Amplification or overexpression of HER2 (ErbB2) has been identified in NSCLC, and somatic HER2 mutations occur in approximately 2 % to 4 % of patients. Response to chemotherapy is poor in the setting of HER2-mutant advanced NSCLC [3]. Similarly, single-agent pan-HER inhibitors appear to have only limited benefit, with rare and short-lived responses.
The 8th edition of the TNM classification has recently come into effect. Compared to the 7th edition published in 2009, several important adjustments have been made to lung cancer staging with the aim of improving prognostication and research. “Research is of particular significance in the context of smaller tumours that can be treated with a variety of therapeutic options,” said Ramón Rami-Porta, MD, PhD, Department of Thoracic Surgery, Hospital Universitari Mútua Terrassa, Terrassa, Barcelona, Spain.
Malignant pleural mesothelioma generally has poor patient prognosis, as it is often diagnosed at an advanced stage. The only approved regimen consists of the combination of pemetrexed and cisplatin, which gives rise to a median OS of approximately 1 year. The randomised, double-blind, placebo-controlled, phase II LUME-Meso trial tested the oral multikinase inhibitor nintedanib for treatment of mesothelioma.
When we look at immunotherapy for NSCLC, we should realize that approximately 20 % of treated patients show a response. To direct treatment to patients with a higher likelihood of response, biomarkers might be of value. One biomarker that is established in clinical practice is PD-L1 expression on the tumour, according to immunohistochemistry.
As compared to anti-PD-1 antibodies, the advantage of antibodies directed against PD-L1 is that they can inhibit PD-1/ PD-L1 interactions while leaving the PD-1/ PD-L2 pathway intact, thus potentially preserving peripheral immune homoeostasis. OAK was the first randomised phase III trial to assess an anti-PD-L1 agent in advanced NSCLC.
Compared to tissue biopsy and re-biopsy, liquid biopsy offers several advantages, including minimal-invasiveness, the opportunity for serial measurements over time to monitor tumour response, and detection of resistance mutations in the plasma prior to radiographic detection. The issue of tumour heterogeneity, which is an important factor in therapeutic failure, is also considered.
Treatment with the ALK tyrosine kinase inhibitor (TKI) crizotinib has been established as a standard first-line option in patients with ALK-rearranged advanced NSCLC. Before the advent of crizotinib, a platinum–pemetrexed doublet followed by pemetrexed maintenance was standard of care in non-squamous NSCLC. However, after an initial response to crizotinib, acquired resistance invariably develops due to multiple mechanisms, which can include secondary mutations in the ALK tyrosine kinase domain.
The irreversible ErbB family blocker afatinib and the reversible EGFR TKIs gefitinib and erlotinib have been approved as first-line therapies for treatment of NSCLC patients with EGFR-sensitising mutations. However, resistance frequently develops, which indicates the need for new agents. The EGFR T790M mutation has been identified as the most common resistance mutation.
From 4th to 7th December, 2016, the IASLC 17th World Conference on Lung Cancer (WCLC) took place in Vienna, Austria, attracting more than 6,500 participants from 93 countries. Scientific insights presented at the IASLC WCLC 2016 are summarised in this memo inOncology congress report that covers a range of topics relating to the diagnosis and treatment of lung cancer.
