Multicenter Phase I/II Study of Cetuximab With Paclitaxel and Carboplatin in Untreated Patients With Stage IV Non–Small-Cell Lung Cancer

Abstract

The combination of cetuximab, paclitaxel, and carboplatin was safe and well tolerated in this population of stage IV patients. The response rate, time to progression, and median survival were slightly superior to historical controls treated with paclitaxel and carboplatin alone. A randomized phase II trial has completed accrual.

Outcomes of Patients with Advanced Non-Small Cell Lung Cancer Treated in a Phase I Clinic

“…The median PFS interval in our study was 2.8 months, similar to previously reported data [37]. However, some studies of less heavily pretreated or treatment-naïve patients with NSCLC reported better outcomes, with median PFS times of 4 -5 months [32,38]. In advanced/metastatic NSCLC, the median OS time on first-line therapy rarely exceeds 11 months and the median PFS duration is usually around 5 months [39 -42].…”

Molecular mechanisms of resistance to the EGFR monoclonal antibody cetuximab

“…A series of phase II trials suggested the benefit of cetuximab in combination with platinum doubles in the first-line treatment setting. [113][114][115][116][117] [77][78][79][80] M225 has slightly more effective anti-EGFR activity than M528, which is in turn more effective than M579. The phase I trial with M225 was successful, but all patients produced human-anti-mouse antibodies (HAMA).…”

Amphiregulin Confers Regulatory T Cell Suppressive Function and Tumor Invasion via the EGFR/GSK-3β/Foxp3 Axis

“…Importantly, the majority of human epithelial cancers are marked by functional activation of growth factors and receptors of the EGFR. Targeting the EGFR is currently available for the treatment of different types of epithelial cancers, such as non-small-cell lung cancer, squamous cell carcinoma of the head and neck, colorectal cancer, and pancreatic cancer (3)(4)(5)(6). The treatment demonstrated that EGFR inhibitors bind to the extracellular domain of the EGFR when it is in the inactive configuration, compete for receptor binding by occluding the ligand-binding region, and thereby directly block ligand-induced EGFR tyrosine kinase activation on cancer cells (7,8).…”