In 3 % to 5 % of cases, lung cancer is associated with ALK rearrangement and can therefore be targeted with the ALK inhibitors crizotinib and ceritinib. While crizotinib is the standard first-line therapy, ceritinib has gained approval for use with patients who are crizotinib-refractory. Ceritinib showed clinical activity in both crizotinib-pretreated and ALK-inhibitor-naïve patients in the single-arm, multicentre, phase II, ASCEND-2 and ASCEND-3 studies.

The basis underlying the toxicities of immune checkpoint inhibitors is their promotion of T-cell activity in a physiological manner. “The amplification of the immune system results in autoimmunity,” explained Ross Soo, MD, FRACP, National University Cancer Institute, Singapore.  Common AEs include fatigue, anorexia and arthralgia. Terms that denote immune-related adverse events (irAEs) typically end in -itis or -opathy.

here are two issues that are tied to the topic of biomarkers in immunotherapies. First, all attempts to define biomarkers have focused primarily on response as a marker of efficacy. We have to be aware, however, that immunotherapies are not targeted therapies, and fast tumor shrinkage is not necessarily observed with this kind of treatment. The efficacy of an immunotherapy is defined by long-lasting tumor stabilization.

The anti-PD-1-antibodies pembrolizumab and nivolumab have been shown to be active in lung cancer. Pembrolizumab is a high-affinity, humanised, monoclonal IgG4κ antibody against PD-1 that prevents the interaction of the receptor with PD-L1 and PD-L2. The KEYNOTE-001 trial demonstrated significant anti-tumour activity of pembrolizumab in advanced NSCLC, with improved outcomes in terms of PD-L1 Tumor Proportion Scores (TPS) ≥ 50 %.

Against the background of improved systemic therapies, there are rising expectations with regard to the potential cure of NSCLC patients who have a limited number of haematogeneous metastases. “Most studies define oligometastasis as one to three, or one to five lesions,” explained Suresh Senan, MRCP, FRCR, PhD, VU University Medical Centre, Amsterdam, The Netherlands.

The most common mechanism of acquired resistance is the T790M mutation within exon 20 of the EGFR gene (Figure 1). Indolent slow tumour growth typically occurs when this mutation emerges. “Repeated imaging may be necessary to identify progression,” explained Pasi A. Jänne, MD, PhD, Lowe Center for Thoracic Oncology, Dana Farber Cancer Institute, Boston, USA, during a symposium at the ESMO Asia Congress.

Non–small-cell lung cancer (NSCLC) with activating epidermal growth factor receptor (EGFR) mutations represents a defined molecular subset of lung cancer that can be targeted with EGFR tyrosine kinase inhibitor (TKI) therapies. Erlotinib, gefitinib and afatinib have been approved as first-line treatment options for EGFR-mutation-positive NSCLC.

My career in lung cancer care started at a time when nihilism prevailed and the standard approach in advanced disease consisted of best supportive measures. No treatments were available in which the benefits outweighed the toxicity. The arrival of chemotherapy eventually rendered improvements in survival possible; in addition, this strategy allowed for symptom relief and increases in quality of life.