Optimizing chemotherapy for patients with advanced non-small cell lung cancer

AbstractPlatinum-based therapy remains the standard of care for the first-line treatment of patients with advanced non-small cell lung cancer (NSCLC). When combined with a third-generation agent, platinum-based doublets improve survival compared with the third-generation agent given alone. Controversy remains, however, regarding the relative risks and benefits of the third-generation agents. Four large phase III trials have addressed this question, with only one trial finding a survival benefit in one of the treatment arms. TAX 326 compared docetaxel-based therapy with vinorelbine/cisplatin, and found that survival, response, and quality of life outcomes all favoured the docetaxel/cisplatin regimen. Consistent benefits have been reported with this regimen in other studies. The non-platinum-based docetaxel/gemcitabine combination is an alternative for patients who are not suitable candidates for platinum-based therapy. Other results have shown that single-agent docetaxel is an appropriate option for elderly patients and those with poor performance status. Overall, the wealth of data with docetaxel in advanced NSCLC suggests that it plays an important role in first-line treatment and, as a single agent, can be considered a reasonable approach in elderly and frail patients

Tivantinib added to erlotinib in nonsmallcell lung cancer: The primary end point was not MET..

D ow nloaded from 2 The transmembrane tyrosine kinase receptor Mesenchymal-Epithelial Transition (MET) factor, activated by its ligand hepatocyte growth factor (HGF), is involved in cell proliferation, survival, motility, and metastasis [1]. The MET pathway is known to crosstalk with the epidermal growth factor receptor (EGFR) and KRAS signaling pathways, which are critical in the molecular pathogenesis of many solid tumors, including non-small lung cancer (NSCLC) with intrinsic or acquired resistance to EGFR inhibitors [2]. While MET amplification is a quite uncommon event in lung cancer, MET protein overexpression has been detected, by immunohistochemistry, in 27 % to 77 % of NSCLC samples with non-squamous histology and 1 % to 57 % of NSCLC samples with squamous cell histology [1]. Tivantinib is an oral drug that binds to the dephosphorylated MET kinase [3]. Although it has shown cytotoxic activity via molecular mechanisms that are independent from its ability to bin