Afatinib Demonstrates Activity in EGFR Mutation-positive NSCLC

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Afatinib may demonstrate clinical activity in patients with EGFR mutation-positive non-small cell lung cancer and brain metastasis.
Afatinib may demonstrate clinical activity in patients with EGFR mutation-positive non-small cell lung cancer and brain metastasis.

Afatinib may demonstrate clinical activity in patients with epidermal growth factor receptor (EGFR) mutation-positive non-small cell lung cancer (NSCLC) and asymptomatic brain metastasis, according to a study published in the Journal of Thoracic Oncology.

Researchers led by Martin Schuler, MD, of the University Duisburg-Essen in Germany looked at results of a phase 3 study of afatinib or cisplatin plus pemetrexed in patients with metastatic lung adenocarcinoma with EGFR mutations (LUX-Lung 3) as well as a randomized, open-label phase 3 study of BIBW 2992 vs chemotherapy as first-line treatment for patients with stage 3B or 4 adenocarcinoma of the lung with EGFR-activating mutation (LUX-Lung 6).

In both studies, prespecific subgroup analyses were conducted for progression-free survival, overall survival, and objective response rate in patients with asymptomatic brain metastases at baseline.

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The researchers noted a trend toward improved progression-free survival with afatinib compared to chemotherapy in both studies among patients with brain metastases, with a similar magnitude in progression-free survival improvement with afatinib among patients without brain metastases.

Upon combined analysis, progression-free survival was significantly improved with afatinib compared with chemotherapy in patients with brain metastases. Afatinib was also found to improve objective response rate compared to chemotherapy in these patients.

Reference

  1. Schuler M, Wu Y, Hirsh V, et al. First-line afatinib versus chemotherapy in patients with non-small cell lung cancer and common epidermal growth factor receptor gene mutations and brain metastases [published online ahead of print January 24, 2016]. J Thorac Oncol. doi: http://dx.doi.org/10.1016/j.jtho.2015.11.014.

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