<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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MDPI AG
2021-08-01
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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. |
first_indexed | 2024-03-10T08:44:20Z |
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institution | Directory Open Access Journal |
issn | 1661-6596 1422-0067 |
language | English |
last_indexed | 2024-03-10T08:44:20Z |
publishDate | 2021-08-01 |
publisher | MDPI AG |
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series | International Journal of Molecular Sciences |
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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