초록접수 현황
| 19F-042 | 구연 발표 |
Genetic Features of Ground-glass Opacity-type Lung Adenocarcinoma: What Causes the Invasiveness of Lung Adenocarcinoma?
Jong-Young Lee¹, Jin Young Yoo², Jun Yeun Cho³, Dohun Kim⁴
¹Institute of Genomic Health, Oneomics Co., Ltd., Seoul, Republic of Korea, ²Department of Radiology, Chungbuk National University Hospital, Chungbuk National University College of Medicine, Chungcheongbuk-do, Republic of Korea, ³Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Chungbuk National University Hospital, Chungbuk National University College of Medicine, Chungcheongbuk-do, Republic of Korea, ⁴Department of Thoracic and Cardiovascular Surgery, Chungbuk National University Hospital, Chungbuk National University College of Medicine, Chungcheongbuk-do, Republic of Korea
Purpose : The purpose of this study is to investigate the genetic features of GGO adenocarcinoma, using next-generation sequencing techniques, by comparing similarly sized solid ones.
Methods : GGO and non-GGO type lung adenocarcinoma confirmed by radiologists were collected. After a pathologist confirmed the tumor and non-tumor portions, whole-exome sequencing using genomic DNA was performed using an Illumina HiSeq 4000. The top 10 altered genes were identified in each step, and they were aligned according to the progression of the lung adenocarcinoma.
Results : In total, 20 samples (n=10 in GGO and paired normal, n=10 in non-GGO and paired normal) were analyzed. Of these, mutations were found in GGO (n=227), non-GGO (n=212), and both (n=48). Tumor mutational burden (TMB) were 8.8 in the GGO and 7.8 in the non-GGO. Mutations having clinical implications were FCGBP and SFTPA1 in the GGO, FOXQ1, IRF5, and MAGEC1 in both, and CDC27 and NOTCH4 in the non-GGO. Protein interacting network revealed that IRF5 of both group had a function of cellular response to cytokine and CDC27 of non-GGO had biologic function with the APC dependent catabolic process, cell division, and cell cycle. Mutations of EGFR and TP53 were detected but KRAS were not.
Conclusion : The GGO type lung adenocarcinoma showed higher TMB than the others. EGFR and TP53 were found but they were not predominant mutations in both group. Moreover, there were no clinically important mutations in the stage of GGO, but frequent mutations having functions related to EMT or the cell cycle were found in the common or non-GGO-specific stages.
Methods : GGO and non-GGO type lung adenocarcinoma confirmed by radiologists were collected. After a pathologist confirmed the tumor and non-tumor portions, whole-exome sequencing using genomic DNA was performed using an Illumina HiSeq 4000. The top 10 altered genes were identified in each step, and they were aligned according to the progression of the lung adenocarcinoma.
Results : In total, 20 samples (n=10 in GGO and paired normal, n=10 in non-GGO and paired normal) were analyzed. Of these, mutations were found in GGO (n=227), non-GGO (n=212), and both (n=48). Tumor mutational burden (TMB) were 8.8 in the GGO and 7.8 in the non-GGO. Mutations having clinical implications were FCGBP and SFTPA1 in the GGO, FOXQ1, IRF5, and MAGEC1 in both, and CDC27 and NOTCH4 in the non-GGO. Protein interacting network revealed that IRF5 of both group had a function of cellular response to cytokine and CDC27 of non-GGO had biologic function with the APC dependent catabolic process, cell division, and cell cycle. Mutations of EGFR and TP53 were detected but KRAS were not.
Conclusion : The GGO type lung adenocarcinoma showed higher TMB than the others. EGFR and TP53 were found but they were not predominant mutations in both group. Moreover, there were no clinically important mutations in the stage of GGO, but frequent mutations having functions related to EMT or the cell cycle were found in the common or non-GGO-specific stages.
책임저자: Dohun Kim
Department of Thoracic and Cardiovascular Surgery, Chungbuk National University Hospital, Chungbuk National University College of Medicine, Chungcheongbuk-do, Republic of Korea
발표자: Dohun Kim, E-mail : mwille@naver.com