial tissues [1]. These tissues—lining organs such as the intestine, breast, and pancreas—are constantly exposed to oncogenic insults, including somatic mutations and microenvironmental stressors that threaten their structural and functional integrity [2]. To preserve homeostasis, epithelia deploy intrinsic quality-control mechanisms capable of recognizing and eliminating aberrant cells before malignant transformation occurs [3].  \nEDAC has gained attention for its role as a first-line, non-immunological barrier to tumor initiation, acting through a sequential process of fitness-based recognition (cell competition) and mechanical clearance (extrusion) coordinated by tightly regulated cell–cell interactions and biomechanical signals [3]. By coupling the recognition of oncogenic changes with directed extrusion and programmed cell death, EDAC suppresses  \n© The Author(s) 2025. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://creativecommons.org/l](http://creativecommons.org/l)icenses/by-nc-nd/4.0/.  \nRiofrio-Chung and Rivera Discover Oncology (2025) 16:1836 Page 2 of 21  \nthe clonal expansion of potentially tumorigenic cells [4]. In this review, we dissect the molecular and biomechanical underpinnings of EDAC, highlight its experimental modeling in vitro and in vivo, and ex","cbCaibZgJHkKYlL0","https://ap.wps.com/l/cbCaibZgJHkKYlL0","pdf",1511437,21,"English","# Introduction\n## EDAC and cellular competition: fundamentals and experimental models\n### Biological basis of EDAC and its relationship with cell competition","[{\"question\":\"What does epithelial defense against cancer (EDAC) consist of?\",\"answer\":\"EDAC is defined by two complementary processes: cell competition and extrusion, which collectively help epithelial tissues eliminate transformed cells early.\"},{\"question\":\"How does cell competition contribute to early tumor control?\",\"answer\":\"Cell competition relies on fitness-based recognition through short-range cell-cell interactions, where less fit or potentially oncogenic neighbors are selectively eliminated.\"},{\"question\":\"Which cancer types are discussed in the review’s EDAC models?\",\"answer\":\"The review examines cancer models focused on pancreatic, colorectal, and mammary cancers.\"}]","Epithelial guardians against cancer: integrating cell competition and extrusion in early tumor control | PDF",1790146294,53]