{"@context":"https://schema.org","@type":"ScholarlyArticle","headline":"Modeling the MYC-driven normal-to-tumour switch in breast cancer","author":[{"@type":"Person","name":"Corey Lourenco"},{"@type":"Person","name":"M. Kalkat"},{"@type":"Person","name":"Kathleen E. Houlahan"},{"@type":"Person","name":"J. D. Melo"},{"@type":"Person","name":"Joseph Longo"},{"@type":"Person","name":"S. Done"},{"@type":"Person","name":"P. Boutros"},{"@type":"Person","name":"L. Penn"}],"datePublished":"2018","identifier":"https://doi.org/10.1101/380931","description":"ABSTRACT\n \n The potent MYC oncoprotein is deregulated in many human cancers, including breast carcinoma, and is associated with aggressive disease. To understand the mechanisms and vulnerabilities of MYC-driven breast cancer, we have generated an\n in vivo\n model that mimics human disease in response to MYC deregulation. MCF10A cells ectopically expressing a common breast cancer mutation in the PI3 kinase pathway (PIK3CA\n H1047R\n ) lead to the development of organized acinar structures in mice. However, expressing both PIK3CA\n H1047R\n and deregulated-MYC lead to the development of invasive ductal carcinoma, thus creating a model in which a MYC-dependent normal-to-tumour switch occurs\n in vivo\n . These MYC-driven tumors exhibit classic hallmarks of human breast cancer at both the pathological and molecular levels. Moreover, tumour growth is dependent upon sustained deregulated MYC expression, further demonstrating addiction to this potent oncogene and regulator of gene transcription. We therefore provide a MYC-dependent human model of breast cancer which can be assayed for\n in vivo\n tumour initiation, proliferation, and transformation from normal breast acini into invasive breast carcinoma. Taken together, we anticipate that this novel MYC-driven transformation model will be a useful research tool to both better understand MYC’s oncogenic function and identify therapeutic vulnerabilities.\n \n \n Conflict of interest statement\n The authors declare no potential conflicts of interest.\n ","url":"https://innscience.ca/es/community/literature/9efc7956-6238-4a4b-9c08-e2a2cad8c2dd"}