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Cell Competition in Carcinogenesis.
Madan, Esha; Palma, António M; Vudatha, Vignesh; Trevino, Jose G; Natarajan, Kedar Nath; Winn, Robert A; Won, Kyoung Jae; Graham, Trevor A; Drapkin, Ronny; McDonald, Stuart A C; Fisher, Paul B; Gogna, Rajan.
Afiliación
  • Madan E; Champalimaud Centre for the Unknown, Lisbon, Portugal.
  • Palma AM; Champalimaud Centre for the Unknown, Lisbon, Portugal.
  • Vudatha V; Department of Surgery, Virginia Commonwealth University, School of Medicine, Richmond, Virginia.
  • Trevino JG; Department of Surgery, Virginia Commonwealth University, School of Medicine, Richmond, Virginia.
  • Natarajan KN; VCU Massey Cancer Center, Virginia Commonwealth University, School of Medicine, Richmond, Virginia.
  • Winn RA; Technical University of Denmark, Kongens Lyngby, Denmark.
  • Won KJ; VCU Massey Cancer Center, Virginia Commonwealth University, School of Medicine, Richmond, Virginia.
  • Graham TA; Department of Computational Biomedicine, Cedars-Sinai Medical Center, Los Angeles, California.
  • Drapkin R; Evolution and Cancer Laboratory, Centre for Cancer Genomics and Computational Biology, Barts Cancer Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, United Kingdom.
  • McDonald SAC; Department of Obstetrics and Gynecology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
  • Fisher PB; Clonal Dynamics in Epithelia Laboratory, Centre for Cancer Genomics and Computational Biology, Barts Cancer Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square. London, United Kingdom.
  • Gogna R; VCU Massey Cancer Center, Virginia Commonwealth University, School of Medicine, Richmond, Virginia.
Cancer Res ; 82(24): 4487-4496, 2022 12 16.
Article en En | MEDLINE | ID: mdl-36214625
The majority of human cancers evolve over time through the stepwise accumulation of somatic mutations followed by clonal selection akin to Darwinian evolution. However, the in-depth mechanisms that govern clonal dynamics and selection remain elusive, particularly during the earliest stages of tissue transformation. Cell competition (CC), often referred to as 'survival of the fittest' at the cellular level, results in the elimination of less fit cells by their more fit neighbors supporting optimal organism health and function. Alternatively, CC may allow an uncontrolled expansion of super-fit cancer cells to outcompete their less fit neighbors thereby fueling tumorigenesis. Recent research discussed herein highlights the various non-cell-autonomous principles, including interclonal competition and cancer microenvironment competition supporting the ability of a tumor to progress from the initial stages to tissue colonization. In addition, we extend current insights from CC-mediated clonal interactions and selection in normal tissues to better comprehend those factors that contribute to cancer development.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Competencia Celular / Neoplasias Límite: Humans Idioma: En Revista: Cancer Res Año: 2022 Tipo del documento: Article País de afiliación: Portugal Pais de publicación: Estados Unidos
Texto completo
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Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Competencia Celular / Neoplasias Límite: Humans Idioma: En Revista: Cancer Res Año: 2022 Tipo del documento: Article País de afiliación: Portugal Pais de publicación: Estados Unidos