Given the importance of EGFR signaling in lung cancer etiology, we examined the role of Drosophila gene Dachshund DACH1 expression in lung cancer development. We conclude that DACH1 binds p53 to inhibit NSCLC cellular growth.
Updated results from a clinical trial showed that patients who were treated with the drug erlotinib (Tarceva) had better quality of life than those receiving standard chemotherapy. The OPTIMAL study is a phase III clinical trial investigating erlotinib (Tarceva) as a first-line treatment for people with advanced non-small cell lung cancer (NSCLC) who have a mutation in the EGFR gene. Tarceva-treated patients scored higher on questionnaires assessing physical, social/family, emotional, and functional well-being. The updated results also confirmed that Tarceva-treated patients experienced longer periods without worsening of their cancer compared to chemotherapy-treated patients.
The OPTIMAL study found that erlotinib improved progression-free survival (PFS) versus standard chemotherapy in Chinese patients with advanced EGFR mutation-positive non-small-cell lung cancer (NSCLC). This report describes the quality of life (QoL) and updated PFS analyses from this study.
Erlotinib improves QoL compared with standard chemotherapy in the first-line treatment of patients with EGFR mutation-positive advanced NSCLC.
We summarize the literature and present an overview of the subject of less common EGFR mutations and their clinical significance, with an emphasis on EGFR TKI sensitivity or resistance.
Our aim was to investigate the presence and association of EGFR and K-Ras mutations in 50 primary NSCLC patients with a smoking history by using real-time PCR and sequencing. EGFR mutations were detected in four patients (8%). Two of these mutations were L858R mutations and the remaining two were deletion mutations spanning between codons 746 and 750. The L858R mutation was significantly associated with smoking status (P=0.003). K-Ras codon 12 and 61 mutations were also observed in four patients. However, no association was observed between K-Ras mutations and the tumor staging, gender, histology and smoking status of the patients.
PHA-E has been reported to induce cell apoptosis by blocking EGFR on lung cancer cells. It was extracted from red kidney beans. Before clinical application, PHA-E has to be proved to have better affinity to EGFR than that of EGF due to the major in vivo competitor. The study would focus on how PHA-E tightly bind to EGFR and the results would compare with that of EGF.
From the studies, we could conclude that PHA-E had better affinity to EGFR than that of the EGF. The interaction between PHA-E and EGFR could block EGF binding and then inhibit phosphorylation of EGFR on lung cancer cells. PHA-E could be developed into a new therapeutic molecule for lung cancer treatment and could be immobilized on the drug carrier as a targeting molecule to guide therapeutic particles to the tumor site.
Interstitial lung disease (ILD), especially idiopathic pulmonary fibrosis, has been shown to be associated with lung carcinogenesis. However, an association between epidermal growth factor receptor (EGFR) mutation status and preexisting ILD in patients with lung adenocarcinoma is unknown.
This study showed that patients with pulmonary adenocarcinoma and ILD had a lower probability of carrying tumor EGFR mutations.