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RON tyrosine kinase mutations in brain metastases from lung cancer

2018; European Respiratory Society; Volume: 4; Issue: 1 Linguagem: Inglês

10.1183/23120541.00083-2017

2312-0541

Melissa Milan, Silvia Benvenuti, Alice Maria Balderacchi, Anna Rita Virzì, Alessandra Gentile, Rebecca Senetta, Paola Cassoni, Paolo M. Comoglio, Giulia Maria Stella,

Neuroendocrine Tumor Research Advances

Brain metastases originate from cancer cells that have spread through the bloodstream and reached the brain from primary tumours in other organs. Metastatic masses are among the most common intracranial neoplasms, occurring in ∼25% of cancer patients. Most brain metastases derive from lung cancers (40–50% of cases), breast cancers (10–16%), melanoma (5–20%), kidney and ovarian cancers (5–10%) and more rarely colorectal cancers. Sometimes (5–10%) no primary site is detectable [1]. The onset of brain lesions from primary solid cancers is associated with poor prognosis with a median survival of 4–5 months [2]. Molecular mechanisms regulating metastatic spreading to the brain are largely unknown. RON (Recepteur d'Origine Nantais), also known as macrophage-stimulating receptor-1 (MSTR1) or stem cell derived tyrosine kinase (STK) in mice, belongs to the family of tyrosine kinase receptors of which MET is the prototype. It has been shown that RON regulates cellular proliferation, adhesion, motility and protection from apoptosis, all events resulting in the invasive growth genetic programme [3], which occurs in specific physiological conditions ( i.e. embryonic development) and, when aberrantly regulated, contributes to tumour onset, progression and, above all, metastatic dissemination. RON mutations might identify actionable targets in highly aggressive lung tumours