Ockham’s razor for the MET-driven invasive growth linking idiopathic pulmonary fibrosis and cancer

Journal of Translational Medicine

Review

Silvia Benvenuti¹  Alessandra Gentile¹  Melissa Milan¹  Alice Balderacchi²  Federica Meloni³  Giulia M. Stella⁴ 

[1] Experimental Clinical Molecular Oncology (ECMO), IRCCS Candiolo Cancer Institute-FPO, Candiolo, 20060, Turin, Italy;Investigational Clinical Oncology (INCO), IRCCS Candiolo Cancer Institute-FPO, Candiolo, 20060, Turin, Italy;Pneumology Unit, Cardiothoracic and Vascular Department, IRCCS Policlinico San Matteo Foundation and University of Pavia Medical School, Piazzale Golgi 19, 27100, Pavia, Italy;Pneumology Unit, Cardiothoracic and Vascular Department, IRCCS Policlinico San Matteo Foundation and University of Pavia Medical School, Piazzale Golgi 19, 27100, Pavia, Italy;Investigational Clinical Oncology (INCO), IRCCS Candiolo Cancer Institute-FPO, Candiolo, 20060, Turin, Italy;

关键词: Cancer;    Idiopathic pulmonary fibrosis;    Invasive growth;    Epithelial-to-mesenchymal transition;    Precision medicine;   

DOI  :  10.1186/s12967-016-1008-4

 received in 2016-07-13, accepted in 2016-08-16,  发布年份 2016

来源: Springer

【 摘 要 】

BackgroundIdiopathic pulmonary fibrosis (IPF) identifies a specific lung disorder characterized by chronic, progressive fibrosing interstitial pneumonia of unknown etiology, which lacks effective treatment. According to the current pathogenic perspective, the aberrant proliferative events in IPF resemble those occurring during malignant transformation.Main bodyReceptor tyrosine kinases (RTK) are known to be key players in cancer onset and progression. It has been demonstrated that RTK expression is sometimes also altered and even druggable in IPF. One example of an RTK—the MET proto-oncogene—is a key regulator of invasive growth. This physiological genetic program supports embryonic development and post-natal organ regeneration, as well as cooperating in the evolution of cancer metastasis when aberrantly activated. Growing evidence sustains that MET activation may collaborate in maintaining tissue plasticity and the regenerative potential that characterizes IPF.ConclusionThe present work aims to elucidate—by applying the logic of simplicity—the bio-molecular mechanisms involved in MET activation in IPF. This clarification is crucial to accurately design MET blockade strategies within a fully personalized approach to IPF.

【 授权许可】

CC BY   
© The Author(s) 2016