Abstract
Circulating tumoral DNA (ctDNA), commonly named “liquid biopsy”, has emerged as a new promising noninvasive tool to detect biomarker in several cancers including lung cancer. Applications involving molecular analysis of ctDNA in lung cancer have increased and encompass diagnosis, response to treatment, acquired resistance and prognosis prediction, while bypassing the problem of tumor heterogeneity. ctDNA may then help perform dynamic genetic surveillance in the era of precision medicine through indirect tumoral genomic information determination. The aims of this review were to examine the recent technical developments that allowed the detection of genetic alterations of ctDNA in lung cancer. Furthermore, we explored clinical applications in patients with lung cancer including treatment efficiency monitoring, acquired therapy resistance mechanisms and prognosis value.
Highlights
Lung cancer is the most common cause of cancer death around the world
EGFR-mutated patients can benefit from a specific first-line treatment the tyrosine kinase (TK) inhibitors (TKI) that competitively inhibits fixation of adenosine triphosphate (ATP) in the catalytic binding site of TK domain
Among the different materials derived from liquid biopsies, Circulating tumoral DNA (ctDNA) has been successfully applied to detect EGFR mutations in non-small-cell lung cancer (NSCLC) patients and can give similar molecular information as those given by invasive tumor biopsies [10] (Figure 1)
Summary
Lung cancer is the most common cause of cancer death around the world. About 80%–85% of lung cancer cases are non-small-cell lung cancer (NSCLC) patients, the remaining 15%–20% are small-cell lung cancer (SCLC) [1]. The discovery of several oncogenic driver mutations in patients with NSCLC, adenocarcinoma cases in particular, has allowed the development of personalized treatments based on these specific molecular alterations. EGFR-mutated patients can benefit from a specific first-line treatment the TK inhibitors (TKI) that competitively inhibits fixation of adenosine triphosphate (ATP) in the catalytic binding site of TK domain. The T790M mutation is present in about half of the lung cancer patients with acquired resistance, and is reported to increase the affinity of the receptor to ATP, relative to its affinity to TKIs [2]. Identification of such mutations is required to propose second-line treatment. Third-generation EGFR inhibitors, such as osimertinib, mereletinib or rociletinib, have been proposed as relevant therapeutics that could disrupt the growth of EGFR T790M-positive tumors and increase patient survival [3,4,5]
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