<i>Ras<sup>V12</sup>; scrib<sup>−/−</sup></i> Tumors: A Cooperative Oncogenesis Model Fueled by Tumor/Host Interactions

The phenomenon of how oncogenes and tumor-suppressor mutations can synergize to promote tumor fitness and cancer progression can be studied in relatively simple animal model systems such as <i>Drosophila melanogaster.</i> Almost two decades after the landmark discovery of cooperative onc...

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Main Authors: Caroline Dillard, José Gerardo Teles Reis, Tor Erik Rusten
Format: Article
Language:English
Published: MDPI AG 2021-08-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/22/16/8873
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author Caroline Dillard
José Gerardo Teles Reis
Tor Erik Rusten
author_facet Caroline Dillard
José Gerardo Teles Reis
Tor Erik Rusten
author_sort Caroline Dillard
collection DOAJ
description The phenomenon of how oncogenes and tumor-suppressor mutations can synergize to promote tumor fitness and cancer progression can be studied in relatively simple animal model systems such as <i>Drosophila melanogaster.</i> Almost two decades after the landmark discovery of cooperative oncogenesis between oncogenic <i>Ras<sup>V12</sup></i> and the loss of the tumor suppressor <i>scribble</i> in flies, this and other tumor models have provided new concepts and findings in cancer biology that has remarkable parallels and relevance to human cancer. Here we review findings using the <i>Ras<sup>V12</sup>; scrib<sup>−/−</sup></i> tumor model and how it has contributed to our understanding of how these initial simple genetic insults cooperate within the tumor cell to set in motion the malignant transformation program leading to tumor growth through cell growth, cell survival and proliferation, dismantling of cell–cell interactions, degradation of basement membrane and spreading to other organs. Recent findings have demonstrated that cooperativity goes beyond cell intrinsic mechanisms as the tumor interacts with the immediate cells of the microenvironment, the immune system and systemic organs to eventually facilitate malignant progression.
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spelling doaj.art-dec4f8ba8bda4c6c8613d58e755fb0832023-11-22T08:01:53ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-08-012216887310.3390/ijms22168873<i>Ras<sup>V12</sup>; scrib<sup>−/−</sup></i> Tumors: A Cooperative Oncogenesis Model Fueled by Tumor/Host InteractionsCaroline Dillard0José Gerardo Teles Reis1Tor Erik Rusten2Centre for Cancer Cell Reprogramming, Faculty of Medicine, Institute of Clinical Medicine, University of Oslo, 0372 Oslo, NorwayCentre for Cancer Cell Reprogramming, Faculty of Medicine, Institute of Clinical Medicine, University of Oslo, 0372 Oslo, NorwayCentre for Cancer Cell Reprogramming, Faculty of Medicine, Institute of Clinical Medicine, University of Oslo, 0372 Oslo, NorwayThe phenomenon of how oncogenes and tumor-suppressor mutations can synergize to promote tumor fitness and cancer progression can be studied in relatively simple animal model systems such as <i>Drosophila melanogaster.</i> Almost two decades after the landmark discovery of cooperative oncogenesis between oncogenic <i>Ras<sup>V12</sup></i> and the loss of the tumor suppressor <i>scribble</i> in flies, this and other tumor models have provided new concepts and findings in cancer biology that has remarkable parallels and relevance to human cancer. Here we review findings using the <i>Ras<sup>V12</sup>; scrib<sup>−/−</sup></i> tumor model and how it has contributed to our understanding of how these initial simple genetic insults cooperate within the tumor cell to set in motion the malignant transformation program leading to tumor growth through cell growth, cell survival and proliferation, dismantling of cell–cell interactions, degradation of basement membrane and spreading to other organs. Recent findings have demonstrated that cooperativity goes beyond cell intrinsic mechanisms as the tumor interacts with the immediate cells of the microenvironment, the immune system and systemic organs to eventually facilitate malignant progression.https://www.mdpi.com/1422-0067/22/16/8873cold-blooded cancercooperative oncogenesistumor/stroma interactions
spellingShingle Caroline Dillard
José Gerardo Teles Reis
Tor Erik Rusten
<i>Ras<sup>V12</sup>; scrib<sup>−/−</sup></i> Tumors: A Cooperative Oncogenesis Model Fueled by Tumor/Host Interactions
International Journal of Molecular Sciences
cold-blooded cancer
cooperative oncogenesis
tumor/stroma interactions
title <i>Ras<sup>V12</sup>; scrib<sup>−/−</sup></i> Tumors: A Cooperative Oncogenesis Model Fueled by Tumor/Host Interactions
title_full <i>Ras<sup>V12</sup>; scrib<sup>−/−</sup></i> Tumors: A Cooperative Oncogenesis Model Fueled by Tumor/Host Interactions
title_fullStr <i>Ras<sup>V12</sup>; scrib<sup>−/−</sup></i> Tumors: A Cooperative Oncogenesis Model Fueled by Tumor/Host Interactions
title_full_unstemmed <i>Ras<sup>V12</sup>; scrib<sup>−/−</sup></i> Tumors: A Cooperative Oncogenesis Model Fueled by Tumor/Host Interactions
title_short <i>Ras<sup>V12</sup>; scrib<sup>−/−</sup></i> Tumors: A Cooperative Oncogenesis Model Fueled by Tumor/Host Interactions
title_sort i ras sup v12 sup scrib sup sup i tumors a cooperative oncogenesis model fueled by tumor host interactions
topic cold-blooded cancer
cooperative oncogenesis
tumor/stroma interactions
url https://www.mdpi.com/1422-0067/22/16/8873
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AT josegerardotelesreis irassupv12supscribsupsupitumorsacooperativeoncogenesismodelfueledbytumorhostinteractions
AT torerikrusten irassupv12supscribsupsupitumorsacooperativeoncogenesismodelfueledbytumorhostinteractions