AI Summary & Key Takeaways
AI InsightThis article will be useful for researchers in this field and will help them choose a model that serves their ideas and contributes to the development of appropriate treatments and understanding of changes in the c-ROS1 oncogene.
📌 3 Key Takeaways
Abstract
The rearrangement of ROS proto-oncogene 1 (ROS1, a receptor tyrosine kinase) was first detected in glioblastoma, then recognised in non-small cell lung cancer (NSCLC) in 2007. These alterations generate fusion proteins, which constitutively activate the kinase domain of ROS1 and hence promote cell prolif eration. NSCLC is the most common type of lung cancer, accounting for approximately 85% of all cases. It is also a very aggressive form of the disease. It is distinguished by genetic differences that affect its biological behaviour and present diverse pathological features. In addition, ROS1 fusions are linked to sensitivity to tyrosine kinase inhibitors, such as crizotinib, which have "off-target" activity against ROS1. Creating new Pre-clinical models, both in vivo and in vitro, that use gene editing and cutting-edge cell culture methods has a huge potential to help make tyrosine kinase inhibitors that are more effective and can target groups of tumours cells that are resistant. Our review focuses on Pre-clinical models developed to date, both in vivo and in vitro, for ROS1+NSCLC and examines their strengths and limitations. This article will be useful for researchers in this field and will help them choose a model that serves their ideas and contributes to the development of appropriate treatments and understanding of changes in the c-ROS1 oncogene.