We show that inhibition of arsenic trioxide (ATO)-mediated epidermal growth factor receptor (EGFR) activation can be used to potently sensitize diverse solid cancer types against ATO. A combination of ATO and EGFR inhibitors is a promising therapeutic strategy against various solid tumors harboring wild-type EGFR.
“In patients with non-small cell lung cancer (NSCLC), knowledge of the epidermal growth factor receptor (EGFR) mutation status is fundamental for selecting the treatment involving EGFR-tyrosine kinase inhibitors (EGFR-TKIs). Little information is available regarding the response and progression-free survival (PFS) in platinum-based chemotherapy (CT) versus EGFR-TKIs in the presence or absence of KRAS mutation, particularly in patients without EGFR mutation…”
“The clinical efficacy of tyrosine kinase inhibitors supports the dependence of distinct subsets of cancers on specific driver mutations for survival, a phenomenon called “oncogene addiction.” We demonstrate that PUMA and BIM are the key apoptotic effectors of tyrosine kinase inhibitors in breast cancers with amplification of the gene encoding human epidermal growth factor receptor 2 (HER2) and lung cancers with epidermal growth factor receptor (EGFR) mutants…”
Neutropenia (a reduction in white blood cells) is a rare, but potentially serious side effect of the cancer drug gefitinib (Iressa). Iressa is used to treat non-small cell lung cancer (NSCLC) with mutations in the EGFR gene. A patient with EGFR-mutant advanced adenocarcinoma of the lung (a type of NSCLC) was treated with Iressa. Her tumor shrank, but she experienced severe neutropenia, leaving her at risk of dangerous infections. She was switched to erlotinib (Tarceva), another EGFR inhibitor, after which her neutropenia cleared up. The patient has since continued on Tarceva without neutropenia or cancer progression for over 9 months. This case suggests that Iressa-induced neutropenia can be safely treated by switching to Tarceva, although caution should be used in drawing conclusions from a single case study.
This week, we borrow a post from the excellent website of the Global Resource for Advancing Cancer Education (GRACE). GRACE founder and president Dr. Jack West is an oncologist who treats people with lung cancer. In the video below, he discusses his evolving views on molecular testing. To see the original post, and to explore the many other resources offered by GRACE, click here.
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.