Abstract
BackgroundLung adenocarcinoma in young adults is a rare entity with the oncogenic genetic alterations associated being poorly understood. In the present study, the effect of genetic alterations in lung adenocarcinoma patients diagnosed in young patients is reported.MethodsTwenty young lung adenocarcinoma patients (age years: median: 33.5, range: 24‐36) were enrolled in the current study and 24 patients who were at common age of the disease onset (age years: median: 61.5, range: 52‐79) were selected for comparison. Paraffin sections of lung adenocarcinoma were analyzed using the whole‐exome sequencing platform.ResultsSimilar number of somatic mutations per tumor were found in the young patients and their older counterparts. Although no age‐related differences were detected in the numbers of lung adenocarcinoma patients harboring well‐known gene variants, mutations in FRG1 and KMT2C were associated with a younger age especially after correcting for tobacco smoking and sex (FRG1: P = 0.027, KMT2C: P = 0.046). Five genetic variants showed higher alteration frequencies in young patients compared to the unclassified East Asian population, suggesting these mutations as disease‐related hereditary germline variants.ConclusionsThese results suggest different characteristics of lung adenocarcinoma between the young and the patients at common age of onset. Young patients with lung adenocarcinoma have a distinctly unique prevalence of oncogenic genetic alterations.
Highlights
Non–small‐cell lung cancer (NSCLC) is widely understood as its heterogeneity, from the profile of both its clinical characteristics and geneticmakeup.[1]
Twenty East Asian young adult patients who had lung cancer diagnosed as adenocarcinoma before 36 years of age were enrolled in the current study
We established that genetic variants associated with lung adenocarcinoma differed between patients diagnosed when young or diagnosed at the common age of onset
Summary
Non–small‐cell lung cancer (NSCLC) is widely understood as its heterogeneity, from the profile of both its clinical characteristics and geneticmakeup.[1] Molecularly targeted therapy has largely revolutionized the treatment of NSCLC in genomically defined subsets of patients.[2] The identification of specific types of EGFR mutation and ALK fusions classically confer sensitivity to matched therapies and implies a significant survival benefit from approved targeted agents.[3,4] In comprehensive genomic profiling analysis, driver genetic alterations have been identified in approximately 50% of lung adenocarcinomas, including variants in EGFR, KRAS, BRAF, HER2, RET, and ROS1.2,5-7. Genetic variants fundamentally associated with a younger age at diagnosis were further investigated with other confounding factors in order to establish more clinically meaningful interpretations
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