Carcinoma initiation via RB tumor suppressor inactivation: a versatile approach to epithelial subtype-dependent cancer initiation in diverse tissues.

Carcinomas arise in a complex microenvironment consisting of multiple distinct epithelial lineages surrounded by a variety of stromal cell types. Understanding cancer etiologies requires evaluating the relationship among cell types during disease initiation and through progression. Genetically engin...

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Autores principales:	Yurong Song, Debra Gilbert, T Norene O'Sullivan, Chunyu Yang, Wenqi Pan, Alisan Fathalizadeh, Lucy Lu, Diana C Haines, Philip L Martin, Terry Van Dyke
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f8f8cf11eed944918839ab4509abf069
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spelling	oai:doaj.org-article:f8f8cf11eed944918839ab4509abf0692021-11-18T08:44:01ZCarcinoma initiation via RB tumor suppressor inactivation: a versatile approach to epithelial subtype-dependent cancer initiation in diverse tissues.1932-620310.1371/journal.pone.0080459https://doaj.org/article/f8f8cf11eed944918839ab4509abf0692013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24312475/?tool=EBIhttps://doaj.org/toc/1932-6203Carcinomas arise in a complex microenvironment consisting of multiple distinct epithelial lineages surrounded by a variety of stromal cell types. Understanding cancer etiologies requires evaluating the relationship among cell types during disease initiation and through progression. Genetically engineered mouse (GEM) models facilitate the prospective examination of early oncogenic events, which is not possible in humans. Since most solid tumors harbor aberrations in the RB network, we developed an inducible GEM approach for the establishment and assessment of carcinoma initiation in a diverse range of epithelial tissues and subtypes upon inactivation of RB-mediated tumor suppression (RB-TS). The system allows independent assessment of epithelial subtypes that express either cytokeratins (K) 18 or 19. By Cre-dependent expression of a protein that dominantly inactivates RB and functionally redundant proteins p107 and p130, neoplasia could be initiated in either K18 or K19 expressing cells of numerous tissues. By design, because only a single pathway aberration was engineered, carcinomas developed stochastically only after long latency. Hence, this system, which allows for directed cell type-specific carcinoma initiation, facilitates further definition of events that can progress neoplasms to aggressive cancers via engineered, carcinogen-induced and/or spontaneous evolution.Yurong SongDebra GilbertT Norene O'SullivanChunyu YangWenqi PanAlisan FathalizadehLucy LuDiana C HainesPhilip L MartinTerry Van DykePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 12, p e80459 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yurong Song Debra Gilbert T Norene O'Sullivan Chunyu Yang Wenqi Pan Alisan Fathalizadeh Lucy Lu Diana C Haines Philip L Martin Terry Van Dyke Carcinoma initiation via RB tumor suppressor inactivation: a versatile approach to epithelial subtype-dependent cancer initiation in diverse tissues.
description	Carcinomas arise in a complex microenvironment consisting of multiple distinct epithelial lineages surrounded by a variety of stromal cell types. Understanding cancer etiologies requires evaluating the relationship among cell types during disease initiation and through progression. Genetically engineered mouse (GEM) models facilitate the prospective examination of early oncogenic events, which is not possible in humans. Since most solid tumors harbor aberrations in the RB network, we developed an inducible GEM approach for the establishment and assessment of carcinoma initiation in a diverse range of epithelial tissues and subtypes upon inactivation of RB-mediated tumor suppression (RB-TS). The system allows independent assessment of epithelial subtypes that express either cytokeratins (K) 18 or 19. By Cre-dependent expression of a protein that dominantly inactivates RB and functionally redundant proteins p107 and p130, neoplasia could be initiated in either K18 or K19 expressing cells of numerous tissues. By design, because only a single pathway aberration was engineered, carcinomas developed stochastically only after long latency. Hence, this system, which allows for directed cell type-specific carcinoma initiation, facilitates further definition of events that can progress neoplasms to aggressive cancers via engineered, carcinogen-induced and/or spontaneous evolution.
format	article
author	Yurong Song Debra Gilbert T Norene O'Sullivan Chunyu Yang Wenqi Pan Alisan Fathalizadeh Lucy Lu Diana C Haines Philip L Martin Terry Van Dyke
author_facet	Yurong Song Debra Gilbert T Norene O'Sullivan Chunyu Yang Wenqi Pan Alisan Fathalizadeh Lucy Lu Diana C Haines Philip L Martin Terry Van Dyke
author_sort	Yurong Song
title	Carcinoma initiation via RB tumor suppressor inactivation: a versatile approach to epithelial subtype-dependent cancer initiation in diverse tissues.
title_short	Carcinoma initiation via RB tumor suppressor inactivation: a versatile approach to epithelial subtype-dependent cancer initiation in diverse tissues.
title_full	Carcinoma initiation via RB tumor suppressor inactivation: a versatile approach to epithelial subtype-dependent cancer initiation in diverse tissues.
title_fullStr	Carcinoma initiation via RB tumor suppressor inactivation: a versatile approach to epithelial subtype-dependent cancer initiation in diverse tissues.
title_full_unstemmed	Carcinoma initiation via RB tumor suppressor inactivation: a versatile approach to epithelial subtype-dependent cancer initiation in diverse tissues.
title_sort	carcinoma initiation via rb tumor suppressor inactivation: a versatile approach to epithelial subtype-dependent cancer initiation in diverse tissues.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/f8f8cf11eed944918839ab4509abf069
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Carcinoma initiation via RB tumor suppressor inactivation: a versatile approach to epithelial subtype-dependent cancer initiation in diverse tissues.

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