Guide to Targeted Therapies: EGFR mutations in NSCLC 2014th Edition

Guide to Targeted Therapies: EGFR mutations in NSCLC 2014th Edition

Guide to Targeted Therapies: EGFR Mutations in NSCLC is a speedy and up-to-date review, which discusses EGFR mutations, testing methods and technology, current and emerging therapies, and resources that clinicians can provide to their patients. Busy healthcare professionals who want a quick review of EGFR gene mutations as well as a summary of current therapies will benefit from this succinct guide.

Non-small cell lung cancer (NSCLC) tumors with specific mutations in the epidermal growth factor receptor (EGFR) tyrosine kinase have been defined as ‘oncogene addicted’ to indicate their dependence on EGFR and their high susceptibility to the inhibitory effects induced by EGFR tyrosine kinase inhibitors (EGFR-TKIs; eg, gefitinib, erlotinib, afatinib). The most common EGFRmutations include a deletion in exon 19 (del E746_A750) and a point substitution in exon 21 (L858R). During the last few years, eight phase III randomized studies comparing an EGFR-TKI versus platinumbased chemotherapy demonstrated that gefitinib, erlotinib, or afatinib are superior to chemotherapy in terms of response rate, progression-free survival, quality of life, and toxicity profile only in patients harboring activating EGFRmutations. Moreover, these mutations are also prognostic of a 
relatively indolent course of disease, regardless of treatment, as compared with classical NSCLC. Although the vast majority of patients harboring EGFRmutations respond to EGFR-TKI treatment, no patient achieves a 
definitive cure and inevitably acquired resistance occurs. The aim of the present handbook is to summarize the role of EGFRmutations in NSCLC and to describe the strategies for treating patients

Lung canceris the most lethal disease in Western countries, with a case mortality rate of 85% [1] . The combination of high incidence and mortality makes lung cancer the leading cause of cancer-related deaths worldwide and it is estimated that it is responsible for more deaths than colorectal, breast, and prostate cancer combined [1] .Non-small cell lung cancer (NSCLC) accounts for 75% of all lung cancers and is divided into different subtypes (adenocarcinoma, squamous cell carcinoma, large cell carcinoma), underlying relevant biological differences (Figure 1.1). Disease stage is the most relevant factor influencing mortality. Approximately 70–80% of patients with NSCLC present with locally advanced or metastatic disease and median survival is approximately 12 months with standard chemotherapy. 
The pathogenesis of lung cancer involves the accumulation of several molecular abnormalities over time. Alterations in gene sequence or expression can occur in the cell-signaling and regulatory pathways involved in cell cycle control, apoptosis, proteasome regulation, and angiogenesis. Genetic changes include mutations, gene silencing, gene amplification or deletion, and whole chromosome gains or losses. Lung adenocarcinoma has been extensively investigated and during the last 10 years several molecular events have been discovered leading to a dramatic change in patient treatment [3–7] . Drugs targeting the tyrosine-kinase domain of the epidermal growth factor receptor (EGFR), such as gefitinib, erlotinib, or afatinib, demonstrated superiority versus standard chemotherapy in patients harboring activating EGFRmutations

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