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Characteristics of Genomic Alterations of Lung Adenocarcinoma in Young Never-Smokers
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A4694 - Characteristics of Genomic Alterations of Lung Adenocarcinoma in Young Never-Smokers
Author Block: W. Luo; Department of Respiratory and Critical Care Medicine, West China Hospital, Chengdu, China.
Abstract
Lung cancer is the top malignancy and a leading cause of cancer related death around the world, with non-small-cell lung cancer (NSCLC) accounting for ~85%. Multiple patient characteristics are considered to be related to the disease signature as well as the treatment outcomes (e.g., smoking status, histological subtype and age). Although genomic profiles have been revealed by large landscape characterizations mainly in Caucasians, no systematically investigation has been done in never-smoker young Asian NSCLC patients, which is considered to be a distinct subset of lung cancer. In this study, we conducted whole genome sequencing to characterize the genomic alterations of 36 never-smoker Chinese patients, who were diagnosed with lung adenocacinomas (LUADs) at 45 years or younger. Besides the well-known lung cancer genes (e.g., TP53and EGFR), our analysis also revealed several potential lung cancer associated genes that were rarely reported (e.g., HOXA4 and MST1). Lung cancer related copy number variants (e.g., EGFR and CDKN2A) were also enriched in our cohort (41.7%, 15/36). Additionally, lung cancer related structure variations (e.g., EML4-ALK, KIF5B-RET) were commonly observed (25%, 8/36), and ALK fusions were the most frequent chromosome translocations enriched in young patients. New fusion partners of ALK(SMG6-ALK)and RET(JMJD1C-RET) were identified. Importantly, our analysis revealed that young never-smoker patients with high prevalence (24/36, 66.7%) carried germline pathologic or likely pathologic alterations in cancer genesaccording ACMG classification, indicating the existence of genetic predisposition as a probable reason for their early-onset of LUADs without smoking history. Our study provides new insights into understanding the genomic landscape underlying LUADs in young never-smoker patients.
Author Block: W. Luo; Department of Respiratory and Critical Care Medicine, West China Hospital, Chengdu, China.
Abstract
Lung cancer is the top malignancy and a leading cause of cancer related death around the world, with non-small-cell lung cancer (NSCLC) accounting for ~85%. Multiple patient characteristics are considered to be related to the disease signature as well as the treatment outcomes (e.g., smoking status, histological subtype and age). Although genomic profiles have been revealed by large landscape characterizations mainly in Caucasians, no systematically investigation has been done in never-smoker young Asian NSCLC patients, which is considered to be a distinct subset of lung cancer. In this study, we conducted whole genome sequencing to characterize the genomic alterations of 36 never-smoker Chinese patients, who were diagnosed with lung adenocacinomas (LUADs) at 45 years or younger. Besides the well-known lung cancer genes (e.g., TP53and EGFR), our analysis also revealed several potential lung cancer associated genes that were rarely reported (e.g., HOXA4 and MST1). Lung cancer related copy number variants (e.g., EGFR and CDKN2A) were also enriched in our cohort (41.7%, 15/36). Additionally, lung cancer related structure variations (e.g., EML4-ALK, KIF5B-RET) were commonly observed (25%, 8/36), and ALK fusions were the most frequent chromosome translocations enriched in young patients. New fusion partners of ALK(SMG6-ALK)and RET(JMJD1C-RET) were identified. Importantly, our analysis revealed that young never-smoker patients with high prevalence (24/36, 66.7%) carried germline pathologic or likely pathologic alterations in cancer genesaccording ACMG classification, indicating the existence of genetic predisposition as a probable reason for their early-onset of LUADs without smoking history. Our study provides new insights into understanding the genomic landscape underlying LUADs in young never-smoker patients.
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