title: Resistance to Therapy.
abstract: Identification of driver mutations in adenocarcinoma of the lung has revolutionized the treatment of this disease. It is now standard of care to look for activating mutations in epidermal growth factor receptor (EGFR), and translocations in anaplastic lymphoma kinase (ALK) or ROS1 in all newly diagnosed adenocarcinoma of the lung, and in many patients with squamous cell carcinoma as well. Recognition of multiple other lung cancer driver mutations has also expanded treatment options. Targeted treatments of these mutations lead to rapid and prolonged responses, but resistance inevitably develops. Until recently, traditional chemotherapy was the only alternative at that time, but better understanding of resistance mechanisms has lead to additional therapeutic options. These mechanisms of resistance and treatments are the focus of this chapter. Understanding of mechanisms of chemotherapy resistance is touched upon, along with a brief discussion of immune checkpoint inhibitors.
authors.affiliation: Stanford University, Kaiser Permanente Fresno, Stanford, USA.
authors.forename: Gabriel
authors.initials: G
authors.lastname: Rivera
authors.affiliation: Stanford University, Stanford Cancer Institute, 875 Blake Wilbur Drive, Stanford, CA, 94305-5826, USA. hwakelee@stanford.edu.
authors.forename: Heather A
authors.initials: HA
authors.lastname: Wakelee
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy* / Q000235:genetics; D000970:Antineoplastic Agents / Q000627:therapeutic use; D019008:Drug Resistance, Neoplasm / Q000235:genetics*; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000235:genetics; D058990:Molecular Targeted Therapy / Q000379:methods / Q000639:trends
chemical_list: D000970:Antineoplastic Agents
keywords: ALK resistance; Chemotherapy resistance; EGFR resistance