title: Systemic treatment in EGFR-ALK NSCLC patients: second line therapy and beyond.
abstract: Lung cancer is the most frequently diagnosed cancer and a leading cause of cancer mortality worldwide, with adenocarcinoma being the most common histological subtype. Deeper understanding of the pathobiology of non-small cell lung cancer (NSCLC) has led to the development of small molecules that target genetic mutations known to play critical roles in progression to metastatic disease and to influence response to targeted therapies. The principle goal of precision medicine is to define those patient populations most likely to respond to targeted therapies. However, the cancer genome landscape is composed of relatively few "mountains" [representing the most commonly mutated genes like KRAS, epidermal growth factor (EGFR), and anaplastic lymphoma kinase (ALK)] and a vast number of "hills" (representing low frequency but potentially actionable mutations). Low-frequency lesions that affect a druggable gene product allow a relatively small population of cancer patients for targeted therapy to be selected.
authors.affiliation: 1 Translational Research Unit, Dr Rosell Oncology Institute, Quirón Dexeus University Hospital, 08028 Barcelona, Spain ; 2 Cancer Biology and Precision Medicine Program, Catalan Institute of Oncology, Hospital Germans Trias i Pujol, Ctra Canyet s/n, 08916 Badalona, Barcelona, Spain ; 3 Fundación Molecular Oncology Research (MORe), Sabino Arana 5-19, 08028 Barcelona, Spain.
authors.forename: Niki
authors.initials: N
authors.lastname: Karachaliou
authors.affiliation: 1 Translational Research Unit, Dr Rosell Oncology Institute, Quirón Dexeus University Hospital, 08028 Barcelona, Spain ; 2 Cancer Biology and Precision Medicine Program, Catalan Institute of Oncology, Hospital Germans Trias i Pujol, Ctra Canyet s/n, 08916 Badalona, Barcelona, Spain ; 3 Fundación Molecular Oncology Research (MORe), Sabino Arana 5-19, 08028 Barcelona, Spain.
authors.forename: Rafael
authors.initials: R
authors.lastname: Rosell
keywords: Lung cancer; TKI resistance; anaplastic lymphoma kinase fusions (ALK fusions); epidermal growth factor (EGFR); tyrosine kinase inhibitors (TKIs)